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Study identified a stringent requirement for Mre11 (show MRE11A ELISA Kits)-Rad50-Nbs (show NLRP2 ELISA Kits) (MRN) function in telomere protection during early embryonic development.
MRN (Mre11 (show MRE11A ELISA Kits), Rad50, and Nbs1 (show NLRP2 ELISA Kits)) complex, CtIP (show RBBP8 ELISA Kits), and BRCA1 are required for both the removal of Top2 (show TOP2 ELISA Kits)-DNA adducts and the subsequent resection of Top2 (show TOP2 ELISA Kits)-adducted DSB ends.
MRN (MRE11 (show MRE11A ELISA Kits)-RAD50-NBS1 (show NLRP2 ELISA Kits)) complex has role in ATR (show ATR ELISA Kits) activation via TOPBP1 (show TOPBP1 ELISA Kits) recruitment.
Results indicate a role for the X. laevis Mre11 (show MRE11A ELISA Kits)/Rad50/Nbs1 (show NLRP2 ELISA Kits) complex in microhomology-mediated end joining.
These findings suggest that the MRN complex is a crucial mediator in the process whereby ATM (show ATM ELISA Kits) promotes the TopBP1 (show TOPBP1 ELISA Kits)-dependent activation of ATR (show ATR ELISA Kits)-ATRIP (show ATRIP ELISA Kits) in response to double-stranded DNA breaks.
suggests that Mre11 (show MRE11A ELISA Kits)-Rad50-Nbs1 (show NLRP2 ELISA Kits) inactivation participates in the down-regulation of damage signaling during checkpoint recovery following double-strand breaks repair.
Data show that the product of the PHS1 (show PTGS1 ELISA Kits) gene is a cytoplasmic protein that functions by controlling transport of RAD50 from cytoplasm to the nucleus.
The protective role of Rad50 protein on shortened telomeres results from its action in constraining recombination to sister chromatids and thus avoiding end-to-end interactions.
Mre11 (show MRE11A ELISA Kits)-Rad50-Nbs1 (show NBN ELISA Kits) complex initiates DNA double strand break repair.
symmetrical engagement of the Rad50 catalytic head domains with ATP bound at both sites is important for MRN functions in eukaryotic cells.
The results illuminate the important role of Nbs1 (show NBN ELISA Kits) and CtIP (show RBBP8 ELISA Kits) in determining the substrates and consequences of human Mre11 (show MRE11A ELISA Kits)/Rad50 nuclease (show DCLRE1C ELISA Kits) activities on protein-DNA lesions.
identification of a novel association for longevity in the RAD50/IL13 (show IL13 ELISA Kits) region on chromosome 5q31.1; the lead SNP rs2706372 is located in the intronic region of the RAD50 gene and is in strong linkage disequilibrium with other associated SNPs close to IL13 (show IL13 ELISA Kits) and IL5 (show IL5 ELISA Kits)
the structure of the human Rad50 hook and coiled-coil domains, was determined.
although Mre11 (show MRE11A ELISA Kits) is required for efficient HR-dependent repair of ionizing-radiation-induced DSBs, Mre11 (show MRE11A ELISA Kits) is largely dispensable for DSB resection in both chicken DT40 and human TK6 B cell lines.
The high expression of MRE11 (show MRE11A ELISA Kits)-RAD50-NBS1 (show NBN ELISA Kits) complex constituents could be a predictor for poor prognosis and chemoresistance in gastric cancer
Germline mutation in RAD50 gene is associated with familial breast cancer.
The MRN complex is essential to restrain MYCN (show MYCN ELISA Kits)-induced replication stress during neural cell proliferation.
study identified the copy number deletion of RAD50 as a candidate marker for survival
Low RAD50 expression is associated with B-cell lymphomas.
The authors demonstrate that ATM (show ATM ELISA Kits) can be activated by DNA double-strand breaks in the absence of the Mre11 (show MRE11A ELISA Kits)-Rad50-NBS1 (show NBN ELISA Kits) (MRN) sensor complex.
Rad50 hook domain strongly influences Mre11 (show MRE11A ELISA Kits) complex-dependent DDR (show DDR1 ELISA Kits) signaling, tissue homeostasis, and tumorigenesis.
RAD50, DNA-PKcs (show PRKDC ELISA Kits) kinase activity, and transcription context are each important to limit incorrect end use during EJ repair of multiple DSBs, but each has distinct roles during repair events requiring end processing
Data show that CS-mediated SCC (show CYP11A1 ELISA Kits) lethality was mitigated in irradiated gain-of-function Rad50(s/s) mice, and epistasis studies order Rad50 upstream of Mre11 (show MRE11A ELISA Kits).
MRE11-RAD50-NBS1 complex dictates DNA repair independent of H2AX.
Rad50 mutant mice (Rad50(S/S) mice) exhibited growth defects and cancer predisposition.
the RAD50 LCR has a complex and dual role in Th1 (show HAND1 ELISA Kits) and Th2 differentiation, communicating early T cell antigen receptor and cytokine signals to the IL-4 (show IL4 ELISA Kits)/IL-13 (show IL13 ELISA Kits) locus in both differentiating cell types
enhancer region with four DNase I (show DNASE1 ELISA Kits) hypersensitive clusters, three of which are highly conserved and predominantly expressed in Th2 cells
The MRE11 (show MRE11A ELISA Kits)-RAD50-Nijmegen breakage syndrome 1 (NBS1 (show NLRP2 ELISA Kits) [MRN]) complex accumulates at sites of DNA double-strand breaks (DSBs) in microscopically discernible nuclear foci.
The protein encoded by this gene is highly similar to Saccharomyces cerevisiae Rad50, a protein involved in DNA double-strand break repair. This protein forms a complex with MRE11 and NBS1. The protein complex binds to DNA and displays numerous enzymatic activities that are required for nonhomologous joining of DNA ends. This protein, cooperating with its partners, is important for DNA double-strand break repair, cell cycle checkpoint activation, telomere maintenance, and meiotic recombination. Knockout studies of the mouse homolog suggest this gene is essential for cell growth and viability. Mutations in this gene are the cause of Nijmegen breakage syndrome-like disorder.
DNA repair protein RAD50
, RAD50 homolog (S. cerevisiae)
, RAD50 homolog
, Subunit of MRX complex, with Mre11p and Xrs2p, involved in processing double-strand DNA breaks in vegetative cells, initiation of meiotic DSBs, telomere maintenance, and nonhomologous end joining
, Rad50 DNA repair/recombination protein
, DNA repair protein RAD50-like