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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 Pubmed References
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 Pubmed References
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 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.
Data show that helicases RHAU, BLM, and WRN exhibit distinct G-quadruplex (GQ) conformation specificity, but use a common mechanism of repetitive unfolding that leads to disrupting GQ structure multiple times in succession.
there was no consistent association between WRN promoter hypermethylation and loss of WRN expression at the mRNA or protein level in CRC (show CALR Antibodies) cell lines or tumors.
Low WRN expression is associated with aggressive tumor phenotype in breast cancer.
WRN is essential for survival of ATLL cells
The authors show that the helicase of hDNA2 functionally integrates with BLM or WRN helicases to promote double-stranded DNA degradation by forming a heterodimeric molecular machine. This collectively suggests that the human DNA2 motor promotes the enzyme's capacity to degrade double-stranded DNA in conjunction with BLM or WRN and thus promote the repair of broken DNA.
In meta-analyses including 59,190 individuals in 5 studies, the hazard ratio for ischemic stroke for C1367R TT homozygotes versus CC/CT was 1.14 . The study suggests that common genetic variation in WRN is associated with increased risk of ischemic stroke in the general population.
The findings suggest that the epidermis is among the tissue types that do not display symptoms of premature ageing caused by loss of function of wrn. This is in support that Werner's syndrome is a segmental progeroid syndrome.
Active control of repetitive structural transitions between replication forks and Holliday junctions by WRN has been reported.
Evaluation of localization of WRN signals demonstrated that WRN does not leave the nucleolus after irradiation. The WRN signal was not detected at the telomere sides, but H2AX was detected at the telomeric sides. Thus, the WRN protein is not involved in irradiation-induced DNA damage/repair, even at telomeric sides in human mesenchymal stem cells (hMSC) and hMSC-telomere 1.
In humans, mutations in WRN give rise to Werner syndrome characterized by premature development of features associated with aging.
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