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310-152 - Sun Certified Backup and Recovery Engineer (emphasis on Solstice Backup) - Dump Information

Vendor	:	SUN
Exam Code	:	310-152
Exam Name	:	Sun Certified Backup and Recovery Engineer (emphasis on Solstice Backup)
Questions and Answers	:	115 Q & A
Updated On	:	October 25, 2017
PDF Download Mirror	:	310-152 Brain Dump
Get Full Version	:	Pass4sure 310-152 Full Version

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310-152 Questions and Answers

QUESTION: 107

You are engaged to deliver a backup and recovery solution for an Enterprise data center. A gap analysis has been performed. The hardware and software have been sized to meet the customers expectation. Based on this effort, what can you expect?

The solution may need to be redesigned while on-site.
The delivery and implementation phase may go smoothly.
The hardware and software will not meet customer expectations.
The customer will be disappointed with the delivery and implementation effort.

Answer: B

QUESTION: 108

You have a small datacenter consisting of five Ultra-10 machines, one E450 server, and an L1000 tape library. Your next project is to come up with a backup and recovery software solution for this datacenter. Management has decided to put you in charge of this task, however, they have a couple of requirements for the software solution:

The software must allow for automatic recycling of tapes because the datacenter will not be staffed every day.
The software must also allow scheduled cloning of tapes. This way the tapes that are cloned can be taken away for offsite storage. Which software solution should you choose based on the hardware configuration and the requirements from management?

Solstice Backup network edition
Solstice Backup workgroup edition
VERITAS NetBackup datacenter edition
VERITAS NetBackup business server edition

Answer: A

QUESTION: 109

You are the Backup and Recovery Administrator for a server centric datacenter. There are five servers that have DLT based autoloaders directly attached to each server via SCSI connections. You have been asked to use VERITAS NetBackup software. Which is the correct NetBackup

product?

NetBackup Datacenter version 3.2
NetBackup Datacenter version 3.4
NetBackup Business Server version 3.2
NetBackup Business Server version 3.4

Answer: B

QUESTION: 110

You are the Backup and Recovery Administrator for a server-centric datacenter, with five servers each with one DLT 7000 based autoloader (total of five) directly attached to each server. The servers and ten workstations all need to be backed up. Each server contains 100 GBytes of data while each workstation has 5 GBytes of data. You have an 8-hour window to back up the data. What is the minimum number of DLT 7000 drives that will enable full backups in native mode to finish during the backup window?

Answer: C

QUESTION: 111

You need to configure a backup system that meets requirements to:

Minimize the amount of manual tape handling required to do restores from backups performed in the last 30 days
Minimize the number of tapes used for backups

Which should you consider in order to meet the requirements?

Purchase a small tape library and schedule daily full backups.
Purchase a large tape library and schedule daily full backups.
Purchase a small tape library and schedule full backups once a week, and daily incremental backups.
Purchase a large tape library, and schedule monthly full backups, weekly cumulative incrementals, and daily incremental backups.

QUESTION: 112

You have 80 backup clients to backup. You see that 75 of the clients have 100 GB of data to back up or less. Five of the clients have between 250 GB to 500 GB of data to backup. You have 8 hours every night in which to complete all backups. You must design a backup infrastructure that allows all clients to meet backup windows that are approximately one hour each, and minimizes the cost. Additionally:

Full backups must be performed once a week on all clients.
Library = 10 tape drives, 3000 tape slots.
Fast Ethernet throughput = 100 Mb/second
Gigabit Ethernet throughput = 400 Mb/second
Fibre Channel (SCSI over FC) = 1000 Mb/second
Tape hardware: Direct attach Fiber Channel switch, with full fabric login support.
Tape Speed = 20 MB/second

Which connectivity type should you use for 75 small backup clients?
1. Install Fast Ethernet cards on the small clients to be used solely for backups.
2. Install gigabit Ethernet cards on the small clients to be used solely for backups.
3. Install redundant fiber channel host bus adapters on each client. Connect one tape drive directly to each small client for dedicated use by that client.
4. Install and configure a backup SAN, using a fibre channel switch with enough ports for all small backup clients. Install redundant fiber channel host bus adapters on each client for connectivity to the SAN.
Answer: A

QUESTION: 113

You have 80 backup clients to backup. You see that 75 of the clients have 100 GB of data to back up or less. Five of the clients have between 250 GB to 500 GB of data to backup. You have 8 hours every night in which to complete all backups. You must design a backup infrastructure that allows all clients to meet backup windows that are approximately one hour each and minimizes the cost. Additionally:
Full backups must be performed once a week on all clients.
Library = 10 tape drives, 3000 tape slots.
Fast Ethernet throughput = 100 Mb/second
Gigabit Ethernet throughput = 400 Mb/second
Fibre Channel (SCSI over FC) = 1000 Mb/second
Tape hardware: Direct attach Fiber Channel switch, with full fabric login support.
Tape Speed = 20 MB/second

Which is the minimum software needed on each of the 75 small clients?

a backup client license
SAN media server license and a backup client license
Shared Storage Option (SSO) and a backup client license
a media server license and a Shared Storage Option (SSO)

Answer: A

QUESTION: 114

For company XYZ, a monthly full backup spans four DLT tapes and has a retention policy of six months. The monthly backup tape pool starts with 100 DLT tapes. How many tapes will be available for backups after one year?

Answer: C

QUESTION: 115

Company XYZ performs a full backup every Sunday and daily incremental backups Monday through Saturday night. A full backup is 100 GBytes of data and each incremental backup is 10 GBytes. The full backup has a retention policy of one month and the incremental backup has a retention policy of two weeks. How much data is backed up in four weeks?

160 GBytes
320 GBytes
640 GBytes
1.28 TBytes

Answer: C

SUN 310-152 Exam (Sun Certified Backup and Recovery Engineer (emphasis on Solstice Backup)) Detailed Information

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Certification Watch Volume 7 #16

Written by Anne Martinez 15 October 2004

Certification News regarding Apple exams, retired Sun exams, HP AIS certification, and cSAGE certification.

Apple Max OS X Exam Promotion
Apple is running a special promotion offering a free certification exam. To get the freebie, you must pass any exam in the Apple Certified System Administrator (ACSA), Apple Certified Technical Coordinator (ACTC), or Apple Certified Help Desk Specialist (ACHDS) certification tracks between October 1 and December 31, 2004. This will earn you a free Mac OS X exam in 2005. the Apple Web site for full details.
Sun to Discontinue Exams as of December 15, 2004
Sun Microsystems has announced plans to retire seven of its older certification exams as of December 15, 2004. According to a Sun Microsystems spokesperson, only one of them (Sun Certified Web Component Developer) is slated to be replaced by a newer version covering the same subject. The retiring exams are:

Sun Certified Web Component Developer for the Java 2 Platform, Enterprise Edition 1.3 (CX-310-080). To be replaced by a newer version, CX-310-081.

Sun Certified Developer for Sun ONE Application Server 6.0 (CX-310-540).

Sun Certified Data Management Engineer (emphasis on VERITAS Volume Manager (CX-310-101).

Sun Certified Data Management Engineer (emphasis on Solstice DiskSuite Software) (CX-310-102).

Sun Certified Backup and Recovery Engineer (emphasis on VERITAS NetBackup) (CX-310-151).

Sun Certified Backup and Recovery Engineer (emphasis on (CX-">310-152) Solstice Backup).

Sun Certified Storage Architect (CX-310-130).

Accredited Integration Specialist (AIS) ProLiant + NetWare, Windows, Linux Retired, Replaced by New Credential Hewlett-Packard's AIS ProLiant + NetWare, AIS ProLiant + Windows and AIS ProLiant + Linux certifications have been retired as of October 1, 2004. However, the exams will be available for completion until the 1st Dec 2004 and accepted for certification until 31 Dec 2004. New candidates will be required to complete the new 'HP ProLiant Servers' certification track.
cSAGE Suspended
The cSAGE certification program for system administrators has been suspended until further notice. Certification Update will keep you posted on future developments.
That's all for this edition of Certification Watch. Please keep your certification news and tips coming to the This email address is being protected from spambots. You need JavaScript enabled to view it..

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STATE v. POULTON

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 [1995] ).
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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Article by ArticleForge

Feedback regulation of cholesterol synthesis: sterol-accelerated ubiquitination and degradation of HMG CoA reductase

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.

Figure 1.
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.

Figure 2.
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.

Figure 3.
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.

Figure 4.
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.

Figure 5.
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.

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Top of page Acknowledgements

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.

Resale Sales Oct. 29-Nov. 5

Editor’s note: Listings include the resale home’s parcel number. Occasionally, the address listed is the homebuyer’s mailing address and not the actual location of the home. Check the parcel number to make sure. Also, a few transactions do not reflect the market value of the homes.
HENDERSON
89002
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117 Grandview Drive, $130,000,
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89012
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27 Trailside Court, $213,000,
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307 Laguna Glen Drive, $200,000,
178-09-614-069
89015
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152 Spinnaker Drive, $164,900,
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212 Pretty Sunset Terrace, $200,000,
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261 Melody Vista Place, $156,000,
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350 Citrus Circle, $124,000, 179-20-514-014
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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677 pansy pl henderson nv 89052 $207,000, 178-29-612-071
837 fulfort ct henderson nv 89052 $202,450, 137-26-717-051
950 seven hills dr #2523 henderson nv 89052 $425,000, 178-18-419-033
1092 broomfield dr henderson nv 89074 $285,000, 178-10-314-022
141 cologne ct henderson nv 89074 $185,000, 177-13-212-033
1431 clipperton ave henderson nv 89074 $315,000, 178-09-711-017
1731 millstream way henderson nv 89074 $250,000, 178-09-414-055
2127 tyler dr henderson nv 89074 $387,000, 178-17-420-003
2422 legacy island cir henderson nv 89074 $530,000, 163-12-403-009
2450 avenida cortes henderson nv 89074 $165,000, 178-19-110-065
2605 glen green ave henderson nv 89074 $162,000, 177-13-313-034
27 rue de degas henderson nv 89074 $204,250, 178-19-110-058
287 kershner ct henderson nv 89074 $250,000, 178-08-711-023
2881 skowhegan dr henderson nv 89074 $299,169, 164-25-713-090
320 bradford dr henderson nv 89074 $217,000, 178-07-613-006
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
NORTH LAS VEGAS
3022 harewood cir north las vegas nv 89030 $60,000, 139-13-116-010
3300 emmons ave north las vegas nv 89030 $70,000, 139-24-710-071
919 carey grove ave north las vegas nv 89030 $157,000, 139-16-815-050
1032 nawkee dr north las vegas nv 89031 $205,500, 124-28-718-004
1065 appleblossom time ave north las vegas nv 89031 $120,500, 124-33-719-016
112 melon aroma ave north las vegas nv 89031 $160,000, 124-34-711-010
1234 pagentry dr north las vegas nv 89031 $164,000, 124-33-713-030
1621 paradise reef ave north las vegas nv 89031 $142,900, 139-02-112-008
1702 council bluff ln north las vegas nv 89031 $143,000, 124-28-214-018
1825 casa verde dr north las vegas nv 89031 $152,000, 124-33-313-031
1934 la villa dr north las vegas nv 89031 $141,500, 124-33-412-046
2117 silver clouds dr north las vegas nv 89031 $250,000, 124-29-713-056
2201 spanish town ave north las vegas nv 89031 $131,000, 139-05-615-001
2423 old town dr north las vegas nv 89031 $150,000, 139-05-510-016
2715 coral cliffs ct north las vegas nv 89031 $130,000, 124-29-614-048
2923 sunrise bay ave north las vegas nv 89031 $119,000, 124-29-410-070
2924 sunrise bay ave north las vegas nv 89031 $123,000, 124-29-410-022
3105 extravagant ave north las vegas nv 89031 $199,000, 124-29-210-011
3 sunrise rose ave north las vegas nv 89031 $215,000, 124-29-415-069
3725 saint phillip ct north las vegas nv 89031 $202,000, 125-16-716-021
3734 saint philip ct north las vegas nv 89031 $100,000, 125-18-614-059
4034 annendale ave north las vegas nv 89031 $164,500, 124-31-515-030
snow dome ave north las vegas nv 89031 $148,000, 124-27-710-030
4123 farmdale ave north las vegas nv 89031 $165,000, 124-31-514-018
4613 sergeant ct north las vegas nv 89031 $175,000, 139-03-512-003
4737 vista del rey ct north las vegas nv 89031 $185,000, 139-03-510-009
5330 daywood st north las vegas nv 89031 $150,000, 124-34-611-103
5343 reardon ct north las vegas nv 89031 $160,000, 124-31-220-010
5416 flying arrow pl north las vegas nv 89031 $147,500, 124-32-112-012
5616 granville lake st north las vegas nv 89031 $265,000, 124-30-812-017
5820 willis st north las vegas nv 89031 $188,500, 124-30-710-007
5917 sea hunter st north las vegas nv 89031 $270,000, 124-30-315-124
5928 puka shell st north las vegas nv 89031 $140,000, 124-29-710-073
6031 red glitter st north las vegas nv 89031 $185,000, 124-29-213-037
6121 river belle st north las vegas nv 89031 $299,900, 124-30-210-086
6333 bunch grass ct north las vegas nv 89031 $265,000, 124-28-517-058
1125 indian hedge dr north las vegas nv 89032 $173,000, 139-09-614-010
140 unity crest ave north las vegas nv 89032 $145,000, 139-03-811-079
1713 ronzard ave north las vegas nv 89032 $170,000, 139-09-417-010
2708 w san miguel ave north las vegas nv 89032 $235,000, 139-05-714-008
3012 w logan ave north las vegas nv 89032 $186,650, 139-08-219-003
3322 shonna way north las vegas nv 89032 $147,000, 139-09-411-008
3330 wild filly ln north las vegas nv 89032 $157,000, 139-07-414-043
3813 blairmoor st north las vegas nv 89032 $155,000, 139-08-513-011
3869 ankara walk dr north las vegas nv 89032 $165,000, 139-07-514-039
1517 saxophone ln north las vegas nv 89081 $278,761, 124-35-715-003
2012 turtle beach ave north las vegas nv 89081 $158,000, 124-26-711-046
3136 mclennan ave north las vegas nv 89081 $170,000, 124-25-613-029
3413 barada heights ave north las vegas nv 89081 $167,000, 124-25-615-076
3504 colby creek ave north las vegas nv 89081 $185,000, 123-31-212-016
3637 terneza ave north las vegas nv 89081 $160,000, 123-30-215-039
3760 hollycroft dr north las vegas nv 89081 $160,000, 123-30-212-099
3840 van ness ave north las vegas nv 89081 $210,000, 123-31-114-085
3905 red trumpet ct north las vegas nv 89081 $165,000, 123-31-511-015
5612 clotidle soupert ct north las vegas nv 89081 $201,000, 124-22-813-036
5808 sagamore canyon st north las vegas nv 89081 $235,000, 123-30-313-062
5821 black sand beach st north las vegas nv 89081 $182,000, 124-26-711-051
6064 camden cove st north las vegas nv 89081 $176,000, 124-25-212-027
6329 beige bluff st #101 north las vegas nv 89081 $100,000, 123-30-510-092
805 seneca heights ave north las vegas nv 89081 $174,900, 124-35-215-040
1823 diamond bluff ave north las vegas nv 89084 $237,000, 124-28-115-019
3037 dowitcher ave north las vegas nv 89084 $195,000, 124-20-211-047
3908 elderdown pl north las vegas nv 89084 $170,000, 124-19-713-030
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

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310-152 - Sun Certified Backup and Recovery Engineer (emphasis on Solstice Backup) - Dump Information

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310-152 Questions and Answers

QUESTION: 107

Answer: B

QUESTION: 108

Answer: A

QUESTION: 109

Answer: B

QUESTION: 110

Answer: C

QUESTION: 111

QUESTION: 112

Answer: A

QUESTION: 113

Answer: A

QUESTION: 114

Answer: C

QUESTION: 115

Answer: C

SUN 310-152 Exam (Sun Certified Backup and Recovery Engineer (emphasis on Solstice Backup)) Detailed Information

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