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Hamster Polyclonal RAD50 Primary Antibody for IP, SimWes - ABIN151086
Giannini, Ristori, Cerignoli, Rinaldi, Zani, Viel, Ottini, Crescenzi, Martinotti, Bignami, Frati, Screpanti, Gulino: Human MRE11 is inactivated in mismatch repair-deficient cancers. in EMBO reports 2002
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Human Polyclonal RAD50 Primary Antibody for IP, PLA - ABIN258735
Wen, Scorah, Phear, Rodgers, Rodgers, Meuth: A mutant allele of MRE11 found in mismatch repair-deficient tumor cells suppresses the cellular response to DNA replication fork stress in a dominant negative manner. in Molecular biology of the cell 2008
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Polyclonal RAD50 Primary Antibody for IP, WB - ABIN540319
Petrini: The mammalian Mre11-Rad50-nbs1 protein complex: integration of functions in the cellular DNA-damage response. in American journal of human genetics 1999
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Human Polyclonal RAD50 Primary Antibody for IP, WB - ABIN2476305
Dolganov, Maser, Novikov, Tosto, Chong, Bressan, Petrini: Human Rad50 is physically associated with human Mre11: identification of a conserved multiprotein complex implicated in recombinational DNA repair. in Molecular and cellular biology 1996
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These evidences suggest that NBS1 (show NBN Antibodies) is regulated by two kind of mechanisms: complex formation dependent on ATM (show ATM Antibodies), and protein degradation mediated by an unknown MG132-resistant pathway.
Five out of twelve patients with defects in either of MSH2 (show MSH2 Antibodies), RAD50 and NBN (show NBN Antibodies) genes suffered from rare life-threatening AE, more frequently than in control group (p = 0.0005). When all detected variants were taken into account, the majority of patients (8 out of 15) suffered from life-threatening toxicity during chemotherapy.
Low RAD50 expression is associated with low-grade epithelial ovarian cancer.
although recruitment of the MRE11 (show MRE11A Antibodies)-RAD50-NBS1 (show NBN Antibodies) (MRN) DSB-sensing complex to viral genomes and activation of the ATM (show ATM Antibodies) kinase can promote KSHV replication, proteins involved in nonhomologous end joining (NHEJ) repair restrict amplification of viral DNA.
Mre11 (show MRE11A Antibodies)-Rad50-Nbs1 (show NBN Antibodies) 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 Antibodies) and CtIP (show RBBP8 Antibodies) in determining the substrates and consequences of human Mre11 (show MRE11A Antibodies)/Rad50 nuclease (show DCLRE1C Antibodies) activities on protein-DNA lesions.
identification of a novel association for longevity in the RAD50/IL13 (show IL13 Antibodies) 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 Antibodies) and IL5 (show IL5 Antibodies)
the structure of the human Rad50 hook and coiled-coil domains, was determined.
although Mre11 (show MRE11A Antibodies) is required for efficient HR-dependent repair of ionizing-radiation-induced DSBs, Mre11 (show MRE11A Antibodies) is largely dispensable for DSB resection in both chicken DT40 and human TK6 B cell lines.
RHS6 is a critical regulatory element for allergic airway inflammation and for coordinate regulation of Th2 cytokine genes by recruiting GATA3 (show GATA3 Antibodies), SATB1 (show SATB1 Antibodies), and IRF4 (show IRF4 Antibodies).
Low RAD50 expression is associated with B-cell lymphomas.
The authors demonstrate that ATM (show ATM Antibodies) can be activated by DNA double-strand breaks in the absence of the Mre11 (show MRE11A Antibodies)-Rad50-NBS1 (show NBN Antibodies) (MRN) sensor complex.
Rad50 hook domain strongly influences Mre11 (show MRE11A Antibodies) complex-dependent DDR (show DDR1 Antibodies) signaling, tissue homeostasis, and tumorigenesis.
RAD50, DNA-PKcs (show PRKDC Antibodies) 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 Antibodies) lethality was mitigated in irradiated gain-of-function Rad50(s/s) mice, and epistasis studies order Rad50 upstream of Mre11 (show MRE11A Antibodies).
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 Antibodies) and Th2 differentiation, communicating early T cell antigen receptor and cytokine signals to the IL-4 (show IL4 Antibodies)/IL-13 (show IL13 Antibodies) locus in both differentiating cell types
enhancer region with four DNase I (show DNASE1 Antibodies) hypersensitive clusters, three of which are highly conserved and predominantly expressed in Th2 cells
Study identified a stringent requirement for Mre11 (show MRE11A Antibodies)-Rad50-Nbs (show NLRP2 Antibodies) (MRN) function in telomere protection during early embryonic development.
MRN (Mre11 (show MRE11A Antibodies), Rad50, and Nbs1 (show NLRP2 Antibodies)) complex, CtIP (show RBBP8 Antibodies), and BRCA1 are required for both the removal of Top2 (show TOP2 Antibodies)-DNA adducts and the subsequent resection of Top2 (show TOP2 Antibodies)-adducted DSB ends.
MRN (MRE11 (show MRE11A Antibodies)-RAD50-NBS1 (show NLRP2 Antibodies)) complex has role in ATR (show ATR Antibodies) activation via TOPBP1 (show TOPBP1 Antibodies) recruitment.
Results indicate a role for the X. laevis Mre11 (show MRE11A Antibodies)/Rad50/Nbs1 (show NLRP2 Antibodies) complex in microhomology-mediated end joining.
These findings suggest that the MRN complex is a crucial mediator in the process whereby ATM (show ATM Antibodies) promotes the TopBP1 (show TOPBP1 Antibodies)-dependent activation of ATR (show ATR Antibodies)-ATRIP (show ATRIP Antibodies) in response to double-stranded DNA breaks.
suggests that Mre11 (show MRE11A Antibodies)-Rad50-Nbs1 (show NLRP2 Antibodies) 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 Antibodies) gene is a cytoplasmic protein (show BLZF1 Antibodies) 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.
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