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image: Robin Zielinski, AP
photograph 1 of 3Pictured is a screenshot taken from the lapel digicam pictures of Las Cruces, N.M. Police branch Officer Johnathan Boehne as he elements his his gun at suspect Juan Gabriel Torres on SUNday, Aug. 21, on the Lohman Avenue overpass in Las Cruces. Officers were dominated justified within the deadly capturing of Torres. programs in Houston and Santa Fe may well be fashions for the way area law enforcement groups reply to crises sparked with the aid of americans whose moves are determined as much through mental disease and substance abuse as willful defiance of the law. (Robin Zielinski/The Las Cruces solar-information via AP) less Pictured is a screenshot taken from the lapel digital camera photos of Las Cruces, N.M. Police branch Officer Johnathan Boehne as he points his his gun at suspect Juan Gabriel Torres on SUNday, Aug. 21, on the ... more image: Robin Zielinski, AP
image 2 of 3In a Saturday, June 24, 2017 picture, Maggie Calderon, Juan Gabriel Torres' ex-girlfriend and mother of his little ones, Juan Gabriel Torres Jr., core, Breeana Torres, heritage, and Jerry Torres no longer pictured, accumulate collectively for the birthday of Juan Gabriel Torres, on the Lohman Avenue bridge where they made a memorial. The 36-year-ancient Torres changed into fatally shot with the aid of LCPD officers SUNday, Aug. 21, 2016, on Lohman Avenue after allegedly committing a theft and stealing a pickup truck past in the day. programs in Houston and Santa Fe may well be models for a way area legislations enforcement corporations reply to crises sparked by americans whose movements are determined as much by using mental disease and substance abuse as willful defiance of the legislations. (Robin Zielinski/The Las Cruces SUN-information by the use of AP) less In a Saturday, June 24, 2017 photo, Maggie Calderon, Juan Gabriel Torres' ex-female friend and mom of his toddlers, Juan Gabriel Torres Jr., middle, Breeana Torres, history, and Jerry Torres not pictured, ... greater photo: Robin Zielinski, AP
image three of threeIn a June 24, 2017 picture, Maggie Calderon, Juan Gabriel Torres' ex-female friend and mother of his infants, Juan Gabriel Torres Jr., Breeana Torres, and Jerry Torres wear black t-shirts in reminiscence of their loved one. TThe 36-yr-ancient Torres changed into fatally shot by means of LCPD officers SUNday, Aug. 21, 2016, on Lohman Avenue after allegedly committing a theft and stealing a pickup truck prior in the day. courses in Houston and Santa Fe may be fashions for the way area legislations enforcement agencies reply to crises sparked by way of people whose moves are determined as an awful lot by mental illness and substance abuse as willful defiance of the law. (Robin Zielinski/Las Cruces SUN-information by way of AP) much less In a June 24, 2017 photograph, Maggie Calderon, Juan Gabriel Torres' ex-female friend and mother of his babies, Juan Gabriel Torres Jr., Breeana Torres, and Jerry Torres wear black t-shirts in memory of their cherished ... more image: Robin Zielinski, AP
Police look for more desirable methods to contend with individuals in disaster
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LAS CRUCES, N.M. (AP) — Juan Gabriel Torres twice drank a beer in entrance of police officers while in possession of a knife in 2016. the first time, he changed into arrested. The next time, he become shot useless.
the primary, in April, looked as if it would had been a cry for assist. Torres talked about he changed into hooked on methamphetamine and wanted to move back to detention center to get clean, a police record mentioned. The 2nd time, in August, he abandoned a stolen pickup truck within the core of a busy overpass and was armed with a big searching knife when he appeared to lunge at officers.
Torres, reportedly clinically determined with schizophrenia and bipolar disease, spent the remaining years of his existence in and out of reformatory and reformatory for crimes often tied to addiction and intellectual ailment.
And now his three babies are with no father.
"I hope he changed into nevertheless right here so he could see the kids, be there for them, see them develop up. It hurts, it hurts my coronary heart," pointed out Maggie Calderon, Torres' ex-female friend and the mom of his little ones.
In June, Calderon and the three children visited the bridge where Torres became fatally shot to commemorate what would were his 37th birthday.
"I should face the proven fact that he's long past," Calderon said. ". I just at all times had that hope in my heart that he could be here for them."
The district attorney decided the deadly police taking pictures of Torres on Aug. 21, 2016, changed into justified. but might it had been averted? programs in Houston and Santa Fe can be models for the way area legislation enforcement organizations reply to crises sparked by people whose actions are determined as a good deal by means of mental affliction and substance abuse as willful defiance of the legislations.
The system of care designed to help individuals dealing with mental fitness concerns in Doña Ana County and New Mexico has taken many hits in contemporary years — most primarily in mid-2013 when Gov. Susana Martinez's administration iced over Medicaid payments to fifteen community mental fitness and dependancy care suppliers throughout New Mexico, including four that provided features in Doña Ana County, over allegations of fraud.
The allegations were answered in 2016 when the attorney regularly occurring found no sample of wrongdoing or fraud in any of the corporations.
The funding freeze caused chaos for health workers and heaps of sufferers in Doña Ana County alike. The equipment has not yet recovered.
in the meantime, law enforcement is increasingly filling the societal want of dealing with individuals in crisis, an evaluation of 911 name information indicates.
The year after Martinez's Medicaid freeze, calls to 911 for behavioral health-linked issues or suicidal ideations rose in Doña Ana County — and the number of calls climbed once more in 2015 and 2016.
Such emergency calls to the Mesilla Valley Regional Dispatch Authority hit a six-year high in 2016 — with a total of 5,771, a rise of pretty much 20 p.c for the reason that 2011.
those calls place a heavy burden on law enforcement officers and other first responders. They tie up time and elements. First responders are not always trained or outfitted to take care of such situations. And by the point society's infrastructure to help americans in disaster has failed, and officers with weapons face people in disaster, all of their lives, and people of any one else nearby, may also be in danger.
it truly is what happened the day Torres died.
He changed into purported to be in the back of bars, however miscommunication between the court and penal complex allowed him to bond out days past. Then, on a SUNday afternoon when people in Doña Ana County have been mourning a police officer who had been shot and killed days previous, Torres performed a violent crime spree that resulted in the center of the Lohman Avenue bridge over Interstate 25. He became armed and shirtless.
Police video suggests him taking a swig from the beer bottle while an officer commanded him to drop his knife. Seconds later, Torres lunged and two Las Cruces police officers fired seven times.
A troubled lifestyles
via dozens of pages of police reports and courtroom filings, a portrait emerges of Torres as a man who did not stay away from quandary or get manage of his addictions, even though he every now and then expressed a want to get clear.
Between 1999 and 2016, he turned into jailed 17 instances on the Doña Ana County Detention middle, served seven stints in state prison, and violated parole/probation nine instances, statistics demonstrate.
As a self-proclaimed gang member who went by means of the nickname "Chucky," he also had at the least 22 encounters with Las Cruces police between 2003 and 2016 earlier than the bridge shooting, in keeping with police reviews.
His first prison conviction got here in March 2002, at age 21, when he pleaded no contest to aggravated battery in opposition t a family member. Then in 2004 he led Las Cruces police on a vehicle and foot chase following an assault name. Torres, in 2005, pleaded no contest to 10 costs after that incident and acquired a in part suspended sentence and probation.
A judge revoked his probation in November 2006, and he served two years in detention center. He became launched in January 2008 and out handiest five months before being accused of violently beating his then-girlfriend (not Calderon). He was charged with kidnapping and battery.
That lady friend instructed police that a drunken Torres — who became nevertheless on supervised probation — all started punching her while she changed into drowsing on June 21, 2008. She yelled to awaken others, she advised police. Torres pinned her and punched her many times within the face and head, she stated. She lost awareness.
She woke up later in a "pool of blood on the mattress," she noted. She walked into a bathroom and Torres attacked her once more.
He pulled her by way of her hair into the bedroom, she informed police, "where he threw her on the bed and started to punch her and knee her once more," based on the document. She talked about she woke up round 10 a.m. the subsequent morning. Torres changed into long past.
A decide authorised a warrant for Torres' arrest three days later, court statistics show. but he wasn't arrested if so unless about 9 months later, in February 2009. Months after that, in August 2009, he pleaded no contest to the expenses.
Torres became sentenced to practically 15 years in prison but ordered to serve only four years, adopted by two years of parole and five years of probation, in response to sentencing documents signed by then-judge Stephen Bridgforth.
With credit for good time, Torres become launched from penitentiary in June 2011 — on his 31st birthday — after serving below two years. He became to serve 5 years of probation.
He did not have to any extent further crook issues unless 2013, at which time he begun racking up probation violations and biking out and in of detention center and prison for the final three years of his lifestyles.
Torres served about four months in jail in 2013 for a probation violation earlier than being launched in October. here month he verified wonderful for meth and opioids and admitted to drug use, in accordance with a petition to revoke his probation that became later disregarded via prosecutors.
That become the yr Martinez's administration iced up funding to the 15 behavioral health suppliers — a circulate that eventually left many prone residents without functions.
it's doubtful if Torres, whose intellectual state gave the impression to be deteriorating, independently sought remedy right through that point. despite the fact, the Parole Board sanctioned Torres and ordered that he effectively complete a medication software in Silver metropolis.
That certainly not came about.
Torres did not document to the Yucca hotel Chemical Dependency medicine core on Dec. 31, 2013 and once again on Jan. 1, 2014, according to a report by means of Parole-Probation Officer Jacob Martinez.
Torres advised Martinez on Jan. 1, 2014 that he turned into on the brink of relapse, the record stated. Martinez arranged for Torres to be picked up by using police and taken to reformatory for an overnight stay.
the following day, when Torres mentioned to the workplace, he pointed out "he become having bad nervousness" and didn't wish to go to Yucca hotel for remedy "because he felt unsafe." He referred to he concept a person became following him and two vehicles had been circling his house the old evening. Martinez described Torres as "anxious and intensely paranoid."
A counselor determined Torres' "intellectual state became not strong" enough to participate within the application at Yucca inn and provided other alternatives, however Torres refused each and every one, in accordance with Martinez's report. as an alternative, Torres pleaded to move to penitentiary as a result of, Martinez's file cited, "he felt superior in a controlled ambiance and would understand how to deal with himself improved."
Torres could not face up to using illegal drugs and become refusing help, Martinez wrote, so he turned into an unsuitable candidate for probation. He informed Torres be incarcerated so he could "take part in the many healing procedures and agencies which are offered in the New Mexico branch of Corrections reformatory device and with a bit of luck he'll learn to make greater choices."
Torres changed into in jail from Jan. 30, 2014, until June 29, 2015.
a typical difficulty
it be no longer unusual for people like Torres to become in jail or reformatory. A 2006 look at via the U.S. Bureau of Justice information found that an estimated 56 percent of state prisoners, forty five % of federal prisoners and sixty four percent of jail inmates nationwide have a intellectual health situation.
In Doña Ana County, about 40 p.c of inmates at the county penal complex acquired treatment for intellectual fitness circumstances in 2016, in accordance with the Doña Ana wellbeing Institute and Stepping Up Partnership, a group of judicial, clinical, legislations enforcement and group stakeholders who work collaboratively to assist individuals with mental fitness disease reside out of reformatory.
"In my 19-12 months profession in law enforcement with LCPD, we've got at all times (encountered) a big variety of individuals that had been dealing with mental crisis," LCPD Deputy Chief Justin Dunivan stated.
Dunivan, who represents LCPD on the wellbeing initiative, pointed out the department has been tackling the concern head-on through crisis intervention practicing and community partnerships.
"We at the moment are doing a far better job, in my view, of working collectively not most effective with legislation enforcement and the clinical box but inside the community to are trying to assist cut back these numbers," he observed.
As of October, 73 % of commissioned officers at LCPD had been certified in disaster intervention working towards, based on spokesman Dan Trujillo. Cadets had been required seeing that 2010 to earn such certification right through LCPD's academy through finishing forty hours of coaching. The eventual aim is practicing for all officers, Dunivan referred to.
Between 2006 and 2016, LCPD officers spoke back to 2,274 calls involving mentally unwell americans, in response to department figures. They additionally replied to three,182 incidents involving americans with suicidal ideations and a pair of,841 incidents involving people who were taken into protecting custody in that eleven-12 months duration.
For Dunivan, the keys questions are: "How will we try to reduce these numbers, and the way can we get these individuals the applicable medication that they need?"
Torres became out of jail for under 10 days in June 2015 earlier than police encountered him again. He referred to as 911 to file that he became being adopted. When police confirmed up, he fled right into a lodge in Las Cruces and tried to barricade himself in a bathroom. "supply me a gun so i can shoot myself," he told officers, based on a police report.
LCPD officers used a Taser to subdue him so that they could take him to MountainView Regional scientific core for evaluation, according to a police file.
Torres become again on the streets below a week later. He known as 911 from quite a few locations, claiming he was being adopted, according to one more file. Officers considered charging him with making false reports, however later learned that he was "bipolar and schizophrenic" and had been currently discharged from Mesilla Valley medical institution, the record cited.
coping with such instances can tax law enforcement resources. by means of legislations, officers taking individuals into protective custody have to accompany them to the hospital and wait via their facet except they're admitted into an emergency room. That may mean an officer is sitting on the sanatorium for any place from one to 5 hours, or once in a while longer, Dunivan pointed out.
Detective Robyn Gojkovich of the Doña Ana County Sheriff's branch, which has been grappling with a deputy shortage for years, stated such calls take resources faraway from different cases.
"We produce other crimes we ought to investigate, and instead we're helping these families out, because who else can they flip to? each person else has really shut the door," Gojkovich stated.
Dunivan spoke of the system must be greater to shorten clinic waits because, "in the end, that grownup needs medical medicine." he is now looking to the Houston Police branch for a likely answer.
About 10 years in the past, Houston established the nation's first intellectual health division in a law enforcement company, beneath the path of then Commander Mike Lee.
The Houston mannequin has groups of officers educated in crisis intervention and intellectual health care workers who respond to calls involving individuals in disaster. Houston police also rolled out a new diversion drop-off facility about 10 years ago. or not it's a place officers can take mentally ill offenders as a substitute of detention center, Lee talked about.
"It begun this huge cultural alternate, and alter in the way of considering for officers of the way to cope with people who're committing offenses or appearing out because of affliction and never as a result of illegal activity," Lee talked about. today, he oversees the newly created mental health & detention center Diversion Bureau on the Houston-enviornment Harris County Sheriff's office, the place he is an enormous.
As a part of their reforms, Houston police additionally streamlined the method of transporting mentally sick people to hospitals. What once took seven pages of forms and needed to be notarized by a judge is now a one-web page kind, Lee pointed out.
"Now, the officer can quit the person rapidly to the group of workers and assist them get treated very right away," he stated. "We a took a technique that become taking 4 to 6 hours of frustration to the officers, buyers and hospitals and became that into a technique that became taking half an hour."
Breaking the Cycle
by way of the conclusion of July 2015, Torres turned into again in detention center after he turned into discovered at a gas station beneath the have an effect on of a synthetic cannabinoid. He changed into launched on April 25, 2016.
He become on the streets for less than in the future.
this is when LCPD Officer Alejandro Rodriguez encountered Torres standing subsequent to his cruiser holding a beer backyard a Las Cruces comfort store. in the report detailing the incident, Rodriguez wrote that Torres refused instructions to step far from the vehicle and taunted him.
Torres chugged the beer and tossed it in a trash can, the document stated. He then advanced on Rodriguez, performing "excessive on whatever or just incredibly intoxicated" and requested the officer what he would do if he shoplifted beer or pulled out the knife that turned into in his pocket. several times, Rodriguez requested Torres to walk away, however Torres didn't.
Rodriguez called for backup. He and Sgt. Feliciano Garcia discovered a handmade shank in Torres' pocket throughout a pat-down search.
Torres informed Rodriguez he wanted to move again to detention center because "he had just gotten out of penal complex and acquired automatically hooked on meth," Rodriguez wrote within the document. Torres believed reformatory "become going to be his means far from it," the document brought up.
Torres received his desire. He walked into the neighborhood comfort shop, grabbed a 24-ounce can of beer, left devoid of paying for it and drank it in entrance of the officers, who then arrested him. He later advised LCPD he planned to make use of the shank "as a tactic to go lower back to detention center."
penitentiary information show Torres become booked into the county prison that evening on expenses of public intoxication, shoplifting, carrying a deadly weapon and assault on a peace officer. He become launched inside two days.
A month later, on might also 29, 2016, he turned into arrested yet once again — this time on expenses of shoplifting alcohol and ingesting in public. His probation changed into revoked. That incident set in action activities that would eventually end with his loss of life.
Some people like Torres combat with lifestyles outdoor the structure of incarceration.
in response to Dunivan, the Doña Ana well being Institute is working to retain people like Torres, who are in disaster, from reoffending by means of improving existing materials, such as capabilities to assist with re-entering society, and developing a complete behavioral health disaster response equipment.
but budget friendly housing, transportation and jobs are also crucial to in the reduction of recidivism, he said.
Calderon, Torres' ex-girlfriend, cautioned that Torres had trouble finding solid housing and protecting on suitable of his medicines when he became now not at the back of bars.
"He changed into on remedy when he obtained out of prison. He instructed me they'd gave him a bunch of medication," she pointed out. "but when his mom kicks him out on the street and he has nowhere to head, where is he going to refill his prescription? How is he going to get anywhere however running right here and there? Of path you're going to be depressed. And if you don't take your medication, it does mess along with your head."
In fiscal 12 months 2011, three,440 inmates had been launched from the brand new Mexico branch of Corrections, based on a 2012 legislative file. inside three years of liberate, forty six percent had been back in jail. within five years it become 53 p.c.
"or not it's paramount if we are looking to smash this cyclical sample — not just selected to individuals if they have a mental fitness crisis but when they have a drug addiction — they ought to have housing, they should have transportation, they must have a job to combine again into society to become a productive member," Dunivan pointed out. regrettably, he talked about, discovering funding for such resources is a problem.
Dunivan is trying to find options in other courses, like Houston's, that have been a success in helping police departments tackle behavioral health considerations. a further program he's discovering is Santa Fe's LEAD (legislations Enforcement Assisted Diversion) software, which is in accordance with a application that bought its delivery in Seattle.
LEAD, which Santa Fe began in 2014, is a pre-arrest diversion software for individuals who have, as "the foundation explanation for their crook activity," an opiate dependancy, stated Santa Fe's LEAD software manager Shelly Moeller.
in its place of going through the cycle of arrest, incarceration and prosecution, offenders are diverted into closely case-managed medication programs and capabilities to help with their addictions, Moeller spoke of.
Santa Fe applied the program in accordance with a spike in property crimes dedicated via americans hooked on heroin and other opiates, mentioned Jerome Sanchez, the previous property crimes sergeant for the Santa Fe Police branch who co-chaired the task drive that created the LEAD software. In an interview, he described discovering that the difficulty "wasn't for a scarcity of law enforcement effort," however as an alternative because of addiction.
"every single person we have been running into on the streets is hooked on heroin. there's no longer a single grownup — no longer one — that we have now interviewed that has no longer been addicted," Sanchez, who is now a consultant for LEAD, recalled telling the police chief.
In Las Cruces, property crimes declined through about 5 % in 2016, based on data launched this year with the aid of the FBI. besides the fact that children, drug offenses expanded by way of about 15 % in 2016, according to LCPD facts.
Moeller talked about she has been in discussions with LCPD and Doña Ana County's fitness and Human features department, amongst others, about establishing a LEAD application in Las Cruces. She mentioned the stakeholders are planning to host their first meeting before the end of the yr.
The LEAD program in Santa Fe starts at the first contact with legislation enforcement, Moeller mentioned. Officers are knowledgeable to establish abilities candidates for the application and ask them to take part.
From there, a case manager is called to the scene to supply "damage reduction" schooling, which emphasizes secure drug use. "Upon first contact with a shopper, case managers supply overdose prevention education and make sure the client has Narcan and entry to clean syringes and other harm reduction features," Moeller referred to. From there, members start individualized treatment plans and set dreams.
capabilities shoppers who don't conform to participate are arrested and charged for his or her alleged crimes. but that is rare, Moeller referred to. Out of about one hundred fifty referrals, only two were arrested because they declined to be a part of the application.
Sanchez spoke of one of the vital greatest challenges in Santa Fe become getting officers on board.
"it's very complex for officers to take note and to wrap their heads around now not arresting people because it's not something that they're used to," he referred to.
nonetheless, Sanchez noted the program has been successful. She recalled its 2nd customer, who got here in barefoot. "I literally failed to feel she would final except the conclusion of the day, and that i truthfully thought she would be lifeless," Sanchez recalled. these days, he said, that client "has completely changed her lifestyles. She's not homeless, she's working, she self-assisting herself and thoroughly functioning."
a different customer, Sanchez mentioned, had been to nine treatment facilities and never had any success before LEAD. "She's additionally absolutely turned round her life and we're even on account that hiring her," he pointed out.
Moeller said LEAD fees about $650,000 to function per 12 months. it is partly funded by means of the metropolis of Santa Fe, with assist from gives you and reimbursements from Medicaid and the U.S. branch of Housing and concrete construction.
according to the LEAD web site, a price-advantage evaluation conducted in 2013 of one hundred people arrested by using Santa Fe police for opiate possession or income published a price of greater than $4 million between 2010 and 2012, or a regular of $forty two,000 per particular person, for incarceration. The projected can charge of a LEAD customer, by contrast, was estimated at $34,000 per individual over a total of three years.
An mistaken release
No such program existed in Las Cruces to present Torres when he turned into arrested in may also 2016 for shoplifting alcohol and ingesting in public. as a substitute, in June of ultimate year, a petition become filed to revoke his probation. He remained at the county detention center, held on a $5,000 secured bond, unless he seemed before judge Douglas Driggers in third Judicial District court on Aug. eleven.
"The petition to revoke probation includes four separate allegations that you violated your probation," Driggers advised Torres, according to a recording of the listening to obtained with the aid of the SUN-information. "As to the allegations contained during this petition . do you admit or deny?"
"I admit the allegations," Torres pointed out.
"The court will accept your admission and hereby revokes your probation," Driggers responded.
before he become sentenced, Torres stated he desired to "thank the court docket for enabling me the chance" to be unsatisfactorily discharged from probation. He changed into sentenced to 12 months and 290 days in prison, the steadiness of his customary 14-12 months time period from the 2008 kidnapping case.
Torres should still have been transported after that from the county reformatory to the state jail device.
Torres wouldn't have been allowed to publish bond. but this is what happened. He turned into released Aug. 12, 2016, the day after the listening to before Driggers, when the Socorro-primarily based precedence 1 Bailbonds Inc. bought dollars to pay the $5,000 bond. The bond had remained in impact despite the fact that Driggers sentenced Torres to detention center.
The mix-up is some thing Driggers stated he had under no circumstances before seen take place before in his 14 years on the bench.
"The jail is to dangle the defendant unless he is transported to the Corrections department to serve his time," Driggers referred to in an interview. but during this case, after Torres become sentenced to jail but earlier than Driggers' order turned into filed, Torres posted bond, in keeping with Driggers. He blamed "a lack of communication between the court and the jail" for enabling Torres to get out.
To make sure an incorrect release does not occur again, Driggers talked about he'll subject a separate detention order in future cases to require that a defendant continue to be in custody "in order that there is never a misstep."
Driggers spoke of he believes the error would had been at last caught after Torres bonded out, and a warrant would had been issued for his arrest. but that hadn't yet came about nine days after Torres' release — when he caught the consideration of police for the closing time on Aug. 21, 2016.
The remaining come upon
It was a somber SUNday as hundreds of mourners, together with rankings of police officers, gathered on the Pan American middle to bid farewell to Officer José Israel Chavez of the Hatch Police branch. Chavez had been shot and killed by means of an armed fugitive on Aug. 12.
in the meantime, police say Torres stole a white Chevrolet pickup from an 86-yr-old man round 3 p.m. near the intersection of Lohman Avenue and Solano power, west of the Lohman bridge over Interstate 25. quickly after, officers spotted and pursued the pickup near the intersection of Lohman and Foothills highway, on the other side of the Lohman bridge. They stopped the pursuit because of heavy traffic.
round four:30 p.m., police saw the pickup drive previous the preliminary crime scene, back on the west side of the Lohman bridge.
Sgt. Michael Henke and Officers Johnathan Boehne and Christopher Gamez followed the pickup east towards the bridge, however they again broke off the pursuit near Walton Boulevard because of heavy site visitors.
under a minute later, officers caught up with the pickup. It became abandoned on Lohman, in the eastbound lanes above the interstate. Torres turned into walking away from the truck, armed with a huge searching knife and carrying a bottle of beer.
A 26-2nd video recorded by way of Boehne's lapel digicam captured the encounter. Boehne swerved round site visitors to get to the deserted pickup. He stopped at the back of an extra patrol unit, stepped out and drew his firearm as he spotted Torres approach a blue Chrysler sedan. in line with police, Torres tried to open the door to the motor vehicle, which was occupied by way of a man and his 10-year son, but couldn't because it was locked.
Boehne's video indicates the blue sedan slowly using away while Torres walked west, took a swig from the beer bottle and held the knife. Boehne yelled:
"Drop the knife! Get out of ways! Drop the knife! Drop the knife, now! Drop the knife. Drop the knife! Put it on the floor! Drop the knife!"
Torres gestured at Boehne and noted anything because the officer issued two final instructions. Then he gave the impression to lunge toward Boehne. besides the fact that children the video cuts off at that aspect, LCPD referred to Boehne and Henke fired their weapons, excellent Torres seven instances.
The bullets ended a lifestyles affected by substance abuse, intellectual disease and many years in incarceration.
a number of weeks later, the district lawyer decided that the shooting became justified under New Mexico legislations, clearing Henke and Boehne of any wrongdoing.
LCPD has declined to talk about the capturing, citing pending litigation. less than a month after the taking pictures, an lawyer representing Torres' household, Gary Mitchell of Ruidoso, sent a tort notice to the metropolis in quest of damages for what he known as Torres' wrongful death. Mitchell has now not returned calls seeking touch upon the ligation.
Torres left at the back of a grieving family unit.
"here is the place the daddy of my youngsters, Gabe Torres, received shot and died," Calderon spoke of while going for walks over the Lohman bridge in June, when she and her children marked Torres' birthday at the spot where he died.
"Ever since then, or not it's been definitely complicated for the youngsters — and for me as a mother to see my children hurt," Calderon observed.
She spoke as passing motors honked at the family. That introduced back painful reminiscences of a candlelight vigil the household held in 2016, soon after Torres' demise. during that gathering, Calderon recalled that motorists honked and a few yelled issues like, "He deserved it; go to hell."
Calderon pointed out she desires americans can be extra sympathetic to households in such situations.
"no person knows what he was going through," she talked about. "All they understand is that, oh, he had a knife. He has tattoos. He has a bottle of beer, and truly they labeled him. and that's what people do — is choose individuals."
This story is a component of a collaboration between NMPolitics.web, the Las Cruces solar-news and KRWG news, supported in part through the Fund for Investigative Journalism, to determine southern New Mexico's struggling behavioral health gadget.
Saturday, March 30, 2013 | 2 a.m.SUN.com/media/img/photos/2013/03/29/Stoker_t198.jpg?cdfb4b79ec677a25380d4d2ab25aad58f36db2ce" alt="Click to enlarge photo"/>
Gordon Stoker, longtime lead tenor for the famed Elvis Presley backup group the Jordanaires, talked about the king of rock 'n’ roll once instructed him and the other members of the gospel concord quartet something that in fact bowled over them, however also licensed their price to him.
"We were all sitting around consuming hamburgers (at 1 a.m. right through the late Nineteen Sixties) and he (Presley) simply looked at us and noted, 'If there hadn't been the Jordanaires, there likely shouldn't have been a me,’” Stoker informed the Las Vegas solar in a 1999 interview while behind the curtain on the Gold Coast lodge, getting ready for a tribute show to Patsy Cline.
"He observed, 'You guys took an interest in me once I did not wish to checklist. You took an interest in me when the cloth was horrific.’ He had a word for the material: crap," Stoker stated, noting that the hit “caught on You” turned into one in all Elvis’ least favorites.
however Stoker spoke of Presley, ever the professional, nonetheless went into the studio with the Jordanaires at his aspect for 15 years and, with out complaining, recorded a lot of songs — the basically first rate ones and the in reality bad ones.
Stoker, who together with the Jordanaires performed Las Vegas continuously over the last 4 many years and changed into elected to the nation music and Gospel song Halls of repute, died Wednesday at his home in Brentwood, Tenn. He changed into 88.
A memorial provider is scheduled for Saturday at 2 p.m. at Christ Presbyterian Church, 2323 historical Hickory Boulevard in Nashville.
Stoker’s voice may also be heard on Presley’s “Viva Las Vegas,” “Hound Dog,” "it be Now or on no account," "Are You Lonesome Tonight?" and “Teddy undergo," among others. within the Nineteen Fifties and '60s, Stoker appeared in movies with Presley, together with "King Creole," "G.I. Blues" and "girls! ladies! girls!"
Stoker and the other Jordanaires can also be heard on Cline’s "crazy," "I Fall to pieces" and "candy desires"; Ricky Nelson’s "traveling Man," “Lonesome town” and "howdy Mary Lou”; Jimmy Dean’s “huge dangerous John”; Johnny Horton’s “The fight of new Orleans”; Tammy Wynette’s “Stand by Your Man”; and Kenny Rogers’ ”Lucille.”
Stoker additionally provided heritage vocals for Sissy Spacek within the 1980 movie concerning the existence and tune of Loretta Lynn, "Coal Miner's Daughter."
among the many estimated 2,500 stars that Stoker and the different Jordanaires backed up as studio vocalists had been Loretta Lynn, Roy Orbison, Vince Gill, Jimmy Buffett, Ringo Starr, Johnny cash, Chicago and Dolly Parton.
Stoker recalled that while Presley’s early-morning hamburger-chomping confession become an exquisite endorsement, he bought one that was just as excellent and just as profitable a few years later from the Beatles’ Paul McCartney.
"He (Paul) talked about, 'When (the Beatles) listened to Elvis' statistics, once we listened to Ricky Nelson's facts, we under no circumstances listened to Elvis or Ricky, we listened to what you guys did, the oohs and ahhs,’” Stoker instructed the SUN. “'We learned to sing harmony by using taking note of (the Jordanaires).’”
although members of the Jordanaires changed through the years, the lineup that become elected to the nation tune hall of reputation in 2001 changed into Stoker, 2d tenor Neal Matthews (who died in 2000), baritone Hoyt Hawkins and bass singer Ray Walker. also in 2001, the group was elected to the gospel tune shrine.
Stoker and the community carried out with Elvis on the Ed Sullivan tv demonstrate in 1957, won a 1964 Grammy for most useful Gospel Recording and carried out for President Gerald Ford at the White condominium in the mid-Nineteen Seventies.
Stoker and the Jordanaires, although, did not function with Presley when he opened his list-surroundings engagement on the hotel international (now LVH) in 1969 as a result of that they had too many studio recording responsibilities in Nashville at the time. The Imperials have been brought in to change the Jordanaires for these Las Vegas shows.
When Presley died in 1977, Stoker and the Jordanaires recorded tribute albums to him.
Born Aug. three, 1924, in Gleason, Tenn., Stoker all started playing piano at age 8. Seven years later, he turned into playing professionally. He joined the John Daniel Quartet after high school and went into the Air drive in 1943.
Stoker joined the Jordanaires in 1950, two years after they had been formed in Missouri, replacing normal pianist Bob cash. He quickly grew to be the longtime lead vocalist.
The Jordanaires caught Presley’s attention in the mid-1950s while they have been performing as backup to Eddy Arnold on the Grand Ole Opry in Nashville.
In an undated interview, Stoker stated he not ever had aspirations of being a celeb himself — singing within the historical past changed into his area within the song world.
"A record producer (as soon as) told us to neglect about the hit parade," Stoker referred to. “(He talked about) stars are right here nowadays and gone day after today. The trade wants decent backup singers. We did not feel he turned into telling the certainty, but, boy, become he ever. For 23 years we had two to 4 periods a day, six days per week."
Stoker is survived by means of wife, Jean Stoker, sons Alan and Brent, daughter Venita, 5 grandchildren and one remarkable grandchild.
Ed Koch is a former longtime solar reporter.
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mother Nature have to be a Lehigh Valley high college soccer fan. just in time for the start of the season, the old gal is providing us a perfect nighttime to kick issues off — sunny skies, now not too sizzling, no longer too bloodless, simply appropriate.
So, right here we go together with the start of an extra scholastic soccer season, and it’s whatever thing like my 35th or thirty sixth here at the Morning call youngsters I did cowl a game or two in 1979 as a newly-employed part-timer at the backside of the totem pole. however considering that 1982, it’s been a large a part of my fall Friday nights.
in fact, excessive school football has always been part of my existence. My father played at Allentown excessive in the late Fifties and our household all the time went to video games when i was a kid.
Going to a game become the only solution to spend a Friday night, however I at all times lamented the proven fact that I couldn’t watch the Brady Bunch or The Partridge family unit, that have been Friday evening tv staples when i used to be a child.
And so it has persisted to be part of my pursuits all through my skilled life.
Do i like excessive college soccer? honestly, i can’t say i like it improved than basketball or anything I do, but there’s nevertheless something special about a Friday nighttime at these stadiums.
If it wasn’t for always being concerned in regards to the cut-off dates, and with all of the offense during this era the games remaining longer than ever, I’d savour it a lot more.
however listed below are 10 things I truly like about it:
10. The groups operating out of the locker room and on to the field. It’s not just like the NFL the place the starters are introduced personally. i like how everyone huddles up and runs out together.
9. The game classes. different sports don’t produce game courses with the frequency of football. i love the schools who put now not most effective rosters in their programs, but additionally all-time information and if there’s ample sponsors, i love how some faculties highlight their different fall programs in the ebook.
8. The cheerleaders.They work hard, they’re athletic and that they work in unison very smartly. terrific choreography with some of these routines. pleased they now have a chance to show off their competencies in various competitions.
7. The refreshment stand. Some are greater than others. Some knock it out of the park with pizza, pierogies, pulled pork, sausage sandwiches, french fries, and many others. Me, I’m just content material with a few scorching canines. but a pretty good refreshment stadium with volunteers working complicated at the back of the scenes is all the time liked.
6. The ticket agents and ticket takers. no one looks ahead to it more than my friend Andy Weaver at Nazareth and he picks his Blue Eagles to win forty four-21 tonight, incidentally. however commonly, this neighborhood gives you carrier with a smile and is satisfied to support you probably have any questions.
5. The pupil sections. i like their theme nights and the style they coordinate their cheers and apparel. Nothing promotes faculty spirit improved than a robust pupil area. sometimes, they ought to be told to preserve it clean and not disparage the different college, however many of the time, they’re high-quality and an asset to the scene.
4. The special nights that are sometimes linked to high college football, whether it’s a adolescence evening, a hall of repute induction ceremony, a unique tribute or a Homecoming. It’s all good stuff.
3. The marching bands. Love the marching bands and if you’ve read me at everywhere the years, you understand i really like Liberty’s Grenadier Band most of all. however Easton, Freedom and Stroudsburg, among others, are all very first rate. Hoping to peer greater of what the Colonial League has to offer this year.
2. the manner everyone stands up for the national Anthem and a few coaches even make sure their children are lined up a undeniable solution to salute the flag. i am completely satisfied that there isn't any controversy about this at this stage and there shouldn’t be.
1. The No. 1 aspect i love about excessive college soccer is that for a couple of hours it brings communities collectively and unifies us. For just a few hours, we’re no longer Democrat or Republican, Liberal or Conservative, Trump-hater or Trump-lover, and we’re not concerned about ethnic backgrounds or religions. We’re Huskies or Vikings or Canaries or Bulldogs or Spartans or Pirates or Rovers or Hurricanes or Patriots or Roughies or Konkrete children or Zephyrs or ... smartly, you get the graphic. high college soccer is among the fantastic things that carry us collectively for a few hours on a Friday nighttime and during this extraordinarily divisive and troubled world we reside in, we definitely might use more solidarity.
Now on to the primary Groller’s nook proper 10 (a quick edition this week).
6. Bethlehem Catholic
8. Southern Lehigh
9. Notre Dame
10. Chicago, the band, no longer the Cubs or White Sox, Bears or Bulls and so forth. . What a beautiful exhibit they put on at Musikfest a few weeks ago. It become some of the highlights of my summer time and brought again the soundtrack of my adolescence for a couple of hours.
April Gamiz /The Morning call
The Seventies band, Chicago, become staggering at Musikfest on Aug. 5.
The Nineteen Seventies band, Chicago, became incredible at Musikfest on Aug. 5. (April Gamiz /The Morning name)
Now on to the Week 1 picks
Parkland 56, Allen 14 — The Canaries are doubtless pleased the agenda alterations subsequent year and that they don’t have to open the season this way.
Emmaus 49, Dieruff 20 — identical goes for the Huskies.
Easton 34, Stroudsburg 14 — New teaching era starts for red Rovers, however with the equal tradition of excellence.
Whitehall 55, PM East 20 — Rob Melosky will make the Cardinals more suitable. It’ll just take time.
Nazareth 42, gratifying Valley 27 — may still be probably the most wonderful video games of the evening with loads of playmakers on either side.
Becahi 40, PM West 20 — The Golden Hawks seem poised for an additional deep state playoff run, however the Panthers are greater than they’ve been.
Northampton 34, ES North 14 — Some k-youngsters americans have counseled their soccer group goes to the EPC North in place of both Becahi or CCHS. They may change their intellect after seeing how long this shuttle to Pike County takes them.
Liberty 28, ES South 20 — The large question right here is whether or not or not Ed Chrsitian may be cleared in time from his concussion protocol to be capable of be on the sidelines for the Cavaliers tonight and what stands out as the delivery of his 37th season in cost.
Freedom 33, CCHS 21 — The Vikings have a lot of new faces. it could possibly make the effort for every little thing to come back to come back together because it did closing year.
Notre Dame 35, Palisades 21 — They can also rating in different ways, however the Crusaders and Pirates should be established guests to the conclusion zone tonight.
Northwestern 27, Palmerton 13 — anticipating decent things out of the Tigers this season. The Blue Bombers pin their hopes on playmaking knowledge of quarterback Tekoah Guedes, a transfer from Northern Lehigh.
Southern Lehigh forty one, Northern Lehigh 21 — The Spartans comprehend they’re already in the district match. but is that this the 12 months they get that first district championship?
Saucon Valley 28, Bangor 14 — Defending league champs know how to combat off challenges and the enhanced Slaters are going to provide them one.
Catasauqua 34, Salisbury 21 — The focus has been on improving the tough Riders protection and taking probably the most drive off the high-flying offense. We’ll see how that’s understanding here.
Pen Argyl 35, Wilson 7 — My first seek advice from to “The Hill” for a game comes Saturday afternoon. Can’t wait to look what it feels like with americans within the stands. also, can’t wait to look Logan Sterner and Job Goodman running round.
Keith Groller / The Morning name
The soccer stadium on the hill in Pen Argyl presents one of the vital excellent views in the Lehigh Valley
The football stadium on the hill in Pen Argyl presents one of the most excellent views in the Lehigh Valley (Keith Groller / The Morning call)
Marian Catholic 21, Fairfield 14 — Pat Morgans takes over the Colts. He performed for Stan Dakosty, who retired after going 310-152-three in 40 seasons. So, expect the Marian program to stay powerful.
Lehighton 28, Fleetwood 7 — Cody Scherer’s return at QB boosts the Indians.
Schuylkill Haven 33, Jim Thorpe 13 — Justin St. Hill is a returning 1,000-yard rusher for the Olympians however Haven will likely have too tons.
Tamaqua 34, Minersville 14 — Thad Zuber, Nick Breiner and Nate Boyle are all playmakers for the Blue Raiders.
Quakertown 30, CB East 20 — The Panthers have come a protracted means given that going 1-10 in 2012. They have been 6-6 remaining yr, however return a lot of pleasant youngsters.
Pennridge 42, Norristown 14 — The Rams, like the Panthers have been 6-6 in 2016, however have excessive hopes of doing much enhanced.
higher Perk 21, Kutztown 14 — The Indians have been rising on account that going 0-10 in 2012. They want to build on their 5-win season in 2016.
adequate, that’s it. It doesn’t matter where you go, simply go to a video game and luxuriate in the exquisite atmosphere that excessive school soccer has to present.
If the Schuylkill League’s soccer coaches were “stars” on the ancient television game exhibit “in shape video game,” it would be easy to be a contestant.
Their solutions are all the equal.
Ask to speak about the title chase in Division I, all six coaches answered with “dogfight,” “battle,” “challenge,” and “tough.”
“There’s on no account per week off,” a couple of coaches said.
“Any team in Division I may fall on the properly,” two coaches noted.
This season, which you can’t fault them.
because the Schuylkill League starts its 2d season, the race for the Division I championship is as balanced as ever.
Pottsville captured the inaugural Schuylkill League Division I title closing season, working the table with a 5-0 record that protected two wins with the aid of 10 aspects or much less and several come-from-at the back of victories.
Which group emerges as the Division I champion this season? right here’s a look on the scorching topics in the Schuylkill League this season:
video game breakers
What makes the Division I race so balanced is that each of the six teams has at least one player who can single-handedly win a game by means of himself:
• All-State tight conclusion Ian Renninger and running lower back Ian Murhon return for the defending champion Crimson Tide. Renninger, who had 24 receptions for 425 yards and four TDs, is also a drive defensively from his shielding handle spot.
• powerful-armed quarterback David Krewson and working again Ben Kramer are again for Blue Mountain, which has the biggest holes to change, having misplaced 23 seniors to graduation. Krewson threw for 782 yards and 7 TDs after taking over the beginning job in Week four final season, whereas Kramer rushed for 617 yards and six rankings.
• Quarterback Doug Weist threw for 1,070 yards final season for North Schuylkill. quickly running again Mitch Wagner also returns for the Spartans.
• At Tamaqua, quarterback Thad Zuber (1,278 passing yards, eleven TDs) and running backs Nick Breiner (861 yards, 15 TDs) and Nate Boyle (584 yards, 5 TD) return to steer the Blue Raiders’ offense.
• Jim Thorpe is boosted by way of the return of junior tailback Justin St. Hill, who rushed for 1,093 yards and 15 TDs.
“Justin is an excellent athlete,” Jim Thorpe educate Mark Rosenberger spoke of. “He has amazing imaginative and prescient, tremendous cutting capacity, outstanding velocity, and for a small child he packs a lot of punch. He’s no longer afraid to reduce his shoulder and try to run someone over. together with his pace, the large play possibility is there as well. We’re excited what Justin is going to provide our offense this 12 months.”
Cody Scherer returns for Lehighton after missing the last three-plus video games with a damaged leg. Scherer become 2d within the area in passing yards with 1,340 a 12 months ago.
The Schuylkill League also noticed a bevy of huge-time soccer players graduate to the faculty ranks.
Eric Wapinsky, Darion Jacoby and Chase Alisauckas of Pottsville; Connor Kerstetter, Erech Noecker, Alex Zimmerman, Danny Greenawalt and Vinny Bobbin of Blue Mountain; essential Jordan, Richie Zahodnick and Bobby Wagner of North Schuylkill; Mike Mayernik and Gavin Zehner of Lehighton; Danny Lozada, Mike Kalyan, Matt Kalyan and Preston Gehring of Schuylkill Haven; Ethan Kuczynski of Marian; and Noah Allegretta of Shenandoah Valley have been family names over the last few seasons. additionally gone is Minersville operating again Kei’dre Taylor, who moved.
Their departures have left their respective groups scrambling for replacements.
The Schuylkill League has three new head coaches this season, with one being a very everyday face.
Former Pottsville train Kevin Keating takes over at Shenandoah Valley (see story, page 13), whereas Pat Morgans replaces legendary head educate Stan Dakosty at Marian and Scott expense takes manage at Panther Valley.
Dakosty coached the Colts for forty seasons, compiling a 310-152-three checklist. Morgans performed for and coached under Dakosty.
“I’m excited,” Morgans pointed out. “certainly, there’s large footwear to fill. but I informed the children that my expectations aren’t going to be any decrease than instruct Dakosty’s.
“I still are expecting them to win games, play challenging, teach challenging, work hard within the lecture room, play for the district championship each year and go to states.”
Defending champions Pottsville and Schuylkill Haven were selected as preseason Schuylkill League division favorites in voting performed through the coaches and media.
in the coaches’ poll, Pottsville obtained four first-area votes and 32 usual facets to lead Division I. They were followed by means of Blue Mountain (28 elements) and North Schuylkill (24), which every grabbed one first-location vote. Tamaqua (18), Lehighton (12) and Jim Thorpe (12) rounded out the Division I poll.
The Hurricanes earned 5 first-vicinity votes and 34 points to true the Division II coaches’ ballot. Haven was followed through Marian (29, one first-region vote), Mahanoy area (20), Minersville (sixteen), Panther Valley (14) and Shenandoah Valley (13).
Coaches ranked teams in the division through which their teams play 1-6 in projected order of finish and facets awarded 6 to 1 in keeping with that rating in each and every division.
while the exact teams didn’t alternate in the media poll, there became some shuffling in both divisions. Sixteen media contributors that cover the 12 colleges within the Schuylkill League took half in the ballot, following the same facets breakdown as the coaches ballot.
The media had Pottsville (68) as the exact team in Division I, followed through Tamaqua (sixty three), Blue Mountain (57), North Schuylkill (56), Jim Thorpe (fifty six) and Lehighton (36). To exhibit the anticipated stability within the division this season, all six groups got as a minimum one first-place vote, with Pottsville getting 5 and Jim Thorpe 4.
In Division II, the media tabbed Schuylkill Haven (ninety one) because the favorite with 13 first-area votes. Marian (77) took the different three first-vicinity votes and changed into second, followed by way of Minersville (56), Mahanoy enviornment (fifty five), Panther Valley (37) and Shenandoah Valley (20).
Division II race
whereas Division I shapes up as a balanced race, Schuylkill Haven is the clear-cut favourite to win Division II for the 2nd straight 12 months.
The Hurricanes return 13 starters from remaining year’s 12-2 club that won the District eleven type AA title and reached the second circular of the PIAA playoffs earlier than falling to Southern Columbia.
Quarterbacks Matt Lewandowski of Mahanoy enviornment and Tanner Kennedy of Panther Valley and working returned Seth Paluck of Marian may still aid their groups be contenders.
Minersville might have the most effective all-around club after Schuylkill Haven, driving the momentum of a strong conclude that saw the Miners location second within the Division II race with a four-1 list.
“Division II is always a fight, a dogfight week to week,” Minersville teach Damian Buggy talked about. “you can’t take any crew flippantly, since you’re in a dogfight per week.
“Haven returns a ton of guys. They made a deep playoff run with a lot of the youngsters which are returning. which you can’t count out Mahanoy, they’re very disciplined with their offense and have respectable athletes in their backfield. Marian at all times reloads every year.
“I consider we’re up there. it will be entertaining to look what instruct Keating does at Shenandoah, as a result of we play them twice. It’s just like the NFC East. Then teach expense at PV, from his lineage in teaching, I’m certain he’ll have Panther Valley capable. properly to backside, I don’t see too many weak links.”
Contact the creator: Lboyer@republicanherald.com; 570-628-6026; @pubsportsboss on Twitter
2016 closing Standings
(average) W L
*Pottsville (9-2) 5 0
Blue Mountain (9-2) 4 1
North Schuylkill (7-5) 3 2
Jim Thorpe (6-5) 2 three
Tamaqua (5-6) 1 4
Lehighton (four-7) 0 5
*Sch. Haven (12-2) 5 0
Minersville (5-6) four 1
Marian (6-6) 3 2
Mahanoy area (5-6) 2 3
Panther Valley (2-8) 1 four
Shen. Valley (0-10) 0 5
* Division champions
Playoff Qualifiers: Pottsville (eleven-AAAA semis), Blue Mountain (EC AAAA champ), North Schuylkill (11-AAA semis), Jim Thorpe (eleven-AAA), Tamaqua (eleven-AAA), Lehighton (11-AAA), Schuylkill Haven (eleven-AA champ, PIAA AA 2nd circular), Minersville (eleven-AA semis), Marian (11-A runner-up), Mahanoy enviornment (11-AA semis)
Schuylkill League agenda
Friday, Sept. 22
Blue Mountain at Tamaqua
Marian at Schuylkill Haven
Friday, Sept. 29
Tamaqua at Pottsville
Jim Thorpe at Blue Mountain
Lehighton at North Schuylkill
Sch. Haven at Mahanoy area
Panther Valley at Marian
Minersville at Shenandoah Valley
Friday, Oct. 6
Pottsville at Blue Mountain
North Schuylkill at Jim Thorpe
Tamaqua at Lehighton
Mahanoy enviornment at Marian
Schuylkill Haven at Minersville
Shen. Valley at Panther Valley
Friday, Oct. 13
Lehighton at Pottsville
Blue Mountain at North Schuylkill
Jim Thorpe at Tamaqua
Minersville at Mahanoy enviornment
Marian at Shenandoah Valley
Panther Valley at Sch. Haven
Friday, Oct. 20
Pottsville at Jim Thorpe
Lehighton at Blue Mountain
Tamaqua at North Schuylkill
Mahanoy enviornment at Panther Valley
Minersville at Marian
Sch. Haven at Shen. Valley
Friday, Oct. 27
North Schuylkill at Pottsville
Jim Thorpe at Lehighton
Shen. Valley at Mahanoy area
Panther Valley at Minersville
(groups bought 6-1 elements in descending order in voting done through division coaches. First-location votes in parentheses)
1. Pottsville (four) 32
2. Blue Mountain (1) 28
three. North Schuylkill (1) 24
4. Tamaqua 18
5. Jim Thorpe 12
(tie) Lehighton 12
1. Schuylkill Haven (4) 34
2. Marian (1) 29
three. Mahanoy enviornment 20
four. Minersville sixteen
5. Panther Valley (1) 14
6. Shenandoah Valley 13
(teams received 6-1 facets in descending order in voting completed with the aid of 16 media members. First-region votes in parentheses)
1. Pottsville (5) 68
2. Tamaqua (2) sixty three
three. Blue Mountain (2) 57
four. Jim Thorpe (4) fifty six
(tie) North Schuylkill (2) 56
6. Lehighton (1) 36
1. Schuylkill Haven (13) 91
2. Marian (three) seventy seven
3. Minersville fifty six
4. Mahanoy area fifty five
5. Panther Valley 37
6. Shenandoah Valley 20
games of the Week
Tri-Valley at Williams Valley, Pottsville at Jim Thorpe, Tamaqua at North Schuylkill, Mount Carmel at Selinsgrove
Marian to dedicate
field for Dakosty
Marian high school will officially dedicate its box at men of Marian Stadium in honor of former teach Stan Dakosty throughout a pre-online game ceremony tonight when the Colts host Minersville.
Dakosty retired after ultimate season. He compiled a 310-152-three ordinary list in forty seasons on the helm.
On the Air
WPPA 1360 AM, Pottsville
Pottsville at Jim Thorpe
WAVT a hundred and one.9 FM, Pottsville
Tri-Valley at Williams Valley
WMGH one zero five.5 FM, Lansford
Tamaqua at North Schuylkill
WLSH 1410 AM, Lansford
Minersville at Marian
WQLV ninety eight.9 FM, Millersburg
Tri-Valley at Williams Valley
WGRC 104.7 FM, Lewisburg
Bloomsburg at Lewisburg
On the information superhighway/television
Tamaqua at North Schuylkill
WLYN television-35, Hazleton
Lake Lehman at Berwick
WQMY television-fifty three, Wilkes-Barre
Towanda at Tunkhannock
Blue Ridge Cable television-13
NW Lehigh at Northern Lehigh
BRC Digital 113
Wallenpaupack at Del. Valley
PCN game of the Week
Meadville at Grove metropolis
Get are living updates
comply with The Republican-Herald activities body of workers on Twitter with are living updates from these video games: Tri-Valley at Williams Valley (@pubsportsboss) and Minersville at Marian (@ChuckCurley). For an entire list of rankings, visit The Republican-Herald sports web page on facebook.
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STATE of Kansas, Appellee, v. Jackie R. POULTON, Appellant.
No. 95,353. Decided: April 04, 2008 Shawn E. Minihan, of Kansas Appellate Defender Office, argued the cause and was on the briefs for the appellant. Thomas R. Stanton, deputy district attorney, argued the cause, and Keith E. Schroeder, district attorney, and Phill Kline, attorney general, were with him on the brief for the appellee.
Jackie R. Poulton was convicted of manufacturing methamphetamine, possessing methamphetamine with intent to sell, possessing drug paraphernalia with intent to manufacture, possessing drug paraphernalia with intent to distribute, possessing drug paraphernalia with intent to consume, possessing marijuana, possessing drugs without a tax stamp, and endangering a child.
Prior to trial, Poulton filed motions to suppress the evidence obtained from two searches of his home, both of which the district court denied. The Court of Appeals reversed the convictions based on the November 20, 2003, search, finding that the search was illegal, but affirmed the convictions based on the December 27, 2003, search without addressing Poulton's suppression issue that the second search constituted fruit of the poisonous tree. State v. Poulton, 37 Kan.App.2d 299, 152 P.3d 678 (2007). We granted Poulton's petition for review, and we now affirm in part and reverse in part the decision of the Court of Appeals.
The relevant facts as stated by the Court of Appeals, follow:
“On November 20, 2003, Ed Mora, a special enforcement officer with the Kansas Department of Corrections, was seeking to serve an arrest warrant on Lisa Lamuz for violating her parole. Mora had been attempting to locate Lamuz for approximately 3 weeks. Deputy Cory Graber told Mora that Lamuz might be staying at a residence at 6112 North Plum in Hutchinson. Mora, Graber, and Deputy Jeremy Hedges went to that address to attempt to serve the arrest warrant on Lamuz.
“Upon arriving at the residence, Graber went to the back of the residence, and Mora and Hedges walked towards the front door. Poulton came out of the house and met the officers on the porch. Mora told Poulton who he was. According to Mora, he asked Poulton if he could speak with him inside, and Poulton responded, ‘[Y]es, come on in.’ Hedges' testimony differed from Mora's in that Hedges never testified that Poulton explicitly consented to them entering the residence. Rather, Hedges testified that Mora asked if he could speak with Poulton and that Poulton responded yes and opened the door and let them in the house.
“According to Mora, once they were inside the residence, he asked Poulton if Lamuz was there. Poulton told Mora that Lamuz was in the back room and that he would go get her. Mora testified that Poulton walked towards the kitchen area of the residence, but he touched Poulton on the arm to stop him. Mora told Poulton that he would get Lamuz. As Mora walked towards the kitchen area, Lamuz walked out of a back room. Mora told Lamuz who he was and that she was under arrest. Mora led her into the front room and attempted to place handcuffs on her. Lamuz told Mora that she was not on parole anymore and that he had made a mistake. Lamuz indicated that she had paperwork showing that she was no longer on parole. Lamuz tried to turn away from Mora, but he forcefully grabbed her and placed her in handcuffs. Approximately five other individuals were in the residence when this incident occurred.
“As Mora was attempting to handcuff Lamuz, Hedges saw Lamuz raise her hand. Hedges immediately called Graber into the residence. Graber entered through the back door as two individuals were attempting to leave the residence. Graber stopped them from leaving. One of the individuals and Poulton went into a back bedroom. Graber saw several rifles and shotguns lying against the doorway. Graber yelled to the other officers that he had seen guns. Graber ordered everyone out of the back bedroom.
“According to Graber, Poulton said that he needed to get Lamuz' shoes out of the bedroom and that Graber could accompany him in there. When Graber went into the back bedroom, he saw a handgun lying on the bed. In addition, Graber saw a test tube containing what appeared to be methamphetamine residue, a razor blade with white powder residue, and an open package of lithium batteries. Graber relayed this information to Hedges who immediately applied for a search warrant.
“The officers confined everyone in the house to one area and handcuffed them. In addition, the officers performed patdown searches for safety reasons. When Poulton was told about the application for a search warrant, he said that his chest was hurting and that he thought he was having a heart attack. Emergency medical services (EMS) personnel were called to the residence.
“Before EMS personnel transported Poulton to the hospital, Graber performed a patdown search. Poulton was not in handcuffs at the time and was not under arrest. Graber testified that the patdown was done for EMS safety purposes. Although Poulton had been in handcuffs earlier, Graber testified that a patdown search had not been performed. During the patdown search, Graber reached for Poulton's right pocket. Poulton told Graber that he should not stick his hand in there. Graber pulled syringes out of Poulton's pocket.
“A search warrant was obtained for the residence. During their search, the officers seized baggies of methamphetamine, drug paraphernalia, and items commonly used in manufacturing methamphetamine.
“On December 27, 2003, Graber and three other officers returned to the residence to serve arrest warrants on four individuals, including Poulton. During the arrests, the officers saw a handgun on a bed in one of the bedrooms, paraphernalia used for methamphetamine, and small baggies containing a white powder that was consistent with methamphetamine. The officers obtained a search warrant for the residence. During their search, the officers seized drug paraphernalia, several baggies of methamphetamine, several baggies of green vegetation, and various items commonly used in manufacturing methamphetamine.
“From the November 20, 2003, incident, Poulton was charged with eight drug-related crimes. Poulton moved to suppress the evidence obtained from the November 20, 2003, search and any statements made by him during or resulting from the search. Poulton argued that the officers never had consent to enter his residence. Poulton contended that the officers' observations, which formed the basis for the search warrant, were made while they were illegally in his residence. The trial court held an evidentiary hearing on Poulton's motion to suppress.
“At the suppression hearing, Poulton testified that he never gave the officers consent to enter his residence. Rather, Poulton testified that the entire conversation concerning Lamuz happened outside of his residence and that he told the officers he would go inside and get Lamuz. Poulton testified that he asked the officers if they would wait on his front porch, but the officers told him no. The officers followed Poulton into his residence.
“At the conclusion of the hearing, the trial court found that the officers had implied consent to enter Poulton's residence. The trial court recognized that there were three different versions of what had occurred at Poulton's residence based on the testimonies of Mora, Hedges, and Poulton. The trial court found that Poulton's testimony that he told the officers to stay outside the residence was not credible. The trial court found that Mora indicated that he was going to get Lamuz, that Poulton indicated that he would do it, and that they all went in the house together. The trial court determined that the officers had implied consent to enter Poulton's residence. The trial court denied Poulton's motion to suppress.
“In a separate criminal case, Poulton was charged with eight additional drug-related crimes along with the crimes of contributing to a child's misconduct and endangering a child. All of these charges resulted from the December 27, 2003, incident. Poulton moved to suppress the evidence obtained from the December 27, 2003, search of his home. The trial court conducted an evidentiary hearing and denied Poulton's motion to suppress.
“Upon motion by the State, the trial court later consolidated Poulton's two criminal cases. Poulton's consolidated case went to a bench trial on stipulated facts. The trial court found Poulton guilty of two counts of manufacture of methamphetamine in violation of K.S.A. 65-4159; two counts of possession of methamphetamine in violation of K.S.A. 65-4161; one count of possession of lithium metal with the intent to manufacture a controlled substance in violation of K.S.A. 65-7006; one count of possession of anhydrous ammonia or pressurized ammonia with the intent to manufacture a controlled substance in violation of K.S.A. 65-7006; five counts of felony possession of drug paraphernalia in violation of K.S.A. 65-4152(a); two counts of possession of methamphetamine without tax stamps affixed in violation of K.S.A. 79-4; one count of possession of marijuana in violation of K.S.A. 65-4162(a)(3); and one count of endangering a child in violation of K.S.A. 21-3608. Poulton was sentenced to a controlling sentence of 30 months in prison.” 37 Kan.App.2d at 301-04, 152 P.3d 678.
The Court of Appeals found, and at oral argument on review the State conceded, that the initial search conducted on November 20, 2003, was illegal. See 37 Kan.App.2d at 308, 310, 152 P.3d 678. We agree and affirm the decision of the Court of Appeals reversing the convictions based on the initial search. The issue relating to the imposition of the Board of Indigents' Defense Services (BIDS) fees is not before us on review, and the decision of the Court of Appeals reversing and remanding the assessment of the BIDS fees to comply with State v. Robinson, 281 Kan. 538, Syl. ¶ 1, 132 P.3d 934 (2006), must stand since it was not appealed.
The Court of Appeals affirmed Poulton's convictions based on the December 27, 2003, search. The Court of Appeals elected not to address Poulton's claim that the evidence seized during the December 27, 2003, search was the fruit of the poisonous tree because Poulton failed to raise the issue in the district court and failed to argue that any exceptional circumstances applied, thereby failing to preserve the issue for appeal. 37 Kan.App.2d at 310-11, 152 P.3d 678.
Appellate courts can consider new issues on appeal in the following circumstances: (1) Cases in which the newly asserted theory involves only a question of law arising on proved or admitted facts and that is finally determinative of the case; (2) cases raising questions for the first time on appeal if consideration of those questions is necessary to serve the ends of justice or to prevent denial of fundamental rights; and (3) cases upholding the judgment of a trial court even though the trial court may have relied on the wrong ground or assigned a wrong reason for its decision. State v. Stevens, 278 Kan. 441, 454, 101 P.3d 1190 (2004) (citing State v. Bell, 258 Kan. 123, 126, 899 P.2d 1000  ).
At least one of the first two exceptions applies in the present case. Poulton and the State entered into a written stipulation of facts for the bench trial. The written stipulation specifically renewed Poulton's objection to the denial of his motions to suppress and preserved the issue of suppression for appeal. Because there are no factual disputes, the question of whether the evidence stemming from the second search should have been suppressed is a purely legal question. The first exception may apply if it is determined that the evidence should have been suppressed and the suppression finally disposes of the case. The second exception applies because the suppression of evidence based on the violation of Poulton's rights under the Fourth Amendment to the United States Constitution implicates a fundamental right.
The fruit of the poisonous tree doctrine bars the admission of evidence directly seized during an illegal search as well as evidence obtained indirectly as a result of information learned or leads obtained from the illegal search. Although not all evidence is fruit of the poisonous tree simply because it would not have become known without the illegal actions of the police, the doctrine bars any evidence that becomes known through exploitation of the illegality. Evidence that is sufficiently distinguishable so as to be purged of the primary taint is not considered fruit of the poisonous tree. See Wong Sun v. United States, 371 U.S. 471, 487-88, 83 S.Ct. 407, 9 L.Ed.2d 441 (1963); State v. Hodges, 252 Kan. 989, 1006, 851 P.2d 352 (1993); State v. Deffenbaugh, 216 Kan. 593, 598, 533 P.2d 1328 (1975).
Although the parties stipulated to the facts leading to the convictions, the State did not have the opportunity to analyze the facts in light of the fruit of the poisonous tree doctrine. The district court found that the initial search was valid, and Poulton did not argue that the second search and arrest constituted fruit of the poisonous tree. Because the parties have not had a full opportunity to argue this issue in light of the conclusion that the first search was illegal, we decline to find that the doctrine of the fruit of the poisonous tree necessarily applies to the facts of this case. We instead vacate the convictions based on the December 27, 2003, search and remand the case to the district court for the purpose of conducting a hearing to determine whether the evidence based on that search should be suppressed as fruit of the poisonous tree. Any appeal taken from that hearing will be docketed as an original appeal in the Court of Appeals.
Judgment of the Court of Appeals is affirmed in part and reversed in part. Judgment of the district court is reversed, and the case is remanded with directions to the district court.
The opinion of the court was delivered by ROSEN, J.:
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Cell Research (2008) 18:609–621. doi: 10.1038cr.2008.61; published online 27 May 2008
Top of page Introduction
3-Hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase catalyzes conversion of HMG CoA to mevalonate (Figure 1), the precursor of isoprenoid groups that are incorporated into many end-products including cholesterol, ubiquinone, heme, dolichol, and the farnesyl and geranylgeranyl groups that can become attached to many cellular proteins 1. HMG CoA reductase has been long recognized as the rate-limiting enzyme in synthesis of cholesterol and as such is a primary focus of regulation. This is underscored by a multivalent system mediated by sterol and nonsterol isoprenoids that exerts stringent feedback control on reductase through multiple mechanisms 2. The complexity of this regulatory system was first revealed in the late 1970s through the use of compactin, a member of the statin family of drugs that are potent competitive inhibitors of reductase 3, 4. Treatment of cultured cells with compactin blocks production of mevalonate, thereby reducing levels of sterol and nonsterol isoprenoids that normally govern feedback regulation of reductase. Cells respond to the inhibition of reductase by developing a drastic increase in reductase protein (~200-fold), owing to the combined effects of enhanced transcription of the reductase gene, efficient translation of reductase mRNA, and extended half-life of reductase protein. Complete reversal of this compensatory increase in reductase requires regulatory actions of both sterol and nonsterol end-products of mevalonate metabolism 2, 5. Sterols inhibit the activity of sterol regulatory element-binding proteins (SREBPs), a family of membrane-anchored transcription factors that enhance cholesterol synthesis and uptake by modulating genes encoding cholesterol biosynthetic enzymes (including reductase) and the low density lipoprotein (LDL)-receptor 6. An unknown nonsterol mevalonate-derived product controls the translational effects through a poorly understood mechanism that may be mediated by the complex 5′-untranslated region of the reductase mRNA 5. Both sterol and nonsterol end-products of mevalonate metabolism combine to accelerate degradation of reductase protein through a mechanism mediated by the ubiquitin-proteasome pathway 7, 8, 9. Through these mechanisms, the multivalent regulation of reductase coordinates mevalonate metabolism such that essential nonsterol isoprenoids can be constantly supplied without risking the potentially toxic overproduction of cholesterol or one of its sterol precursors.
Schematic representation of the cholesterol synthetic pathway in animal cells. Reactions that require molecular oxygen are indicated, and specific inhibitors of various enzymes in the pathway are highlighted in red.
Full figure and legend (120K)
In all mammalian species that have been studied to date (i.e., human, hamster, rat, and mouse), reductase localizes to membranes of the endoplasmic reticulum (ER) and consists of 887 or 888 amino acids that can be separated into two contiguous domains (Figure 2A) 10, 11, 12, 13. The N-terminal domain of reductase is comprised of 339 amino acids and is integrated into membranes by virtue of eight membrane-spanning segments that are separated by short loops (Figure 2B) 14. The 548-amino acid C-terminal domain of reductase projects into the cytosol and exerts all of the enzymatic activity 13. The amino acid sequence of the membrane domain of reductase is strikingly conserved among mammalian species 15, 16, which suggested early on that the region may be important for more than just membrane anchorage. Indeed, two key observations have disclosed an important role for the membrane domain of reductase in sterol-accelerated degradation. (1) Expression of the truncated, cytosolic C-terminal domain of reductase produced a stable, catalytically active protein whose degradation was not influenced by sterols 17. (2) A chimeric protein consisting of a fusion between the membrane domain of reductase and soluble β-galactosidase exhibited sterol-accelerated degradation similar to the wild-type full-length reductase 18. These observations led to the hypothesis that the membrane domain of reductase somehow senses levels of membrane-embedded sterols, which triggers reactions that render the enzyme susceptible to proteolytic degradation 17. This degradation occurs from ER membranes and can be blocked by inhibitors of the 26S proteasome, which leads to the accumulation of ubiquitinated forms of reductase 9, 19.
Domain structure of hamster HMG CoA reductase. (A) HMG CoA reductase consists of two distinct domains: a hydrophobic N-terminal domain with eight membrane-spanning segments that anchor the protein to ER membranes, and a hydrophilic C-terminal domain that projects into the cytosol and exhibits all of the enzyme's catalytic activity. (B) Amino acid sequence and topology of the membrane domain of hamster HMG CoA reductase. The lysine residues implicated as sites of Insig-dependent, sterol-regulated ubiquitination are highlighted in red and denoted by arrows. The YIYF sequence in the second membrane-spanning helix that mediates Insig binding is highlighted in yellow.
Full figure and legend (110K)
Ubiquitin and proteasomes have been implicated in degradation of reductase in the yeast Saccharomyces cerevisiae 20. HMG2p, one of two reductase isozymes in yeast, is rapidly degraded when flux through the mevalonate pathway is high. Degradation of the other isozyme, HMG1p, is not regulated. Although the catalytic domains of yeast HMG2p and mammalian reductase show strong similarity (>50% identity over 540 amino acids), the membrane domains bear limited resemblances (<20% identity over 340 amino acids). Considering that the membrane domains of yeast and mammalian reductase are necessary and sufficient for accelerated degradation 18, 21, limited conservation between these regions provides an explanation for the observation that degradation is not triggered by sterols in yeast, but rather by nonsterol isoprenoids 22. Despite these differences, regulated ubiquitination and degradation of reductase is employed by yeast and mammals to modulate flux through the mevalonate pathway. For further insight into the pathway for degradation of HMG2p in yeast, readers are referred to several excellent reviews 20, 22, 23.
Top of page Insigs, polytopic proteins of the ER that mediate sterol-accelerated degradation of HMG CoA reductase
Crucial insights into the mechanism for sterol-accelerated degradation of reductase have emerged from comparisons made between reductase and Scap (the SREBP cleavage-activating protein). Similar to reductase, Scap contains two distinct domains: a hydrophobic N-terminal domain that spans the membrane eight times and a hydrophilic C-terminal domain that projects into the cytosol 24. The C-terminal domain of Scap mediates a constitutive association with SREBPs; this interaction is required for Scap-dependent translocation of SREBPs from the ER to Golgi in sterol-deprived cells (Figure 3). Upon arrival in the Golgi, SREBPs encounter a pair of proteases (designated site-1 and site-2 proteases) that act successively to release soluble fragments from the membrane into the cytosol 25, 26, 27, 28, 29. These processed forms of SREBPs then migrate from the cytosol into the nucleus and stimulate target gene expression, which results in increased synthesis and uptake of sterols 6. The subsequent accumulation of sterols in ER membranes prevents proteolytic activation of SREBPs by blocking exit of Scap-SREBP complexes from the ER; transcription of SREBP target genes declines and cholesterol synthesis and uptake are suppressed. Inhibition of ER to Golgi transport of SREBPs results from sterol-induced binding of Scap to ER retention proteins called Insig-1 and Insig-2 30, 31. Insig binding occludes a cytosolic binding site in Scap recognized by COPII proteins, which incorporate cargo molecules into vesicles that deliver ER-derived proteins to the Golgi 32. Scap-Insig binding is mediated by a segment of Scap's membrane domain that includes transmembrane helices 2-6 25, 30. A similar stretch of transmembrane helices is found in at least four other polytopic membrane proteins (including the Niemann Pick C1 protein, Patched, Dispatched, and reductase), all of which have been postulated to interact with sterols. Thus, the region has become known as the sterol-sensing domain 33. The importance of the sterol-sensing domain in regulation of Scap is illustrated by findings that point mutations within the region disrupt Insig binding, thereby relieving mutant Scap-SREBP complexes from sterol-mediated ER retention 30, 31, 34, 35, 36.
Model for sterol-regulated Scap-SREBP pathway. SCAP is a sensor of sterols and an escort of SREBPs. In sterol-depleted cells, Scap facilitates export of SREBPs from the ER to the Golgi apparatus, where two proteases, Site-1 protease (S1P) and Site-2 protease (S2P), act to release the transcriptionally active, N-terminal bHLH-Zip domain of SREBPs from the membrane. The released bHLH-Zip domain migrates into the nucleus and binds to a sterol response element (SRE) in the enhancerpromoter region of target genes, activating their transcription. Accumulation of sterols in ER membranes triggers binding of Scap to one of two retention proteins called Insigs, which blocks incorporation of Scap-SREBP complexes into ER transport vesicles. As a result, SREBPs no longer translocate to the Golgi apparatus, the bHLH-Zip domain cannot be released from the membrane, and transcription of all target genes declines.
Full figure and legend (81K)
The recognition of sequence resemblances between the sterol-sensing domains of Scap and reductase stimulated an appraisal of a role for Insigs in degradation of reductase. This effort led to the following observations, which considered together divulge the action of at least one of the Insig proteins in sterol-accelerated degradation of reductase. First, when overexpressed by transfection in Chinese hamster ovary (CHO) cells, reductase cannot be degraded when the cells are treated with sterols 37. Co-expression of Insig-1 restores sterol-accelerated degradation of reductase, suggesting the saturation of endogenous Insigs by the overexpressed reductase. Second, reduction of both Insig-1 and Insig-2 by RNA interference (RNAi) abolishes sterol-accelerated degradation of endogenous reductase 38. Third, mutant CHO cells lacking both Insigs are impervious to sterol-stimulated degradation of reductase as well as sterol-mediated inhibition of SREBP processing 39.
Degradation of reductase coincides with sterol-induced binding of its membrane domain to Insigs 37, an action that requires a tetrapeptide sequence, YIYF, located in the second transmembrane segment of reductase (see Figure 2B) 38. A mutant form of reductase in which the YIYF sequence is mutated to alanine residues no longer binds to Insigs and the enzyme is not subject to rapid degradation. The YIYF sequence is also present in the second transmembrane domain of Scap, where it mediates sterol-dependent formation of Scap-Insig complexes 30, 31. In fact, overexpressing the sterol-sensing domain of Scap in cells blocks Insig-mediated, sterol-accelerated degradation of reductase. Mutation of the YIYF sequence in the Scap sterol-sensing domain ablates this inhibition. This indicates that Scap and reductase bind to the same site on Insigs and the two proteins compete for limiting the amount of Insigs when intracellular sterol levels rise.
Top of page Insig-mediated ubiquitination of HMG CoA reductase
Evidence supporting a major role for the ubiquitin-proteasome pathway in sterol-accelerated degradation of reductase was first provided by the observation that proteasome inhibition blocks the process 19, leading to the accumulation of ubiquitinated forms of reductase on ER membranes 9. This ubiquitination is obligatory for degradation of reductase and exhibits an absolute requirement for the presence of Insigs 38, 39. Reduction of Insig-1 and Insig-2 mRNA by genetic mutation or RNAi-mediated knockdown abrogates sterol-dependent ubiquitination of endogenous reductase, rendering the enzyme refractory to accelerated degradation. Moreover, sterol-induced ubiquitination of reductase exhibits an absolute Insig requirement in transient transfection assays. Mutation of the YIYF sequence in reductase, which blocks Insig binding, prevents regulated ubiquitination and slows the enzyme's degradation. In contrast, conservative substitutions of arginine for lysines 89 and 248 in the membrane domain of reductase (Figure 2B) do not block Insig binding, but the substitutions rather abolish ubiquitination and subsequent degradation of reductase. Thus, lysines 89 and 248 in reductase are implicated as sites for Insig-mediated, sterol-induced ubiquitination. It is important to note that mutation of lysines 89 and 248 blocks ubiquitination and degradation of reductase in the context of the full-length enzyme, suggesting that the catalytic domain does not contribute to ubiquitination. This is consistent with the observation that the soluble catalytic domain is dispensable for sterol-regulated degradation 17.
How might Insig binding impart recognition of reductase by the ubiquitinating machinery? This question was addressed by examining reductase ubiquitination in a permeabilized cell system 40. Sterol-depleted cells were permeabilized with low concentrations of the mild detergent digitonin such that nearly all of the cytosolic proteins were released into the supernatant upon centrifugation, whereas membrane proteins such as reductase remained associated with the pellet fraction. The pellet of permeabilized cells supports Insig-dependent ubiquitination of reductase that is stimulated by additions of ATP, sterols, and rat liver cytosol in vitro. Surprisingly, reductase ubiquitination is potently stimulated by oxygenated derivatives of cholesterol, including 24-, 25-, and 27-hydroxycholesterol, but not by cholesterol itself. The significance of this finding will be discussed in more detail below.
Ubiquitination of proteins is a multistep process, involving the action of at least three types of enzymes 41. In the first step, ubiquitin is activated by the ubiquitin-activating enzyme (E1), which forms a thiol ester between a reactive cysteine residue in E1 and the C-terminus of ubiquitin. Next, ubiquitin is transferred from E1 to a catalytic cysteine of the ubiquitin-conjugating enzyme (E2). The third type of enzyme, ubiquitin ligase (E3), facilitates transfer of activated ubiquitin from E2 to a lysine residue in the substrate (or a previously attached ubiquitin). Once a poly-ubiquitin chain of sufficient size is built, the substrate is recognized and subsequently degraded by proteasomes. Only two E1 enzymes exist, and both are cytosolic proteins. In contrast, a variety of E2s and E3s, both soluble and membrane-bound, have been described 42. The exquisite sensitivity of substrate ubiquitination is ultimately determined by the E3, either alone or in combination with its cognate E2.
Fractionated S100 from Hela cells was utilized to determine which component of the reductase ubiquitinating machinery (E1, E2 and E3) is provided by rat liver cytosol in the permeabilized cell system 40. These fractions were first described by Hershko and co-workers 43, 44 and were generated by separating Hela cell S100 into fractions that bind (Fraction II) or do not bind (Fraction I) an anion exchange resin. It was subsequently determined that Fraction I contained ubiquitin, whereas Fraction II contains E1 45. Fraction II effectively replaces rat liver cytosol for regulated ubiquitination of reductase in permeabilized cells, but Fraction I does not. Two observations indicate that Fraction II provides a source of ubiquitin activation in the permeabilized cell system. First, purified E1 replaces rat liver cytosol for sterol-regulated ubiquitination of reductase in permeabilized cells. Second, immunodepletion of E1 eliminates the reductase ubiquitinating activity of rat liver cytosol. These results demonstrate that E1 is the only cytosolic protein required for reductase ubiquitination, which indicates the reductase E2 and E3 are membrane-associated proteins. This notion is consistent with the localization of apparent sites of reductase ubiquitination, lysines 89 and 248, which are cytosolically exposed and are predicted to lie immediately adjacent to transmembrane helices three and seven (Figure 2B).
Results from the analysis of reductase ubiquitination in permeabilized cells indicated that Insig binding results in recruitment of enzymes that ubiquitinate reductase. Coimmunoprecipitation experiments, coupled with tandem mass spectroscopy, were utilized to identify membrane proteins that associate with the sterol-dependent reductase-Insig complex. These studies revealed that Insig-1 binds to a known membrane-anchored ubiquitin ligase called gp78 46. The cDNA for gp78 predicts a 643-amino acid protein that can be divided into four domains. The N-terminal domain of 298 amino acids contains five to seven membrane-spanning helices that anchor the protein to ER membranes and mediate association with Insig-1. The membrane attachment region of gp78 is followed by a 43-amino acid region with a RING finger consensus sequence that confers ubiquitin ligase activity 47. Following the RING domain is a 42-amino acid region homologous to Cue1p, an ER membrane protein in yeast that serves as a membrane anchor for Ubc7p, a cytosolic ubiquitin-conjugating enzyme 48. Recently, this region of gp78 has been shown to directly bind to Ufd1, a cytosolic protein that modulates gp78 ubiquitin ligase activity, thereby enhancing ubiquitination and degradation of the enzyme's substrates 49. Finally, the extreme C-terminus of gp78 (48 amino acids) mediates an interaction with VCP (Valosin-containing protein, also known as p97), an ATPase that has been implicated in the post-ubiquitination steps of ER-associated degradation (ERAD) 50.
At least three lines of evidence indicate that gp78, through its binding to Insig-1, initiates sterol-accelerated degradation of reductase. (1) Overexpression of the membrane domain of gp78 blocks Insig-mediated, sterol-accelerated degradation of reductase, suggesting that the membrane domain of gp78 competes with full-length gp78 for binding to Insig-1, thereby abolishing reductase ubiquitination. (2) Sterols trigger binding of gp78 to reductase in an Insig-dependent, sterol-regulated manner. The specificity of this binding is illustrated by the inability of gp78 to bind Scap, regardless of the presence or absence of sterols andor Insigs. (3) RNAi-mediated knockdown of gp78 prevents sterol-regulated ubiquitination and degradation of endogenous reductase. Importantly, the effect of gp78 knockdown is specific inasmuch as knockdown of a related membrane-bound ubiquitin ligase, Hrd1, does not affect reductase ubiquitination. Another function of gp78, besides its role as a ubiquitin ligase, is to couple ubiquitination of reductase to degradation through its association with VCP. Indeed, coimmunoprecipitation experiments show that gp78 is an intermediary in association of VCP and Insig-1. Moreover, knockdown of VCP by RNAi prevents sterol-accelerated degradation of endogenous reductase and a dominant-negative ATPase-deficient mutant of VCP blocks sterol-regulated degradation of transfected reductase.
The identification of gp78 as an E3 ubiquitin ligase that mediates reductase ubiquitination has important implications for yet another mode of sterol regulation. The regulation of Insig-1 contrasts that of reductase in that Insig-1 becomes ubiquitinated and is rapidly degraded by proteasomes in sterol-depleted cells 51. Ubiquitination of Insig-1 is mediated by gp78 52. When sterols induce reductase to bind Insig-1, ubiquitination is diverted toward reductase and the enzyme becomes rapidly degraded. However, when sterols cause Scap to bind Insig-1, gp78 is displaced and no longer ubiquitinates Insig-1, thereby stabilizing the protein. This reaction helps to explain why reductase is degraded when it binds to Insig-1, whereas Scap binding to Insig-1 leads to retention in the ER. In addition, gp78-mediated ubiquitination and degradation of Insig-1 provide a mechanism for a recently appreciated process termed “convergent feedback inhibition” 51. In sterol-depleted cells, Scap-SREBP complexes no longer bind Insig-1, which in turn becomes ubiquitinated and degraded. Thus, Scap-SREBP complexes are free to exit the ER and translocate to the Golgi, where the SREBPs are processed to the nuclear form that stimulates transcription of target genes, including the Insig-1 gene. reased transcription of the Insig-1 gene leads to increased synthesis of Insig-1 protein, but the protein is ubiquitinated and degraded until sterols build up to levels sufficient to trigger Scap binding. Thus, inhibition of SREBP processing requires convergence of newly synthesized Insig-1 and newly acquired sterols.
Top of page The HMG CoA reductase sterol-sensing reaction
Oxysterols are derivatives of cholesterol that contain hydroxyl groups at various positions in the iso-octyl side chain 53, 54. These compounds are synthesized in many tissues by specific enzymes called hydroxylases; oxysterols play key roles in cholesterol export and they are also intermediates in the synthesis of bile acids 55. Oxysterols are significantly more soluble than cholesterol in aqueous solution, and thus can readily pass across the plasma membrane and enter cells. This property renders oxysterols such as 24-, 25-, and 27-hydroxycholesterol extremely potent in inhibiting cholesterol synthesis by stimulating binding of both reductase and Scap to Insigs. Oxysterols are present at very low concentrations (104- to 106-fold less than cholesterol) in tissues and blood, which raises questions as to whether they act through a similar mechanism as LDL-derived cholesterol to block cholesterol synthesis. In the case of Scap, the mode of action of these two classes of sterols is becoming clear. Cholesterol directly binds to the membrane domain of Scap in a specific and saturable fashion 56. The interaction causes a conformational change in Scap that promotes Insig binding 57. The addition of cholesterol in vitro to membranes isolated from sterol-depleted cells causes exposure of a cryptic trypsin cleavage site, thereby altering the tryptic digestion pattern of Scap that can be monitored by immunoblot analysis 58. Co-expression of Insigs lowers the amount of cholesterol required to induce the conformational change in Scap. Oxysterols neither alter Scap's conformation in vitro nor bind to the protein's membrane domain, leading to the postulation of the existence of a membrane-bound oxysterol binding protein. Remarkably, Insig-2 has been recently defined as a membrane-bound oxysterol binding protein with binding specificity that correlates with the ability of oxysterols to inhibit SREBP processing 32, 59. Thus, formation of the Scap-Insig complex can be initiated by either binding of cholesterol to the membrane domain of Scap or by binding of oxysterols to Insigs. Both events prevent incorporation of Scap-SREBP into vesicles that bud from the ER en route to the Golgi. By analogy, the likely mechanism by which oxysterols stimulate degradation of reductase is through their binding to Insigs.
In striking contrast to results obtained with Scap, the analysis of reductase ubiquitination in permeabilized cells revealed that the reaction was potently stimulated by oxysterols, but not by cholesterol 40. These results led to a search for endogenous sterol regulators of reductase ubiquitination and degradation. Previous indirect studies implicated that lanosterol, the first sterol produced in the cholesterol biosynthetic pathway (Figure 1), or one of its metabolites participates in feedback inhibition of reductase. For example, genetic mutation or pharmacologic inhibition of lanosterol 14α-demethylase, which catalyzes the first step in conversion of lanosterol to cholesterol (Figure 1), markedly reduces the amount of reductase activity in cells 60, 61. These observations led to the evaluation of lanosterol and its metabolite 24,25-dihydrolanosterol as endogenous regulators of reductase ubiquitination and degradation 62. When added to intact cells, lanosterol and 24,25-dihydrolanosterol potently stimulate ubiquitination and degradation of reductase through a reaction that requires the presence of Insigs. The activity of both sterols is specific inasmuch as they do not inhibit processing of SREBPs. This is consistent with the inability of lanosterol to directly bind to Scap and Insig or alter Scap's conformation in vitro 58. The action of lanosterol and 24,25-dihydrolanosterol is direct and does not require their conversion into an active metabolite as indicated by the reconstitution of reductase ubiquitination by simply incubating isolated membranes with the sterols and purified E1. Using this in vitro assay, the action of lanosterol and 24,25-dihydrolanosterol in stimulating ubiquitination and degradation of reductase was traced to methyl groups present in the 4α, 4β, and 14α positions of the sterol ring.
Insig-mediated regulation of reductase is controlled by three classes of sterols: oxysterols, cholesterol, and methylated sterols such as lanosterol and 24,25-dihydrolanosterol. Oxysterols, which are derived from cholesterol, have dual actions in that they accelerate degradation of reductase and block ER to Golgi transport of Scap-SREBP through their direct binding to Insigs. Cholesterol does not regulate reductase stability directly, but binds to Scap and triggers Insig binding, thereby preventing escape of Scap-SREBP from the ER. On the other hand, lanosterol selectively accelerates degradation of reductase without an effect on ER to Golgi transport of Scap-SREBP. Notably, the demethylation of lanosterol has been implicated as a rate-limiting step in the post-squalene portion of cholesterol synthesis, suggesting the reaction as a potential focal point in sterol regulation 63, 64. Considering that lanosterol is the first sterol produced in cholesterol synthesis, it seems reasonable that it controls early steps in the pathway (i.e., the nonsterol branch) by stimulating reductase degradation. The accumulation of lanosterol is avoided, owing to its inability to block SREBP processing through Scap. This assures that mRNAs encoding enzymes catalyzing reactions subsequent to lanosterol remain elevated and lanosterol is metabolized to cholesterol. The importance of this conversion is highlighted by the observation that lanosterol cannot support cell growth in the absence of cholesterol and may be toxic 65. This toxicity is likely due to the inability to optimize certain physiologic properties of cell membranes with regard to biological functions.
Top of page Oxygen sensing in the cholesterol biosynthetic pathway
The physiologic relevance of lanosterol as an endogenous regulator of reductase ubiquitination and degradation was deduced by the recognition that cholesterol synthesis is a highly oxygen-consumptive process. The synthesis of one molecule of cholesterol from acetyl-CoA requires eleven molecules of dioxygen, nine of which are consumed during the removal of the 4α, 4β, and 14α methyl groups in lanosterol and its metabolite 24,25-dihydrolanosterol by the successive actions of lanosterol 14α-demethylase and C4-methyl sterol oxidase (Figure 1). This led to speculation that oxygen deprivation (hypoxia) might block demethylation of lanosterol and 24,25-dihydrolanosterol and thereby stimulate degradation of reductase. Indeed, a recent study shows that hypoxia blunts cholesterol synthesis by inhibiting lanosterol and 24,25-dihydrolanosterol demethylation, causing both sterols to accumulate in cells 66. Rapid degradation of reductase parallels hypoxia-induced accumulation of lanosterol and 24,25-dihydrolanosterol. This Insig-mediated degradation requires de novo sterol synthesis as indicated by its inhibition by compactin and the squalene monooxygenase inhibitor NB-598, but not the lanosterol 14α-demethylase inhibitor RS-21607 (see Figure 1). Although hypoxia accelerates degradation of reductase, processing of SREBPs remains unaffected. This finding is consistent with the observation described above that exogenous lanosterol stimulates degradation of reductase without inhibiting SREBP processing.
In addition to the accumulation of methylated sterols, the degradation of reductase in hypoxic cells also requires the action of the oxygen-sensitive transcription factor, HIF-1α. In oxygenated cells, HIF-1α is rapidly degraded owing to hydroxylation of specific proline residues in the protein 67. Prolyl hydroxylation enhances binding of HIF-1α to the von Hippel Lindau tumor suppressor protein (pVHL), which is the recognition component of a ubiquitin ligase that targets HIF-1α for proteasomal degradation. Prolyl hydroxylation of HIF-1α is catalyzed by a family of dioxygenases that use 2-oxoglutarate as a co-substrate and exhibit strict dependence for molecular oxygen 68, 69, 70. When cells are deprived of oxygen, prolyl hydroxylation is inhibited, allowing HIF-1α to escape degradation and accumulate to high levels. The stabilized HIF-1α subunits associate with the constitutive HIF-1β subunit, forming a heterodimeric transcription factor (HIF) that modulates expression of more than 70 genes involved in both systemic and cellular responses to oxygen deprivation 71.
Evidence implicating a major role for HIF-1α in the hypoxia-induced degradation of reductase is provided by both pharmacologic and genetic data. Treatment of oxygenated cells with dimethyloxalylglycine (DMOG), a non-specific inhibitor of 2-oxoglutarate-dependent dioxygenases, not only stabilizes HIF-1α 72 but also triggers rapid degradation of reductase through an Insig-dependent mechanism that requires de novo sterol synthesis. Genetic evidence for a role of HIF-1α in reductase degradation is provided by the observation that the enzyme is refractory to hypoxia- and DMOG-induced degradation in mutant cells that are deficient in HIF-1α. While these observations establish the importance of the action of HIF-1α in oxygen-regulated degradation of reductase, they raise questions as to the HIF-target genes that mediate the response. In several DNA microarray analyses, Insig-1 and Insig-2 transcripts have been identified among those increased by either DMOG or hypoxia treatment 73, 74, 75. This observation led to the subsequent discovery that DMOG and hypoxia enhance expression of both Insigs through a HIF-dependent mechanism. Considered together, these observations establish a connection between cholesterol synthesis and oxygen sensing in animal cells (Figure 4). These metabolic pathways are linked by two regulatory actions: (1) hypoxia-induced accumulation of the cholesterol biosynthetic intermediates lanosterol and 24,25-dihydrolanosterol; and (2) HIF-1α mediated induction of Insigs. Convergence of these signals triggers rapid degradation of reductase, which ultimately limits synthesis of cholesterol and helps to guard against the wasting of cellular oxygen in the face of hypoxia.
Mechanism for oxygen sensing in the cholesterol synthetic pathway. The link between synthesis of cholesterol and oxygen sensing in animal cells is provided by hypoxia-induced accumulation of lanosterol and 24,25-dihydrolanosterol and HIF-1α-mediated induction of Insig-1 and Insig-2. Convergence of these responses leads to rapid degradation of HMG CoA reductase, thereby limiting synthesis of cholesterol.
Full figure and legend (65K) Top of page Unanswered questions and future directions
Despite the recent advances in the understanding of molecular mechanisms underlying sterol-accelerated degradation of reductase, much remains to be determined. For instance, what is the mechanism by which lanosterol and 24,25-dihydrolanosterol trigger binding of reductase to Insigs? Do these methylated sterols directly bind the membrane domain of reductase in a reaction analogous to that of cholesterol and Scap? Unfortunately, attempts to demonstrate direct binding of methylated sterols to the membrane domain of reductase have been unsuccessful. Moreover, addition of lanosterol or 24,25-dihydrolanosterol to reductase-containing membranes in vitro fails to alter the tryptic pattern of the enzyme. Thus, the possibility exists that a distinct ER membrane protein binds to methylated sterols and, in turn, triggers binding of reductase to Insigs, thereby initiating reductase ubiquitination. Reductase is the target of statins, which are the most widely prescribed cholesterol-lowering drugs in humans. Interest in developing additional strategies that inhibit reductase has led to the discovery of nonsterol compounds, such as vitamin E (tocotrienols) and the bisphosphonate SR-12813, that mimic sterols in accelerating reductase degradation 76, 77. The availability of such reagents may prove useful in the ongoing quest to define the molecular mechanisms for the reductase sterol-sensing reaction.
Another unresolved question in reductase degradation is the mechanism for delivery of ubiquitinated forms of the enzyme from the membrane to the cytosol for proteasomal degradation. Unlike model ERAD substrates that are either completely lumenal or contain one transmembrane domain, proteasome inhibition leads to accumulation of ubiquitinated reductase on membranes, rather than in the cytosol 37. This suggests that degradation of reductase is coupled to its ubiquitination and proceeds through a membrane-bound intermediate. However, reductase must be degraded as a unit without releasing the catalytic domain into the cytosol, which would defeat the purpose of regulated degradation.
Efficient degradation of reductase requires nonsterol isoprenoids derived from mevalonate in addition to sterols. This was borne out of experiments showing that in compactin-treated cells sterols can trigger binding of reductase to Insigs and subsequent ubiquitination of the enzyme. However, the ubiquitinated reductase is not efficiently degraded unless the cells are also treated with mevalonate. This mevalonate requirement can be bypassed by the addition of geranylgeraniol (GG-OH), a 20-carbon isoprenoid, but not by the 15-carbon farnesol 38. GGOH does not appear to trigger reductase ubiquitination, even though it augments sterol-accelerated degradation of the enzyme. This suggests the action of nonsterol isoprenoids in a post-ubiquitination step of reductase degradation.
The current view of sterol-accelerated degradation of reductase is illustrated in the model shown in Figure 5. The reaction is initiated by sensing of membrane-embedded sterols through direct or indirect interactions with the membrane domain of reductase. This interaction causes reductase to bind to a subset of Insigs that are associated with gp78, which mediates transfer of ubiquitin from the E2 Ubc7 to lysines 89 and 248 of reductase. Ubiquitination targets reductase for recognition by gp78-associated VCP, which, together with its cofactors, somehow extract ubiquitinated reductase from membranes and deliver it to proteasomes for degradation. The extraction step appears to be augmented by GG-OH. It seems likely that GG-OH, after its conversion to metabolically active geranylgeranyl-pyrophosphate (GG-PP), is incorporated into a protein that enhances the effect of sterols on reductase degradation. Possible candidates include geranylgeranylated Rab proteins, which are known to play key roles in various aspects of vesicular transport 78. Thus, the possibility exists that a vesicle-mediated transport event delivers ubiquitinated reductase to a specific organelle or subdomain of the ER in which the protein is degraded. Notably, Ufd1 appears to play a key role in this pathway by enhancing gp78 ubiquitin ligase activity and modulating a post-ubiquitination step in reductase degradation. In addition, Ufd1 seems to bind to gp78 in a sterol-regulated fashion 49, but the significance of this is presently unknown. Complete elucidation of reductase degradation will likely require the reconstitution of post-ubiquitination steps of reductase degradation in a cell-free system.
Pathway for sterol-accelerated degradation of HMG CoA reductase. Accumulation of 25-hydroxycholesterol, lanosterol, or 24,25-dihydrolanosterol in ER membranes triggers binding of the reductase to Insigs. A subset of Insigs is associated with the membrane-anchored ubiquitin ligase, gp78, which binds the E2 Ubc7 and VCP, an ATPase that plays a role in extraction of ubiquitinated proteins from ER membranes. Through the action of gp78 and Ubc7, reductase becomes ubiquitinated, which triggers its extraction from the membrane by VCP, and subsequent delivery to proteasomes for degradation. The post-ubiquitination step is postulated to be enhanced by geranylgeraniol through an undefined mechanism that may involve a geranylgeranylated protein, such as one of the Rab proteins.
Full figure and legend (97K)
What is the contribution of reductase degradation to overall cholesterol homeostasis in whole animals? Insigs appear to play a major role in regulation of reductase in the mouse liver. Genetic deletion of Insigs results in the accumulation of reductase to a level approximately 20-fold higher than that in wild type mice 79. This accumulation is presumably attributable to the combination of both transcriptional and post-transcriptional regulation of reductase, but the extent to which each level of regulation contributed to the massive increase in reductase is unknown. Thus, studies that directly focus on reductase degradation are required in order to determine the contribution of protein stability to overall regulation of reductase in mice in vivo under various physiologic conditions, such as hypoxia.
The significance of Insig-mediated regulation of reductase in maintenance of cholesterol homeostasis is highlighted by the effectiveness of reductase inhibition in lowering plasma LDL-cholesterol in humans 80. However, the inhibition of reductase disrupts normal feedback inhibition of the enzyme, and animals respond by developing a compensatory increase in reductase levels in the liver 81, 82. Remarkably, a similar response has been observed in livers of statin-treated humans as well 83. Knowledge of the mechanisms for this compensatory increase, particularly the contribution of degradation, may facilitate development of novel drugs that improve the effectiveness of statins, or in some cases provide alternative treatments. Such a drug would be modeled after lanosterol and 24,25-dihydrolanosterol, which selectively stimulate reductase degradation without affecting the Scap-SREBP pathway or LDL-receptor activity. In addition, elucidation of the underlying mechanisms for sterol-accelerated, ERAD of reductase may have implications for degradation of other clinically important proteins such as the cystic fibrosis transmembrane conductance regulator (CFTR). Thus, further excitement will undoubtedly ensue once questions posed in this review begin to become clear.
Top of page References
Work in the DeBose-Boyd laboratory is supported by grants from the National Institutes of Health (HL20948), the Perot Family Foundation, the American Heart Association (0540128N), and the W.M. Keck Foundation.
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1101 Plumstead St., $255,000,
1116 San Gabriel Ave., $499,900,
1117 Dunrobin Garden St., $180,000,
1149 Midori St., $363,000, 179-31-813-004
117 Grandview Drive, $130,000,
120 Sttingham Park Ave., $264,000,
1661 Arabian Drive, $75,000,
171 Redwood Pond Drive, $200,000,
410 Golden Spears Place, $450,000,
441 Chateau Drive, $165,500,
605 Jade Circle, $133,000, 179-29-110-003
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826 Butch Cassidy Lane, $165,000,
943 Spiracle Ave., $245,487,
982 Klamath River Ave., $179,900,
173 Bear Cove Terrace, $295,974,
18 Pyrenees Court, $905,000,
180 Leaf Tree Ave., $287,340,
29 Montelago Blvd., No. 311, $79,000, 160-22-317-045
500 Punto Vallata Drive, $464,787,
653 Livery Court, $166,000,
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1092 Bootspur Drive, $184,000,
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151 Lemongold St., $250,000,
1556 Harwood Ave., $345,000,
1809 Country Meadows Drive, $445,000, 178-20-814-067
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228 Palmetto Pointe Drive, $355,000,
231 W. Horizon Ridge Parkway, No. 1018, $108,000, 178-24-811-132
27 Trailside Court, $213,000,
315 Dazzling Terrace, $325,000,
339 Pleasant Summit Drive, $457,500,
643 Pacific Cascades Drive, $290,000,
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1690 Normandy Way, No. 824, $70,000, 178-09-116-046
1691 Keepsake Ave., $87,000,
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405 Breeze Way, $175,000, 178-24-616-033
419 Rocky Road, $150,000, 178-24-516-017
For a complete listing, visit .reviewjournalm. Click on the Recent Stories tab on the right corner. Look for Saturday’s date and click on Real Estate. Figures are provided by AccuData, a local research firm.
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346 clayton st henderson nv 89074 $197,000, 178-07-212-013
66 dow jones st #1 henderson nv 89074 $135,000, 178-15-312-007
75 n valle verde dr #912 henderson nv 89074 $120,500, 178-17-719-056
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6436 ruddock dr north las vegas nv 89084 $254,900, 124-19-810-002
6504 boatbill st north las vegas nv 89084 $228,000, 124-20-410-049
6608 lavender lilly ln #2 north las vegas nv 89084 $132,500, 124-20-311-095
6608 night owl bluff ave north las vegas nv 89084 $216,500, 124-21-310-010
6636 evening grosbeak pl north las vegas nv 89084 $207,000, 124-19-715-079
6704 sea swallow st north las vegas nv 89084 $249,900, 124-20-711-141
6944 caspian tern st north las vegas nv 89084 $201,900, 124-19-213-025
6945 diver ave north las vegas nv 89084 $179,000, 124-20-211-033
3913 helens pouroff ave north las vegas nv 89085 $201,000, 124-07-814-064
1008 e rome blvd north las vegas nv 89086 $208,000, 124-23-312-032
1409 peyton stewart ct north las vegas nv 89086 $285,000, 124-23-712-005
2632 lazy leopard ct north las vegas nv 89086 $165,000, 124-24-310-041
2845 swanson ave north las vegas nv 89086 $145,000, 124-24-412-059
1009 palmer st las vegas nv 89101 $83,535, 139-25-612-037
136 cervantes st las vegas nv 89101 $85,000, 139-35-715-017
150 n las vegas blvd #1903 las vegas nv 89101 $394,000, 139-34-613-178
2204 wendell ave las vegas nv 89101 $103,000, 139-26-712-089
2600 constantine ave las vegas nv 89101 $135,000, 139-25-">310-152
2113 fontenelle st las vegas nv 89102 $49,000, 138-24-217-008
2300 w sahara ave #420 las vegas nv 89102 $45,000, 140-04-210-003
2412 mason ave las vegas nv 89102 $278,000, 139-32-410-008
3913 el parque ave las vegas nv 89102 $144,000, 162-06-711-095
3993 spring mountain rd #377 las vegas nv 89102 $63,000, 163-24-710-025
3993 spring mountain rd #377 las vegas nv 89102 $77,150, 163-24-710-062
4621 cinderella ln las vegas nv 89102 $142,000, 162-07-210-039
3594 moraga dr las vegas nv 89103 $68,000, 138-27-419-322
3661 bronco rd las vegas nv 89103 $76,000, 163-24-612-886
4335 thorndale pl las vegas nv 89103 $224,900, 163-23-213-025
4383 thorndale pl las vegas nv 89103 $185,500, 163-23-213-020
4471 dean martin dr #2105 las vegas nv 89103 $132,040, 124-17-615-205
5155 w tropicana ave #2146 las vegas nv 89103 $110,000, 163-25-510-158
5160 indian river dr #335 las vegas nv 89103 $67,200, 163-24-612-335
5415 w harmon ave #1039 las vegas nv 89103 $102,500, 138-25-313-047
5416 winston dr las vegas nv 89103 $229,900, 163-13-710-013
6318 humus ave las vegas nv 89103 $145,000, 176-11-510-115
6349 explorer dr las vegas nv 89103 $205,000, 163-23-712-140
1207 s 15th st las vegas nv 89104 $140,000, 162-02-115-032
1434 lucky st las vegas nv 89104 $136,000, 161-05-112-041
1504 wesley st las vegas nv 89104 $155,000, 161-05-210-025
1800 hassett ave las vegas nv 89104 $122,500, 162-02-712-065
1916 s 6th st las vegas nv 89104 $179,000, 162-03-315-037
1917 bonita st las vegas nv 89104 $83,000, 162-02-616-012
4820 e baltimore ave las vegas nv 89104 $180,000, 161-05-810-055
801 griffith ave las vegas nv 89104 $139,900, 162-03-615-001
1321 w adams ave las vegas nv 89106 $115,000, 139-28-613-001
1716 robin st las vegas nv 89106 $138,000, 139-20-810-021
1844 tourmaline blue st las vegas nv 89106 $108,000, 139-20-420-056
1908 robin st las vegas nv 89106 $110,000, 139-20-810-012
2252 la mark ave las vegas nv 89106 $115,000, 139-29-511-029
2305 holly ave las vegas nv 89106 $110,000, 139-20-711-021
335 arnold st las vegas nv 89106 $115,000, 139-33-210-045
600 s tonopah #300 las vegas nv 89106 $359,000, 178-21-810-028
106 narcissus ln las vegas nv 89107 $132,500, 139-29-812-026
201 falcon ln las vegas nv 89107 $135,000, 138-36-120-035
3025 palomino ln las vegas nv 89107 $146,000, 162-05-114-013
3105 sonia dr las vegas nv 89107 $625,000, 139-32-211-009
4108 fortune dr las vegas nv 89107 $152,000, 139-30-711-130
4313 handford ave las vegas nv 89107 $113,000, 139-19-111-108
4321 w bonanza rd las vegas nv 89107 $133,000, 139-30-410-010
444 wonderstone dr las vegas nv 89107 $156,500, 138-36-611-073
4601 baxter pl las vegas nv 89107 $145,000, 139-31-410-097
516 n wallace dr las vegas nv 89107 $220,000, 138-26-712-037
5700 heron ave las vegas nv 89107 $215,000, 162-06-214-012
5715 heron ave las vegas nv 89107 $116,300, 138-36-315-022
5820 lydia dr las vegas nv 89107 $110,000, 138-36-116-015
5913 granada ave las vegas nv 89107 $158,000, 138-25-314-010
6209 hargrove ave las vegas nv 89107 $135,000, 138-35-512-008
6225 hobart ave las vegas nv 89107 $139,000, 138-26-812-003
6300 garwood ave las vegas nv 89107 $115,000, 138-35-511-063
6609 bourbon way las vegas nv 89107 $269,900, 138-07-718-002
701 pioneer st las vegas nv 89107 $148,000, 139-30-716-016
721 chabot dr las vegas nv 89107 $248,000, 139-30-711-025
777 n rainbow blvd #120 las vegas nv 89107 $545,000, 176-11-710-003
813 stark dr las vegas nv 89107 $48,000, 139-17-712-053
1004 saylor way las vegas nv 89108 $130,000, 138-25-214-005
2109 willowbury dr ut c las vegas nv 89108 $74,000, 138-23-212-059
2433 sweetgum st las vegas nv 89108 $150,000, 138-14-413-077
3024 gentle breeze st las vegas nv 89108 $180,000, 138-14-110-094
3404 san juan dr las vegas nv 89108 $119,900, 139-30-514-060
4300 beth ave las vegas nv 89108 $147,000, 139-19-215-070
4401 caribou way las vegas nv 89108 $187,000, 138-02-212-026
4424 midway ln las vegas nv 89108 $130,000, 138-02-211-032
5809 rae dr las vegas nv 89108 $134,900, 138-25-211-023
6012 vegas dr las vegas nv 89108 $75,000, 138-24-418-001
6304 mint frost way las vegas nv 89108 $160,000, 138-26-512-004
6332 lorille ln las vegas nv 89108 $165,000, 138-20-511-007
6524 moon roses ct las vegas nv 89108 $83,000, 138-25-812-015
6561 gazelle dr las vegas nv 89108 $159,900, 138-23-315-003
6600 coastal breeze ct las vegas nv 89108 $149,000, 138-14-110-001
917 shelton dr las vegas nv 89108 $189,900, 138-26-618-047
210 e flamingo rd #208 las vegas nv 89109 $132,000, 162-16-810-068
222 karen ave # las vegas nv 89109 $380,000, 162-10-114-342
2852 loveland dr #1807 las vegas nv 89109 $50,000, 162-16-810-061
1251 bledso ln las vegas nv 89110 $72,500, 161-17-413-032
129 romero dr las vegas nv 89110 $55,931.97 140-32-311-058
1363 betty ln las vegas nv 89110 $240,000, 140-28-210-048
1580 desertaire way las vegas nv 89110 $99,900, 140-07-311-036
4228 caliper dr las vegas nv 89110 $108,000, 140-30-812-019
4444 berkley ave las vegas nv 89110 $37,000, 140-31-816-048
4617 toadstool ln las vegas nv 89110 $122,500, 140-29-414-048
500 red bandana st las vegas nv 89110 $112,703, 140-31-512-022
513 hall of fame dr las vegas nv 89110 $140,570, 140-33-618-020
528 stanley cup dr las vegas nv 89110 $100,000, 140-30-215-003
5641 gorham ave las vegas nv 89110 $95,000, 140-33-611-074
5657 coaldale pl las vegas nv 89110 $189,995, 140-33-611-056
58 moon chase st las vegas nv 89110 $410,000, 140-34-212-014
5831 goodsprings ct las vegas nv 89110 $139,900, 140-33-614-024
6074 adobe summit ave las vegas nv 89110 $199,000, 140-27-213-078
6134 kadena cir las vegas nv 89110 $165,000, 140-27-415-050
6670 e owens ave las vegas nv 89110 $331,500, 140-22-803-005
7061 montana ave las vegas nv 89110 $230,000, 161-15-410-039
732 summer heights ln las vegas nv 89110 $143,000, 140-33-514-051
806 sun shimmer pl las vegas nv 89110 $248,000, 140-27-816-025
5165 turnberry ln las vegas nv 89113 $275,000, 163-27-210-005
7189 s durango dr #311 las vegas nv 89113 $90,000, 176-05-810-208
7565 frontier ranch ln las vegas nv 89113 $225,000, 163-34-110-066
7923 trail head dr las vegas nv 89113 $269,000, 163-33-610-030
8070 w russell rd #1047 las vegas nv 89113 $93,000, 163-28-811-070
8208 dutch harbor cir las vegas nv 89113 $545,000, 176-16-111-001
2308 colebrook st las vegas nv 89115 $46,000, 140-20-111-153
2354 sandy ln las vegas nv 89115 $125,000, 140-21-210-001
3329 queen st las vegas nv 89115 $109,500, 140-07-410-022
3610 saint bar ct las vegas nv 89115 $75,000, 140-07-311-056
3821 soda springs dr las vegas nv 89115 $33,700, 140-18-215-010
3974 lancome st las vegas nv 89115 $90,000, 140-08-110-073
6150 belmont shores st north las vegas nv 89115 $130,000, 123-29-210-230
2000 jasper bluff st #207 las vegas nv 89117 $120,000, 163-06-320-053
3120 mediterranean dr las vegas nv 89117 $199,900, 163-08-717-051
3205 shallow point cir las vegas nv 89117 $182,900, 163-07-810-011
3265 s tioga way las vegas nv 89117 $600,000, 163-10-405-006
3320 s fort apache rd #1134 las vegas nv 89117 $100,000, 163-17-116-059
7155 coley ave las vegas nv 89117 $425,000, 163-10-705-003
8057 lands end ave las vegas nv 89117 $150,000, 162-24-310-060
8101 meantmore ave las vegas nv 89117 $505,000, 164-12-415-014
8222 stoneheather ct las vegas nv 89117 $275,000, 163-09-212-039
8509 hearst ct las vegas nv 89117 $135,000, 138-33-111-018
8600 w charleston blvd #1020 las vegas nv 89117 $72,500, 138-32-819-036
8709 maritime dr las vegas nv 89117 $177,000, 163-08-819-014
8944 clairton ct las vegas nv 89117 $315,000, 125-27-612-003
9020 cape wood ct las vegas nv 89117 $264,500, 163-08-312-047
9220 vosburgh dr las vegas nv 89117 $168,000, 138-08-613-009
9400 alameda harbor ave las vegas nv 89117 $234,000, 163-07-811-010
6198 island palm ave las vegas nv 89118 $460,000, 163-26-815-001
1065 e flamingo rd #815 las vegas nv 89119 $80,000, 162-27-711-007
1156 placerville st las vegas nv 89119 $115,000, 177-03-813-027
1469 santa anita dr las vegas nv 89119 $240,000, 124-22-510-037
1545 white dr las vegas nv 89119 $230,000, 177-02-413-007
1730 jupiter ct #a las vegas nv 89119 $170,000, 178-10-415-031
1847 misty glade dr las vegas nv 89119 $176,000, 177-02-810-045
1865 hallwood dr las vegas nv 89119 $158,000, 162-24-710-028
1980 sunnyslope ave las vegas nv 89119 $143,000, 162-26-710-172
5438 clydesdale st las vegas nv 89119 $143,000, 162-26-710-283
7010 encore way las vegas nv 89119 $157,000, 177-02-310-024
7099 rusty nail way las vegas nv 89119 $227,000, 177-02-319-019
934 lady marlene ave las vegas nv 89119 $133,500, 162-27-715-043
2881 vista del sol ave las vegas nv 89120 $185,222, 161-20-110-001
3745 braewood south ave las vegas nv 89120 $138,000, 161-30-313-038
3885 e reno ave las vegas nv 89120 $152,000, 161-30-610-008
4002 lucas ave las vegas nv 89120 $145,000, 161-30-714-038
4840 elaina ave las vegas nv 89120 $115,000, 161-29-712-081
5020 mesaview dr las vegas nv 89120 $175,000, 161-30-117-025
5194 brentmead dr las vegas nv 89120 $175,000, 161-30-612-103
5384 hillsboro ln las vegas nv 89120 $125,000, 161-29-712-010
5481 shodall cir las vegas nv 89120 $180,000, 161-30-316-011
5618 s mojave rd las vegas nv 89120 $192,000, 162-25-813-014
5880 s pearl st las vegas nv 89120 $306,000, 161-31-105-016
2444 domingo st las vegas nv 89121 $100,000, 162-13-310-033
2470 e flamingo rd #c las vegas nv 89121 $222,000, 138-29-312-012
2632 topaz sq las vegas nv 89121 $43,000, 162-11-511-045
2725 s nellis blvd #2079 las vegas nv 89121 $32,500, 162-23-210-002
2791 mcleod dr las vegas nv 89121 $160,000, 162-12-214-045
3542 rio mayo dr las vegas nv 89121 $115,000, 161-17-614-033
3691 mckinley ave las vegas nv 89121 $120,000, 161-18-311-033
3925 chinchilla ave las vegas nv 89121 $149,900, 161-19-712-027
3941 placita ave las vegas nv 89121 $124,000, 161-07-610-061
3988 el segundo ave las vegas nv 89121 $115,000, 161-07-610-014
3990 e twain ave las vegas nv 89121 $140,000, 161-18-616-055
4630 dennis way las vegas nv 89121 $154,900, 161-20-712-050
4632 bountiful way las vegas nv 89121 $120,500, 162-24-712-005
4778 fuentes way las vegas nv 89121 $50,000, 161-17-511-022
3234 chimayo ln las vegas nv 89122 $75,000, 161-09-810-213
4057 whispering quail ct las vegas nv 89122 $214,900, 161-15-815-005
4719 madrigal way las vegas nv 89122 $139,900, 161-22-411-021
5070 blanton dr las vegas nv 89122 $135,000, 161-21-411-091
5118 northridge cir las vegas nv 89122 $90,000, 161-28-610-034
5240 petal ave las vegas nv 89122 $80,000, 161-21-112-047
5655 bolton valley dr las vegas nv 89122 $149,000, 161-21-712-017
5678 sentry palm ct las vegas nv 89122 $380,000, 178-20-212-060
5705 mahogany run pl las vegas nv 89122 $138,000, 161-16-511-049
5870 medallion dr #101 las vegas nv 89122 $61,000, 161-27-313-136
6156 wheat penny ave las vegas nv 89122 $105,000, 138-03-819-039
6402 azurelyn ave las vegas nv 89122 $178,000, 161-27-514-113
6 buck jones ave #102 las vegas nv 89122 $118,000, 161-10-710-062
6613 diamond care dr las vegas nv 89122 $118,000, 161-26-211-085
6836 mahogany meadows ave las vegas nv 89122 $158,000, 161-26-310-021
6877 gold nugget dr las vegas nv 89122 $150,000, 161-26-310-047
1438 silver rain ave las vegas nv 89123 $275,000, 177-23-410-128
1675 pecan orchard ln las vegas nv 89123 $245,000, 177-14-112-025
2220 buffalo run ave las vegas nv 89123 $188,000, 177-11-611-113
331 barletta ave las vegas nv 89123 $319,000, 177-21-511-017
671 hermosa palms ave las vegas nv 89123 $182,000, 177-15-116-001
738 fontayne ave las vegas nv 89123 $270,000, 177-22-210-046
7480 puritan ave las vegas nv 89123 $221,000, 177-10-113-018
7577 poppy meadow st las vegas nv 89123 $173,900, 177-10-613-070
7765 meadow creek st las vegas nv 89123 $214,500, 177-11-712-055
8118 tone st las vegas nv 89123 $183,000, 177-15-511-013
8255 s las vegas blvd #1515 las vegas nv 89123 $275,000, 177-17-510-260
8640 emerald grove way las vegas nv 89123 $269,000, 176-20-811-008
8833 haviland rd las vegas nv 89123 $226,600, 177-15-412-035
902 cavaison ave las vegas nv 89123 $250,000, 177-22-714-023
9031 galena crossing st las vegas nv 89123 $335,000, 178-19-413-009
9039 emery lake st las vegas nv 89123 $247,500, 177-23-512-020
9055 purple leaf st las vegas nv 89123 $148,000, 177-20-511-010
9484 corato st las vegas nv 89123 $225,000, 177-23-714-025
950 denberry way las vegas nv 89123 $305,000, 177-10-613-068
986 country wind way las vegas nv 89123 $259,900, 177-15-811-044
5 tyrol way las vegas nv 89124 $410,000, 128-31-210-021
4187 matterhorn way las vegas nv 89124 $295,000, 129-36-610-045
1141 nevada sky st las vegas nv 89128 $128,000, 138-28-224-010
1150 n buffalo dr #1076 las vegas nv 89128 $76,000, 138-27-219-068
2945 channel bay dr las vegas nv 89128 $409,000, 138-16-613-002
3013 blue fin cir las vegas nv 89128 $229,900, 138-16-513-058
3125 n buffalo dr #1136 las vegas nv 89128 $163,000, 125-08-416-007
3150 soft breezes dr #1212 las vegas nv 89128 $75,000, 138-16-516-054
3150 soft breezes dr #2033 las vegas nv 89128 $64,000, 138-16-516-141
3151 soaring gulls dr #2075 las vegas nv 89128 $74,000, 138-16-120-199
7837 desert bell ave las vegas nv 89128 $207,000, 138-21-816-065
7908 waterfalls ave las vegas nv 89128 $278,000, 138-21-612-015
8016 painted clay ave las vegas nv 89128 $220,000, 138-21-425-009
8117 tropic isle cir las vegas nv 89128 $282,500, 138-21-217-015
8201 point view ct las vegas nv 89128 $367,500, 138-16-413-074
10348 faustine ave las vegas nv 89129 $166,000, 137-12-513-015
10533 cliff edge ct las vegas nv 89129 $207,500, 137-01-210-023
10630 shifting breeze ave las vegas nv 89129 $200,000, 137-12-210-057
10728 little horse creek ave las vegas nv 89129 $178,000, 137-01-114-022
3429 round valley way las vegas nv 89129 $170,000, 163-12-603-001
3504 jewel night st las vegas nv 89129 $310,000, 137-12-715-031
3921 braod meadow ct las vegas nv 89129 $56,565, 139-19-311-072
3925 white castle st las vegas nv 89129 $320,000, 138-08-112-004
4128 bennett mountain st las vegas nv 89129 $320,000, 137-01-412-020
4252 sparrow springs ct las vegas nv 89129 $142,000, 138-03-313-038
4425 n chieftain st las vegas nv 89129 $415,000, 138-06-605-016
4 dunlap crossing st las vegas nv 89129 $305,000, 138-03-211-011
7301 breezy night ct las vegas nv 89129 $180,000, 138-03-218-022
8922 indian eagle dr las vegas nv 89129 $172,000, 138-08-315-013
9113 ballad ave las vegas nv 89129 $176,000, 138-08-412-014
4705 gonzales dr las vegas nv 89130 $202,500, 138-01-112-002
4793 hampstead heath ct las vegas nv 89130 $157,000, 138-02-110-020
4894 w lone mountain rd las vegas nv 89130 $175,000, 125-36-515-058
4925 signal dr las vegas nv 89130 $202,000, 125-36-813-004
5704 calm lagoon ave las vegas nv 89130 $242,000, 125-25-211-040
5744 typan st las vegas nv 89130 $179,990, 125-25-814-061
5804 wood petal st las vegas nv 89130 $235,000, 125-25-710-002
5831 rebecca rd las vegas nv 89130 $350,000, 125-26-302-012
5860 thai coast st las vegas nv 89130 $500,000, 125-25-313-031
6402 inwood park ct las vegas nv 89130 $324,500, 125-35-310-092
7065 w ann rd #130-115 las vegas nv 89130 $370,000, 125-10-310-007
7266 crest peak ave las vegas nv 89130 $167,500, 125-27-311-020
5216 whisper lake ave las vegas nv 89131 $277,500, 125-13-711-025
5414 regal willow ct las vegas nv 89131 $272,450, 125-24-110-036
5830 toofer winds ct las vegas nv 89131 $300,004, 125-12-111-062
6150 deep autumn ave las vegas nv 89131
7033 bocaire dr las vegas nv 89131 $237,000, 125-10-511-025
7221 eaglegate st las vegas nv 89131 $240,000, 125-16-820-029
7233 boyd ln las vegas nv 89131 $210,000, 178-31-112-018
7320 misty glow ct las vegas nv 89131 $195,000, 125-16-816-044
7331 hazel plain ave las vegas nv 89131 $380,000, 125-22-113-018
7340 silver spirit st las vegas nv 89131 $95,000, 163-30-519-034
7352 misty glow ct las vegas nv 89131 $165,000, 125-16-816-068
7604 windswept st las vegas nv 89131 $219,000, 125-16-212-009
7623 maple meadow st las vegas nv 89131 $252,000, 125-16-215-007
7679 morning lake dr las vegas nv 89131 $111,777, 124-27-211-067
7725 curiosity ave las vegas nv 89131 $180,000, 125-16-610-056
7729 brilliant forest st las vegas nv 89131 $205,000, 125-16-617-005
8222 sunset horizon st las vegas nv 89131 $411,000, 125-11-310-060
8323 rainbow sky st las vegas nv 89131 $375,000, 125-11-310-010
8724 purple wisteria st las vegas nv 89131 $170,000, 125-13-612-023
9056 walker lake ct las vegas nv 89131 $150,000, 125-17-413-023
2449 n tenaya #33883 las vegas nv 89133 $328,000, 137-34-615-054
10424 trenton pl las vegas nv 89134 $265,000, 137-24-512-073
10504 findlay ave las vegas nv 89134 $270,000, 137-24-211-071
2601 saltbush dr las vegas nv 89134 $128,834, 138-17-813-022
2608 palmridge dr las vegas nv 89134 $155,000, 138-17-713-061
2625 saltbush dr las vegas nv 89134 $170,000, 138-17-714-052
3109 goodhope ct las vegas nv 89134 $120,000, 138-17-111-008
8929 brook bay ct las vegas nv 89134 $305,000, 138-30-515-013
9000 bald eagle dr las vegas nv 89134 $1,145,000, 138-20-213-019
9309 cactus wood dr las vegas nv 89134 $203,000, 138-18-612-006
9432 summer rain dr las vegas nv 89134 $197,500, 138-19-515-116
9716 ridge creek pl las vegas nv 89134 $225,500, 138-19-412-018
9901 trailwood dr #2133 las vegas nv 89134 $165,000, 138-19-324-015
10508 hope mills dr las vegas nv 89135 $500,000, 164-13-615-001
10531 penns creek ct las vegas nv 89135 $228,800, 164-12-514-058
10651 angelo tenero ave las vegas nv 89135 $294,000, 164-25-620-036
10810 sterling forest ave las vegas nv 89135 $815,000, 164-12-415-011
10810 woodstream ct las vegas nv 89135 $715,000, 164-12-411-022
11414 newton commons dr #101 las vegas nv 89135 $240,000, 164-02-226-041
2624 heathrow st las vegas nv 89135 $178,000, 164-12-111-080
4599 denaro dr las vegas nv 89135 $365,000, 164-24-310-063
5085 alfingo st las vegas nv 89135 $299,000, 164-25-515-053
11618 costa linda ave las vegas nv 89138 $366,700, 137-35-114-026
11830 portina dr #2028 las vegas nv 89138 $200,000, 163-07-413-026
321 corsicana st las vegas nv 89138 $161,100, 138-08-412-018
608 doletto st las vegas nv 89138 $280,000, 137-35-619-023
651 hayborn meadows st las vegas nv 89138 $400,000, 137-34-213-063
679 indian garden st las vegas nv 89138 $243,888, 137-35-618-039
820 paseo rocoso pl las vegas nv 89138 $295,000, 137-34-716-033
5047 vacaville ave las vegas nv 89139 $151,000, 176-13-510-050
6225 humus ave las vegas nv 89139 $294,300, 176-14-113-176
6274 oread ave las vegas nv 89139 $134,580, 176-11-510-153
6274 pangea ave las vegas nv 89139 $160,000, 176-11-511-057
6696 coronado palms ave las vegas nv 89139 $181,000, 163-20-714-003
6721 dunraven ave las vegas nv 89139 $175,000, 176-11-112-020
6774 coronado crest ave las vegas nv 89139 $363,000, 176-11-310-013
7568 belgian lion st las vegas nv 89139 $236,250, 177-18-218-042
8059 wards ferry st las vegas nv 89139 $213,000, 176-12-810-212
8127 sorrel st las vegas nv 89139 $292,510, 176-14-113-178
8133 sorrel st las vegas nv 89139 $295,624, 176-14-113-177
8144 sorrel st las vegas nv 89139 $278,300, 176-14-113-159
8228 sorrel st las vegas nv 89139 $315,320, 176-14-113-145
8466 loxton cellars st las vegas nv 89139 $225,500, 177-18-215-105
10 pink dogwood dr las vegas nv 89141 $789,363, 191-07-510-090
10228 nolinas st las vegas nv 89141 $205,000, 124-19-616-016
10535 refugio st las vegas nv 89141 $385,000, 177-31-511-021
10762 rococo ct las vegas nv 89141 $177,000, 177-31-615-065
10795 avenzano st las vegas nv 89141 $207,000, 177-32-213-002
11135 ferragamo ct las vegas nv 89141 $225,000, 177-31-411-029
11171 verismo st las vegas nv 89141 $162,500, 177-32-414-015
11257 lavandou dr las vegas nv 89141 $340,000, 176-36-812-048
4846 graziano ave las vegas nv 89141 $191,000, 177-31-213-043
4949 calvary ct las vegas nv 89141 $76,000, 177-23-817-376
8 sand dollar ave las vegas nv 89141 $117,139, 176-25-810-032
5337 blue oat ave las vegas nv 89141 $155,000, 176-25-810-184
5548 tabernas ct las vegas nv 89141 $200,000, 176-36-416-036
5571 casa palazzo ct las vegas nv 89141 $392,000, 176-36-214-024
56 olympia canyon way las vegas nv 89141 $2,598,750, 191-06-217-024
6088 bassio ave las vegas nv 89141 $245,000, 176-36-216-050
1699 divinity st las vegas nv 89142 $52,000, 140-29-411-149
2529 winterwood blvd las vegas nv 89142 $167,000, 161-09-110-052
2747 sunrise bluff dr las vegas nv 89142 $255,000, 161-11-210-008
5726 slice dr las vegas nv 89142 $149,900, 161-04-813-106
6305 peach orchard rd las vegas nv 89142 $145,000, 161-03-813-040
6775 azure clouds way las vegas nv 89142 $298,000, 161-11-114-002
7501 crooked branch st las vegas nv 89143 $191,500, 125-17-715-031
7509 nicklin st las vegas nv 89143 $175,000, 125-17-715-023
8025 quilted bear st las vegas nv 89143 $221,000, 125-08-122-011
8908 rusty rifle ave las vegas nv 89143 $269,900, 125-08-212-018
9100 picket fence ave las vegas nv 89143 $215,000, 125-08-219-008
1004 duckhorn ct #104 las vegas nv 89144 $148,000, 138-30-215-064
1012 domnus ln #203 las vegas nv 89144 $157,000, 138-30-215-033
10304 huxley cross ln las vegas nv 89144 $375,000, 137-25-717-025
10321 pacific summerset ln las vegas nv 89144 $285,000, 137-24-813-108
10524 pine glen ave #105 las vegas nv 89144 $127,500, 137-36-113-255
10657 royal view ave las vegas nv 89144 $245,000, 137-25-314-023
10709 beringer dr las vegas nv 89144 $800,000, 137-25-118-029
10828 windrose point ave las vegas nv 89144 $12,500, 139-28-612-084
11024 sonoma creek ct las vegas nv 89144 $239,900, 137-26-715-045
116 s ring dove dr las vegas nv 89144 $638,000, 137-36-519-002
6325 juliano rd las vegas nv 89144 $309,900, 125-21-412-003
917 corsica ln las vegas nv 89144 $250,000, 137-25-612-034
9401 canyon mesa dr las vegas nv 89144 $205,000, 139-34-412-072
1001 neil armstrong cir las vegas nv 89145 $132,000, 138-34-415-025
105 redstone st las vegas nv 89145 $125,000, 138-34-519-032
124 sam jonas dr las vegas nv 89145 $167,000, 138-33-518-006
248 jon belger dr las vegas nv 89145 $155,000, 138-33-111-067
357 tobler dr las vegas nv 89145 $132,500, 138-33-216-010
6948 erin cir las vegas nv 89145 $157,500, 125-13-511-028
7709 pheasant ln las vegas nv 89145 $175,000, 138-33-715-024
8000 mount harris ct las vegas nv 89145 $55,000, 138-25-111-033
8104 leger dr las vegas nv 89145 $200,000, 138-33-215-011
8348 san grail ct las vegas nv 89145 $95,000, 138-33-323-039
8409 running deer ave #202 las vegas nv 89145 $72,500, 138-28-616-024
9101 alta dr #1103 las vegas nv 89145 $1,140,000, 138-32-213-090
924 vincent way las vegas nv 89145 $180,000, 138-34-811-031
9724 royal lamb dr las vegas nv 89145 $110,000, 177-13-310-020
1275 westwind rd las vegas nv 89146 $260,590, 163-01-105-005
2835 s bronco st las vegas nv 89146 $440,000, 174-20-401-013
3049 westwind rd las vegas nv 89146 $182,500, 162-06-215-013
5218 stampa ave las vegas nv 89146 $127,500, 163-12-711-002
5883 laredo st las vegas nv 89146 $99,000, 163-12-111-017
5991 w obannon dr las vegas nv 89146 $149,000, 138-36-611-031
3673 spring day ct las vegas nv 89147 $208,000, 163-16-614-046
3716 white peppermint dr las vegas nv 89147 $190,603, 163-15-311-015
3729 broadmead st las vegas nv 89147 $330,000, 163-17-714-006
3730 bombastic ct las vegas nv 89147 $57,000, 163-21-516-255
3766 cape solitude st las vegas nv 89147 $148,500, 163-18-310-084
3864 almondview st las vegas nv 89147 $211,500, 163-15-313-044
4540 avery rock st las vegas nv 89147 $296,000, 163-21-717-007
4579 tidal cove ct las vegas nv 89147 $182,500, 163-21-715-044
4644 altina st las vegas nv 89147 $25,000, 139-27-110-018
4707 desert plains rd las vegas nv 89147 $255,000, 163-21-817-013
4718 stavanger ln las vegas nv 89147 $160,000, 163-20-718-020
4768 skyhawk canyon st las vegas nv 89147 $340,000, 163-19-412-047
4777 crakow ct las vegas nv 89147 $130,000, 138-11-110-150
7140 mountain moss dr las vegas nv 89147 $112,000, 139-31-410-068
7219 empress dr las vegas nv 89147 $123,000, 163-22-616-043
7950 w flamingo rd #1125 las vegas nv 89147 $80,000, 163-16-811-068
8367 flamingo rd #101 las vegas nv 89147 $201,000, 179-29-415-006
8460 birthstone ave las vegas nv 89147 $143,000, 163-21-114-033
8824 prague ct las vegas nv 89147 $409,000, 163-20-716-001
9102 w viking rd las vegas nv 89147 $250,000, 163-17-316-031
9626 blyth rock ave las vegas nv 89147 $90,000, 161-10-710-314
9682 camino capistrano ln las vegas nv 89147 $185,000, 138-36-610-034
10087 canyon hills ave las vegas nv 89148 $284,000, 163-30-415-017
197 country greens ave las vegas nv 89148 $82,500, 162-13-213-019
32 sahalee dr las vegas nv 89148 $450,000, 176-08-210-012
5973 indian sunset st las vegas nv 89148 $210,000, 163-32-611-018
6871 crystal rapids st las vegas nv 89148 $192,500, 176-05-213-036
707 running putt way las vegas nv 89148 $430,000, 176-17-612-037
7162 hedgemaple ct las vegas nv 89148 $51,000, 138-24-110-092
8997 castledowns st las vegas nv 89148 $210,000, 176-20-513-053
9034 vintage wine ave las vegas nv 89148 $215,000, 176-20-110-008
9069 dryland ct las vegas nv 89148 $169,900, 176-08-112-147
9119 westchester hill ave las vegas nv 89148 $195,000, 176-20-210-094
9120 glennon ave las vegas nv 89148 $160,000, 176-08-112-131
9146 hombard ave las vegas nv 89148 $159,000, 176-08-112-068
9191 autumn mist ct las vegas nv 89148 $195,000, 176-05-217-005
9883 canyon hills ave las vegas nv 89148 $165,000, 126-13-313-043
9979 ridgehaven ave las vegas nv 89148 $265,000, 163-30-310-005
4835 byzantine ct las vegas nv 89149 $779,000, 125-31-801-025
5116 jessica joy st las vegas nv 89149 $635,000, 125-33-311-019
5393 painted mirage rd las vegas nv 89149 $179,000, 125-34-610-004
5555 michelli crest way las vegas nv 89149 $650,000, 126-36-501-003
5725 berwick falls ln las vegas nv 89149 $171,000, 125-28-815-007
5801 n butler st las vegas nv 89149 $165,000, 125-35-610-016
6390 buzz aldrin dr las vegas nv 89149 $63,000, 138-27-615-012
6917 gothic marigold st las vegas nv 89149 $135,000, 125-20-211-036
7405 delectable ct las vegas nv 89149 $146,000, 125-17-310-021
7913 aubergine cove ct las vegas nv 89149 $297,500, 125-18-111-064
7941 crimson point st las vegas nv 89149 $154,000, 125-18-110-094
8020 wispy sage way las vegas nv 89149 $575,000, 125-33-210-035
9025 lacey landing ct las vegas nv 89149 $169,900, 125-17-213-039
9105 umberland ave las vegas nv 89149 $358,600, 125-16-214-019
9121 patrick henry ave las vegas nv 89149 $180,000, 125-20-311-008
9168 beautiful flower ct las vegas nv 89149 $179,999, 125-20-410-159
9219 avon park ave las vegas nv 89149 $199,990, 125-19-510-023
9237 apollo heights ave las vegas nv 89149 $245,000, 125-19-516-096
9385 w tropical pkwy las vegas nv 89149 $260,000, 125-30-703-001
9441 biroth ct las vegas nv 89149 $194,000, 125-19-611-024
9747 cathedral pines ave las vegas nv 89149 $739,940, 125-18-311-055
glistening brook ct las vegas nv 89149 $730,000, 125-31-201-029
1710 candice st las vegas nv 89156 $145,000, 140-21-814-028
2261 carlsbad cir las vegas nv 89156 $93,000, 139-30-514-003
2668 grand basin dr las vegas nv 89156 $149,500, 140-15-718-053
5772 camino ramon ave las vegas nv 89156 $111,000, 140-21-611-017
6362 red comet ct las vegas nv 89156 $134,000, 140-15-814-011
6380 diego dr las vegas nv 89156 $143,000, 140-22-714-024
6457 cedar break ave las vegas nv 89156 $138,000, 140-15-817-005
6470 rosemount ave las vegas nv 89156 $140,000, 140-15-710-025
6570 hayden peak ln las vegas nv 89156 $117,000, 140-15-614-020
3750 s las vegas blvd #3209 las vegas nv 89158 $1,728,000, 162-20-712-213
10128 haymarket peak ave las vegas nv 89166 $233,000, 126-13-516-065
10409 walworth ave las vegas nv 89166 $215,000, 126-13-815-065
7128 rosecrans st las vegas nv 89166 $310,000, 126-24-113-032
7430 pine harbor st las vegas nv 89166 $133,000, 126-13-312-033
7759 weavercrest ct las vegas nv 89166 $219,000, 126-13-212-165
7790 scottie st las vegas nv 89166 $465,000, 126-18-601-002
1950 capistrano ave las vegas nv 89169 $129,500, 162-11-712-073
3110 burnham ave las vegas nv 89169 $177,000, 162-11-810-125
3258 pawnce dr las vegas nv 89169 $105,000, 139-35-611-063
10117 glorious moon ct las vegas nv 89178 $254,000, 176-27-312-039
6325 stonily ln las vegas nv 89178 $67,550, 139-23-110-015
7054 mirkwood ave las vegas nv 89178 $380,000, 176-27-610-007
716 quayside ct las vegas nv 89178 $212,000, 176-18-514-044
7220 w meranto ave las vegas nv 89178 $336,000, 176-22-701-003
7926 avalon valley ct las vegas nv 89178 $102,000, 176-04-710-155
8008 base camp ave las vegas nv 89178 $240,000, 176-28-511-056
817 connex ct las vegas nv 89178 $252,500, 176-18-111-007
8759 horizon wind ave #103 las vegas nv 89178 $145,000, 176-20-714-222
8805 traveling breeze ave #101 las vegas nv 89178 $130,000, 176-20-714-133
8934 harmony hall ave las vegas nv 89178 $234,000, 176-29-611-100
8954 catfish stream ave las vegas nv 89178 $225,000, 176-20-712-082
9122 ashiw ave las vegas nv 89178 $154,900, 176-21-315-065
9139 hermosa valley st las vegas nv 89178 $222,500, 176-19-610-063
9372 hosner st las vegas nv 89178 $189,900, 176-20-315-055
9517 dawning heat st las vegas nv 89178 $149,000, 176-20-414-003
9645 stonily ln las vegas nv 89178 $449,000, 176-21-810-023
9729 high alpine st las vegas nv 89178 $269,900, 176-28-511-009
9792 sunflower hill st las vegas nv 89178 $245,000, 176-28-512-017
9918 blue villa ct las vegas nv 89178 $190,000, 176-29-613-008
1460 lawman ct las vegas nv 89179 $165,000, 177-02-412-013
7381 benlomond ave las vegas nv 89179 $225,000, 176-34-310-139
7718 flowering quince dr las vegas nv 89179 $233,734, 176-34-118-026
10179 lemon thyme st las vegas nv 89183 $190,000, 177-27-711-115
10207 rising tree st las vegas nv 89183 $148,000, 177-27-312-076
10213 cupids dart st las vegas nv 89183 $210,000, 177-27-310-184
10378 september flower st las vegas nv 89183 $159,000, 177-26-417-035
10452 cherry brook st las vegas nv 89183 $210,000, 177-26-412-023
10595 placid st las vegas nv 89183 $750,000, 177-33-501-017
10621 medicine bow st las vegas nv 89183 $282,000, 177-34-516-075
121 gilliflower ave las vegas nv 89183 $146,000, 191-04-410-039
217 centocelle ave las vegas nv 89183 $309,000, 191-04-610-014
769 jaded emerald ct las vegas nv 89183 $230,000, 177-27-113-002
930 grand cerritos ave las vegas nv 89183 $207,000, 176-36-618-034
9966 mystic dance st las vegas nv 89183 $260,000, 177-27-612-018
9971 fragile fields st las vegas nv 89183 $135,000, 177-27-614-171
158 oakridge dr dayton nv 89403 $162,300, 126-13-117-051
1322 denver st boulder city nv 89005 $380,000, 186-04-410-005
1516 fifth st boulder city nv 89005 $236,000, 186-09-210-031
631 h ave boulder city nv 89005 $195,000, 186-09-510-123
773 fairway dr boulder city nv 89005 $290,000, 186-16-219-009
795 pebble beach dr boulder city nv 89005 $65,000, 186-08-512-010
315 concord dr mesquite nv 89027 $110,000.00 001-17-810-080
317 tex st mesquite nv 89027 $155,000.00 001-16-512-023
375 poppy ln mesquite nv 89027 $140,000.00 001-16-410-017
467 mesa blvd #202 mesquite nv 89027 $87,500.00 001-09-616-024
699 mesa vw mesquite nv 89027 $128,800.00 001-09-613-027
700 aztec cir #1d mesquite nv 89027 $113,398.95 001-19-512-014
3337 partridge run st laughlin nv 89029 $145,000.00 264-28-122-020
1505 branding iron trail mesquite nv 89034 $188,000.00 002-24-610-004