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anti-Human RAD50 Antikörper:
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Hamster Polyclonal RAD50 Primary Antibody für 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
Show all 29 Pubmed References
Polyclonal RAD50 Primary Antibody für IP, WB - ABIN540427
Sedelnikova, Nakamura, Kovalchuk, Koturbash, Mitchell, Marino, Brenner, Bonner: DNA double-strand breaks form in bystander cells after microbeam irradiation of three-dimensional human tissue models. in Cancer research 2007
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Human Polyclonal RAD50 Primary Antibody für 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 für 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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Expression levels of MRN complex proteins(MRE11/RAD50/NBS1) significantly predict disease-free survival in rectal cancer patients, including those treated with neoadjuvant radiotherapy, and may have value in the management of these patients.
These data suggest that RAD50 foci formation in CTCs and CAMLs may be used to track cells subjected to radiation occurring at primary tumors, and following PD-L1 expression in circulating cells may be used as a surrogate for tracking adaptive changes in immunotherapeutic targets.
These evidences suggest that NBS1 is regulated by two kind of mechanisms: complex formation dependent on ATM, and protein degradation mediated by an unknown MG132-resistant pathway.
Five out of twelve patients with defects in either of MSH2, RAD50 and NBN 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-RAD50-NBS1 (MRN) DSB-sensing complex to viral genomes and activation of the ATM kinase can promote KSHV replication, proteins involved in nonhomologous end joining (NHEJ) repair restrict amplification of viral DNA.
Mre11-Rad50-Nbs1 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 and CtIP in determining the substrates and consequences of human Mre11/Rad50 nuclease activities on protein-DNA lesions.
identification of a novel association for longevity in the RAD50/IL13 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 and IL5
the structure of the human Rad50 hook and coiled-coil domains, was determined.
although Mre11 is required for efficient HR-dependent repair of ionizing-radiation-induced DSBs, Mre11 is largely dispensable for DSB resection in both chicken DT40 and human TK6 B cell lines.
The high expression of MRE11-RAD50-NBS1 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-induced replication stress during neural cell proliferation.
The C allele of rs6871536 was positively associated with atopic asthma in a Chinese population.
study identified the copy number deletion of RAD50 as a candidate marker for survival
Lack of association between RAD50-IL13 polymorphisms and pediatric asthma susceptibility in Northeastern Han Chinese
we present an in-depth genomic and functional genetic analysis identifying RAD50 hypomorphism as a contributing factor to a curative response to systemic combination therapy in a patient with recurrent, metastatic small-cell cancer.
a significant increase in DKC1, RAD50, MRE11 and RPA1 expression in MM cases with high bone marrow infiltration (p=0.03) and a tendency towards cases with advanced ISS stage
RHS6 is a critical regulatory element for allergic airway inflammation and for coordinate regulation of Th2 cytokine genes by recruiting GATA3, SATB1, and IRF4.
Low RAD50 expression is associated with B-cell lymphomas.
The authors demonstrate that ATM can be activated by DNA double-strand breaks in the absence of the Mre11-Rad50-NBS1 (MRN) sensor complex.
Rad50 hook domain strongly influences Mre11 complex-dependent DDR signaling, tissue homeostasis, and tumorigenesis.
RAD50, DNA-PKcs 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 lethality was mitigated in irradiated gain-of-function Rad50(s/s) mice, and epistasis studies order Rad50 upstream of Mre11.
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 and Th2 differentiation, communicating early T cell antigen receptor and cytokine signals to the IL-4/IL-13 locus in both differentiating cell types
enhancer region with four DNase I hypersensitive clusters, three of which are highly conserved and predominantly expressed in Th2 cells
The MRE11-RAD50-Nijmegen breakage syndrome 1 (NBS1 [MRN]) complex accumulates at sites of DNA double-strand breaks (DSBs) in microscopically discernible nuclear foci.
depletion of Rad50 in cultured cells caused extensive DNA damage & death within 3 to 5 days of Rad50 deletion; this was not associated with gross telomere dysfunction, suggesting that telomeric functions of the Mre11 complex are not required for viability
During V(D)J recombination, MRN deficiency leads to the aberrant joining of Rag double-strand breaks (DSBs) and to the accumulation of unrepaired coding ends.
Results suggest a model in which MRN stabilizes distant breaks and processes DNA termini to facilitate repair by both the classical and alternative NHEJ pathways.
The role of Mre11/Rad50/Nbs1 at dysfunctional telomeres is multifaceted, involving both repression of NHEJ in G(2) through end resection and induction of NHEJ in G(1) through ATM-dependent signaling.
Study identified a stringent requirement for Mre11-Rad50-Nbs (MRN) function in telomere protection during early embryonic development.
MRN (Mre11, Rad50, and Nbs1) complex, CtIP, and BRCA1 are required for both the removal of Top2-DNA adducts and the subsequent resection of Top2-adducted DSB ends.
MRN (MRE11-RAD50-NBS1) complex has role in ATR activation via TOPBP1 recruitment.
Results indicate a role for the X. laevis Mre11/Rad50/Nbs1 complex in microhomology-mediated end joining.
These findings suggest that the MRN complex is a crucial mediator in the process whereby ATM promotes the TopBP1-dependent activation of ATR-ATRIP in response to double-stranded DNA breaks.
suggests that Mre11-Rad50-Nbs1 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 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.
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