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anti-Human Nibrin Antibodies:
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Polyclonal Nibrin Primary Antibody for IF - ABIN540667
Compton, Choi, Cesare, Ozgür, Griffith: Xrcc3 and Nbs1 are required for the production of extrachromosomal telomeric circles in human alternative lengthening of telomere cells. in Cancer research 2007
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Human Monoclonal Nibrin Primary Antibody for 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 for 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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Human Polyclonal Nibrin Primary Antibody for 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 for 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 Polyclonal Nibrin Primary Antibody for WB - ABIN6674081
Li, Zhang, Chen, Guo, Zhang, Tang, Xu, Zhang, Tao, Wang, Jiang, Sun, Mao: Impaired DNA double-strand break repair contributes to the age-associated rise of genomic instability in humans. in Cell death and differentiation 2017
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Human Polyclonal Nibrin Primary Antibody for WB - ABIN5663771
Zhang, Tang, Jiang, Mao: The transcription factor GATA3 is required for homologous recombination repair by regulating CtIP expression. in Oncogene 2017
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it is discovered that MRE11 and NBS1 should start diffusion from significantly different starting positions which suggests that diffusion might not be the only transport mechanism of repair protein recruitment to the DNA break.
For rs13312986 A>G genotypes, AA was 78% in prostate cancer patients and 80% in controls. AG was 21% in patients and 20% in controls. GG was 1% in patients and none was detected in control. For rs14448 T>C genotypes, TC was 23% in patients and 20% in controls. TT was 77% in patients and 80% in controls. CC was not detected either in patients or controls.
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.
the present study observed a significantly higher frequency of the rs2735383 variant of the NBS1 gene, indicating that this variant may be a genetic susceptibility factor of laryngeal carcinoma.
The CC genotype of rs2735383 did not confer an increased breast cancer risk, neither in the overall analyses nor in the subgroup analyses.
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.
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-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.
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-Rad50-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 in determining the substrates and consequences of human Mre11/Rad50 nuclease 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.
The CC genotype of NBS1 Glu185Gln may increase lung cancer risk only for males and smokers and may serve as a practical marker for early detective and predictive purposes of lung cancer
surmise that the higher fertility of female c.657del5 carriers reflects a lower miscarriage rate in these women, thereby reflecting the role of the NBN gene product, nibrin, in the repair of DNA double strand breaks and their processing in immune gene rearrangements, telomere maintenance, and meiotic recombination
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.
a somatic missense mutation c.1061C>T (p.P354L) in the NBN gene in a patient with CCS lacking an EWSR1-ATF1 fusion.
The high expression of MRE11-RAD50-NBS1 complex constituents could be a predictor for poor prognosis and chemoresistance in gastric cancer
Loss of Nbn expression is associated with premature hair loss.
the essential role of Nbs1 is via its interaction with Mre11 and that most of the Nbs1 protein is dispensable for Mre11 complex functions and suggest that Mre11 and Rad50 directly activate ATM.
Low NBS1 expression is associated with B-cell lymphomas.
findings show that NBS1 is crucial for macrophage function during normal aging
TRIP13-deficient spermatocytes also progress to an H1t-positive stage if ATM activity is attenuated by hypomorphic mutations in Mre11 or Nbs1 or by elimination of the ATM-effector kinase CHK2
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-Chk2-P53 signaling pathway and the AKT/mTOR signaling pathway are responsible for the enhanced apoptosis of the Nbn-deficient mature oligodendrocytes.
JNK signaling and ATR signaling are likely to converge to regulate the cerebellar apoptosis of newborn Nbn-deficient mice.
Nbn and Atm collaborate to prevent DSB accumulation and apoptosis during development in a tissue- and developmental stage-specific manner.
the antagonism and redundancy of ATMIN and NBS1 constitute a crucial regulatory mechanism for ATM signaling and function.
Nbs1-deficient neocortex shows accumulative endogenous DNA damage and defective activation of Ataxia telangiectasia and Rad3-related (ATR)-Chk1 pathway upon DNA damage.
NBS1 haploinsufficiency results in increased mammary tumor latency and metastasis.
a distinct function of Nbs1 and Atr in neurogenesis
murine cells have evolved mechanisms to ensure the functional redundancy of Pif1 or Nbs1 in the regulation of chromosome healing.
Point mutation at the Nbs1 Threonine 278 site does not affect mouse development, but compromises the Chk2 and Smc1 phosphorylation after DNA damage.
Atm has cellular roles not regulated by Nbs1 in the murine cerebellum.
deletion of the entire Nbs1 protein in T-cell precursors (Nbs1(T-del)) results in severe lymphopenia and a hindrance to the double-negative 3 (DN3)-to-DN4 transition in early T-cell development
Study concludes that Nbs1 and Rad54 function cooperatively, but in separate pathways to counteract DNA double-strand break.
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