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Human Polyclonal Nibrin Primary Antibody für IHC - ABIN966789
Hsu, Shi, Gartenhaus: The MCT-1 oncogene product impairs cell cycle checkpoint control and transforms human mammary epithelial cells. in Oncogene 2005
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Human Polyclonal Nibrin Primary Antibody für WB - ABIN361984
Buscemi, Perego, Carenini, Nakanishi, Chessa, Chen, Khanna, Delia: Activation of ATM and Chk2 kinases in relation to the amount of DNA strand breaks. in Oncogene 2004
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Human Monoclonal Nibrin Primary Antibody für ICC, FACS - ABIN1724942
Zheng, Zhang, Jiang, You, Liu, Lu, Zhou: Functional NBS1 polymorphism is associated with occurrence and advanced disease status of nasopharyngeal carcinoma. in Molecular carcinogenesis 2011
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Human Monoclonal Nibrin Primary Antibody für ICC, FACS - ABIN1724946
Zuhlke, Johnson, Okoth, Stoffel, Robbins, Tembe, Salinas, Zheng, Xu, Carpten, Lange, Isaacs, Cooney: Identification of a novel NBN truncating mutation in a family with hereditary prostate cancer. in Familial cancer 2012
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These evidences suggest that NBS1 is regulated by two kind of mechanisms: complex formation dependent on ATM (zeige ATM Antikörper), and protein degradation mediated by an unknown MG132-resistant pathway.
Five out of twelve patients with defects in either of MSH2 (zeige MSH2 Antikörper), RAD50 (zeige RAD50 Antikörper) 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.
To our knowledge, this is the first report of NBN gene mutation in an individual with lung cancer in the Arab world
Low NBS1 expression is associated with low-grade epithelial ovarian cancer.
although recruitment of the MRE11 (zeige MRE11A Antikörper)-RAD50 (zeige RAD50 Antikörper)-NBS1 (MRN) DSB-sensing complex to viral genomes and activation of the ATM (zeige ATM Antikörper) kinase can promote KSHV replication, proteins involved in nonhomologous end joining (NHEJ) repair restrict amplification of viral DNA.
Data suggest HSP90AA1-dependent regulation of ATM-NBN-CHK2 and ATR-CHK1 axes influences cells capability to repair double-stranded DNA damage; mechanisms include phosphorylation, polyubiquitination, and proteasomal degradation/proteolysis. (HSP90AA1 = heat shock protein 90kDa alpha; ATM = ataxia telangiectasia mutated protein; NBN = nibrin; CHK = checkpoint kinase; ATR = ataxia telangiectasia and Rad3 related kinase)
Mre11 (zeige MRE11A Antikörper)-Rad50 (zeige RAD50 Antikörper)-Nbs1 complex initiates DNA double strand break repair.
Phosphorylation status of NBS1 determines how dysfunctional telomeres are repaired.
The results illuminate the important role of Nbs1 and CtIP (zeige RBBP8 Antikörper) in determining the substrates and consequences of human Mre11 (zeige MRE11A Antikörper)/Rad50 (zeige RAD50 Antikörper) nuclease (zeige DCLRE1C Antikörper) activities on protein-DNA lesions.
The Nbs1 homologs that promote herpes simplex virus 1 infection also interact with the herpes simplex virus 1 ICP0 protein.
Loss of Nbn expression is associated with premature hair loss.
the essential role of Nbs1 is via its interaction with Mre11 (zeige MRE11A Antikörper) and that most of the Nbs1 protein is dispensable for Mre11 (zeige MRE11A Antikörper) complex functions and suggest that Mre11 (zeige MRE11A Antikörper) and Rad50 (zeige RAD50 Antikörper) directly activate ATM (zeige ATM Antikörper).
Low NBS1 expression is associated with B-cell lymphomas.
findings show that NBS1 is crucial for macrophage function during normal aging
TRIP13 (zeige TRIP13 Antikörper)-deficient spermatocytes also progress to an H1t (zeige HIST1H1T Antikörper)-positive stage if ATM (zeige ATM Antikörper) activity is attenuated by hypomorphic mutations in Mre11 (zeige MRE11A Antikörper) or Nbs1 or by elimination of the ATM (zeige ATM Antikörper)-effector kinase CHK2 (zeige CHEK2 Antikörper)
In the absence of wild type nibrin, the repair of spontaneous errors, presumably arising during DNA replication, makes a major contribution to the basal mutation rate.
Nbs1 mutants initially accumulate replication intermediate, not DSBs.
This report showed that ATM (zeige ATM Antikörper)-Chk2 (zeige CHEK2 Antikörper)-P53 (zeige TP53 Antikörper) signaling pathway and the AKT (zeige AKT1 Antikörper)/mTOR (zeige FRAP1 Antikörper) signaling pathway are responsible for the enhanced apoptosis of the Nbn-deficient mature oligodendrocytes.
JNK (zeige MAPK8 Antikörper) signaling and ATR (zeige ATR Antikörper) signaling are likely to converge to regulate the cerebellar apoptosis of newborn Nbn-deficient mice.
Mutations in this gene are associated with Nijmegen breakage syndrome, an autosomal recessive chromosomal instability syndrome characterized by microcephaly, growth retardation, immunodeficiency, and cancer predisposition. The encoded protein is a member of the MRE11/RAD50 double-strand break repair complex which consists of 5 proteins. This gene product is thought to be involved in DNA double-strand break repair and DNA damage-induced checkpoint activation.
, Nijmegen breakage syndrome 1 (nibrin)
, cell cycle regulatory protein p95
, p95 protein of the MRE11/RAD50 complex
, nijmegen breakage syndrome protein 1 homolog