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Human Polyclonal RECQL2 Primary Antibody for ChIP, ICC - ABIN151918
Harrigan, Piotrowski, Di Noto, Levine, Bohr: Metal-catalyzed oxidation of the Werner syndrome protein causes loss of catalytic activities and impaired protein-protein interactions. in The Journal of biological chemistry 2007
Show all 9 references for ABIN151918
Human Monoclonal RECQL2 Primary Antibody for IF, WB - ABIN394233
Ehrenberg, Dratviman-Storobinsky, Avraham-Lubin, Goldenberg-Cohen: Lack of association of the WRN C1367T polymorphism with senile cataract in the Israeli population. in Molecular vision 2010
Show all 5 references for ABIN394233
Human Polyclonal RECQL2 Primary Antibody for IHC (p), IP - ABIN151919
Sidorova, Li, Folch, Monnat: The RecQ helicase WRN is required for normal replication fork progression after DNA damage or replication fork arrest. in Cell cycle (Georgetown, Tex.) 2008
Show all 5 references for ABIN151919
Human Polyclonal RECQL2 Primary Antibody for EIA, FACS - ABIN955584
Perry, Asaithamby, Barnebey, Kiamanesch, Chen, Han, Tainer, Yannone: Identification of a coiled coil in werner syndrome protein that facilitates multimerization and promotes exonuclease processivity. in The Journal of biological chemistry 2010
Show all 5 references for ABIN955584
Human Monoclonal RECQL2 Primary Antibody for ICC, IF - ABIN2668372
Opresko, Calvo, von Kobbe: Role for the Werner syndrome protein in the promotion of tumor cell growth. in Mechanisms of ageing and development 2007
A mislocalization of the Wrn mutant protein in the liver endoplasmic reticulum fraction increased oxidative stress in that cellular compartment. Vitamin C reversed this oxidative stress.
The deleterious effects of the helicase-deficient Wrn protein are mediated by the dysfunction of several cellular organelles.
Data suggest that, in the context of Wrn deficiency-related telomere dysfunction, loss of p16Ink4a (show CDKN2A Antibodies) function could prevent cells from senescence.
The FEN1 (show FEN1 Antibodies) E359K germline mutation disrupts the FEN1 (show FEN1 Antibodies)-WRN interaction and FEN1 (show FEN1 Antibodies) GEN (show GEN1 Antibodies) activity, causing aneuploidy-associated cancers.
Studies show that in the context of Myc-associated tumorigenesis, loss of Wrn amplifies the DNA damage response, both in preneoplastic and neoplastic tissue, engaging activation of tumor suppressor pathways.
embryonic fibroblasts lacking a functional Wrn helicase (show DNA2 Antibodies) inhibited the immortalization of Safb1 (show SAFB Antibodies)-null cells. These results indicate that an intact Wrn protein is required for immortalization and tumorigenesis in Safb1 (show SAFB Antibodies)-null mice.
BCR/ABL-mediated stimulation of WRN modulates the efficiency and fidelity of major DSB repair mechanisms to protect leukemia cells from apoptosis and to facilitate genomic instability.
WRN has a role in processing specific types of homologous recombination intermediates as well as an important function in nonhomologous recombination
results demonstrate that WRN loss confers a strong cellular phenotype in early passage human - though not mouse - primary fibroblasts.
Genetic cooperation between this protein and poly(ADP-ribose) polymerase-1 (show PARP1 Antibodies) prevent chromatid breaks, complex chromosomal rearrangements, and cancer in mice.
WRN or the Bloom syndrome helicase (BLM) stimulates DNA polymerase delta (show POLD1 Antibodies) progression across telomeric G-rich repeats, only WRN promotes sequential strand displacement synthesis and FEN1 (show FEN1 Antibodies) cleavage.
This study identified residues in the WRN RQC domain that are involved specifically in the interaction with G-quadruplex DNA.
findings indicate that WRN interacts with HDACs 1 and 2 to facilitate activity of stalled replication forks under conditions of replication stress.
We found statistically significant association with AAO for three genes (WRN, NTN4 and LAMC3 (show LAMC3 Antibodies)) with common associated variants.
Finfings indicate a role for Werner syndrome helicase WRN as a modulator of DNA repair, replication, and recombination.
The WRN Cys1367Arg (T>C) polymorphism is not associated with overall cancer risk, although subgroup analyses suggested an association with breast cancer and overall cancer specifically in European populations. [meta-analysis]
The CC genotype of WRN rs1346044 may contribute to an increased risk and a premature onset of breast cancer.
Japanese subjects bearing at least one A allele of rs2230009 of the WRN gene are at a significantly higher risk of femoral fracture, possibly due to decreased bone density.
WRN prefers to act on DNA strand invasion intermediates in a manner that favours strand invasion and exchange.
we provide a proof of concept for applying the external guide sequence (EGS) approach in directing an RNase P RNA to efficiently cleave the WRN mRNA in cultured human cell lines.
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.
, Werner syndrome ATP-dependent helicase homolog
, exonuclease WRN
, DNA helicase, RecQ-like type 3
, Werner syndrome ATP-dependent helicase
, recQ protein-like 2