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Werner syndrome, RecQ helicase-like

WRN, Werner syndrome protein
This gene encodes a member of the RecQ subfamily and the DEAH (Asp-Glu-Ala-His) subfamily of DNA and RNA helicases. DNA helicases are involved in many aspects of DNA metabolism, including transcription, replication, recombination, and repair. This protein contains a nuclear localization signal in the C-terminus and shows a predominant nucleolar localization. It possesses an intrinsic 3' to 5' DNA helicase activity, and is also a 3' to 5' exonuclease. Based on interactions between this protein and Ku70/80 heterodimer in DNA end processing, this protein may be involved in the repair of double strand DNA breaks. Defects in this gene are the cause of Werner syndrome, an autosomal recessive disorder characterized by premature aging. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Blm, CAN, AGE, POLYMERASE, p53
Papers using WRN antibodies
Activation of Stat3 sequence-specific DNA binding and transcription by p300/CREB-binding protein-mediated acetylation.
Harris Reuben S., In PLoS ONE, 2004
... Anti-WRN antibody (H300) was purchased from Santa Cruz Biotechnology (Santa Cruz, CA) ...
Papers on WRN
Nucleotide Pool Depletion Induces G-Quadruplex-Dependent Perturbation of Gene Expression.
Sale et al., Cambridge, United Kingdom. In Cell Rep, Jan 2016
Genome-wide, gene expression changes induced by HU significantly overlap with those resulting from loss of the G4-helicases FANCJ, WRN, and BLM.
Replication stress induced site-specific phosphorylation targets WRN to the ubiquitin-proteasome pathway.
Asaithamby et al., Dallas, United States. In Oncotarget, Jan 2016
WRN, the protein defective in Werner syndrome, plays critical roles in preventing replication stress, chromosome instability, and tumorigenesis.
The Caenorhabditis elegans Werner syndrome protein participates in DNA damage checkpoint and DNA repair in response to CPT-induced double-strand breaks.
Ahn et al., Ulsan, South Korea. In Cell Signal, Jan 2016
Our previous studies found that the Caenorhabditis elegans WRN-1 RecQ protein (a human WRN ortholog) exhibits ATP-dependent 3'-5' helicase activity and that the WRN-1 helicase is stimulated by RPA-1 on a long forked DNA duplex.
RECQL5 has unique strand annealing properties relative to the other human RecQ helicase proteins.
Bohr et al., Baltimore, United States. In Dna Repair (amst), Jan 2016
Five different homologs are present in humans, three of which are implicated in accelerated aging genetic disorders: Rothmund Thomson (RECQL4), Werner (WRN), and Bloom (BLM) syndromes.
Mechanisms of Origin, Phenotypic Effects and Diagnostic Implications of Complex Chromosome Rearrangements.
Haaf et al., Würzburg, Germany. In Mol Syndromol, Sep 2015
Therefore, the putative functions of the proteins encoded by ATM, BLM, WRN, ATR, MRE11, NBS1, and RAD51 in preventing CCRs are discussed.
Methylation of Werner syndrome protein is associated with the occurrence and development of invasive meningioma via the regulation of Myc and p53 expression.
Ren et al., Beijing, China. In Exp Ther Med, Aug 2015
UNASSIGNED: The aim of the present study was to investigate the positive rate of Werner syndrome protein (WRN) methylation in meningioma patients, and further assess the association between WRN methylation and the occurrence of meningioma.
Stem Cell Depletion by Global Disorganization of the H3K9me3 Epigenetic Marker in Aging.
Larrick et al., Sunnyvale, United States. In Rejuvenation Res, Aug 2015
Zhang et al. (2015) report that decreasing levels of WRN, Werner's syndrome (WS) helicase, with increasing age results in loss of heterochromatin marks in mesenchymal stem cells (MSCs) and correlates with an increased rate of cellular senescence.
Aging stem cells. A Werner syndrome stem cell model unveils heterochromatin alterations as a driver of human aging.
Belmonte et al., Beijing, China. In Science, Jul 2015
Werner syndrome (WS) is a premature aging disorder caused by WRN protein deficiency.
Protein degradation pathways regulate the functions of helicases in the DNA damage response and maintenance of genomic stability.
Brosh et al., Baltimore, United States. In Biomolecules, 2014
Stability of the Werner syndrome helicase-nuclease (WRN) involved in the replication stress response is regulated by its acetylation.
Werner Syndrome-specific induced pluripotent stem cells: recovery of telomere function by reprogramming.
Tahara et al., Hiroshima, Japan. In Front Genet, 2014
The function of the DNA helicase encoded by WRN, the gene responsible for WS, has been studied extensively.
Human RecQ helicases in DNA repair, recombination, and replication.
Bohr et al., Baltimore, United States. In Annu Rev Biochem, 2013
The importance of these proteins in cellular homeostasis is underscored by the fact that defects in BLM, WRN, and RECQL4 are linked to distinct heritable human disease syndromes.
RECQL1 and WRN DNA repair helicases: potential therapeutic targets and proliferative markers against cancers.
Furuichi et al., Kamakura, Japan. In Front Genet, 2013
RECQL1 and WRN helicases in the human RecQ helicase family participate in maintaining genome stability, DNA repair, replication, and recombination pathways in the cell cycle.
The Werner syndrome protein promotes CAG/CTG repeat stability by resolving large (CAG)(n)/(CTG)(n) hairpins.
Li et al., Lexington, United States. In J Biol Chem, 2012
WRN stimulates (CTG)(n) HPR on the template DNA strand by resolving the hairpin so that it can be efficiently used as a template for repair or replicative synthesis.
Perturbed replication induced genome wide or at common fragile sites is differently managed in the absence of WRN.
Franchitto et al., Roma, Italy. In Carcinogenesis, 2012
the role of WRN in response to perturbation of replication along common fragile sites is functionally distinct from that carried out at stalled forks genome wide.
The Werner syndrome gene product (WRN): a repressor of hypoxia-inducible factor-1 activity.
Richard et al., Québec, Canada. In Exp Cell Res, 2012
The results indicate that WRN protein regulates HIF-1 activation by affecting mitochondrial ROS production and intracellular ascorbate levels.
Teaching neuroimages: a prematurely aging patient presenting with severe leukoaraiosis and stroke.
Barsottini et al., São Paulo, Brazil. In Neurology, 2012
The patient presents with 5 cardinal and 3 minor features of Werner syndrome, which is an unusual autosomal recessive inherited disorder caused by mutations in the WRN gene on chromosome 8.
Nucleolin inhibits G4 oligonucleotide unwinding by Werner helicase.
Bohr et al., Baltimore, United States. In Plos One, 2011
WRNp interacts with the RNA-binding protein, NCL.
Cdk2 suppresses cellular senescence induced by the c-myc oncogene.
Amati et al., Milano, Italy. In Nat Cell Biol, 2010
Myc also causes senescence in cells lacking the DNA repair protein Wrn.
SIRT6 is a histone H3 lysine 9 deacetylase that modulates telomeric chromatin.
Chua et al., Stanford, United States. In Nature, 2008
At telomeric chromatin, SIRT6 deacetylates H3K9 and is required for the stable association of WRN, the factor that is mutated in Werner syndrome.
Human telomeric protein TRF2 associates with genomic double-strand breaks as an early response to DNA damage.
Meyn et al., Toronto, Canada. In Nat Genet, 2005
The TRF2 DSB response requires the TRF2 basic domain but not its Myb domain and occurs in the absence of functional ATM and DNA-PK protein kinases, MRE11/Rad50/NBS1 complex and Ku70, WRN and BLM repair proteins.
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