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Study identified a stringent requirement for Mre11 (show MRE11A Proteins)-Rad50-Nbs (show NLRP2 Proteins) (MRN) function in telomere protection during early embryonic development.
MRN (Mre11 (show MRE11A Proteins), Rad50, and Nbs1 (show NLRP2 Proteins)) complex, CtIP (show RBBP8 Proteins), and BRCA1 are required for both the removal of Top2 (show TOP2 Proteins)-DNA adducts and the subsequent resection of Top2 (show TOP2 Proteins)-adducted DSB ends.
MRN (MRE11 (show MRE11A Proteins)-RAD50-NBS1 (show NLRP2 Proteins)) complex has role in ATR activation via TOPBP1 (show TOPBP1 Proteins) recruitment.
Results indicate a role for the X. laevis Mre11 (show MRE11A Proteins)/Rad50/Nbs1 (show NLRP2 Proteins) complex in microhomology-mediated end joining.
These findings suggest that the MRN complex is a crucial mediator in the process whereby ATM (show ATM Proteins) promotes the TopBP1 (show TOPBP1 Proteins)-dependent activation of ATR-ATRIP (show ATRIP Proteins) in response to double-stranded DNA breaks.
suggests that Mre11 (show MRE11A Proteins)-Rad50-Nbs1 (show NLRP2 Proteins) 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 Proteins) gene is a cytoplasmic protein (show BLZF1 Proteins) 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.
Low RAD50 expression is associated with low-grade epithelial ovarian cancer.
although recruitment of the MRE11 (show MRE11A Proteins)-RAD50-NBS1 (show NBN Proteins) (MRN) DSB-sensing complex to viral genomes and activation of the ATM (show ATM Proteins) kinase can promote KSHV replication, proteins involved in nonhomologous end joining (NHEJ) repair restrict amplification of viral DNA.
Mre11 (show MRE11A Proteins)-Rad50-Nbs1 (show NBN Proteins) 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 Proteins) and CtIP (show RBBP8 Proteins) in determining the substrates and consequences of human Mre11 (show MRE11A Proteins)/Rad50 nuclease (show DCLRE1C Proteins) activities on protein-DNA lesions.
identification of a novel association for longevity in the RAD50/IL13 (show IL13 Proteins) 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 Proteins) and IL5 (show IL5 Proteins)
the structure of the human Rad50 hook and coiled-coil domains, was determined.
although Mre11 (show MRE11A Proteins) is required for efficient HR-dependent repair of ionizing-radiation-induced DSBs, Mre11 (show MRE11A Proteins) is largely dispensable for DSB resection in both chicken DT40 and human TK6 B cell lines.
The high expression of MRE11 (show MRE11A Proteins)-RAD50-NBS1 (show NBN Proteins) 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.
Low RAD50 expression is associated with B-cell lymphomas.
The authors demonstrate that ATM (show ATM Proteins) can be activated by DNA double-strand breaks in the absence of the Mre11 (show MRE11A Proteins)-Rad50-NBS1 (show NBN Proteins) (MRN) sensor complex.
Rad50 hook domain strongly influences Mre11 (show MRE11A Proteins) complex-dependent DDR (show DDR1 Proteins) signaling, tissue homeostasis, and tumorigenesis.
RAD50, DNA-PKcs (show PRKDC Proteins) 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 Proteins) lethality was mitigated in irradiated gain-of-function Rad50(s/s) mice, and epistasis studies order Rad50 upstream of Mre11 (show MRE11A Proteins).
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 (show CBR2 Proteins) has a complex and dual role in Th1 (show HAND1 Proteins) and Th2 differentiation, communicating early T cell antigen receptor and cytokine signals to the IL-4 (show IL4 Proteins)/IL-13 (show IL13 Proteins) locus in both differentiating cell types
enhancer region with four DNase I (show DNASE1 Proteins) hypersensitive clusters, three of which are highly conserved and predominantly expressed in Th2 cells
The MRE11 (show MRE11A Proteins)-RAD50-Nijmegen breakage syndrome 1 (NBS1 (show NLRP2 Proteins) [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