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anti-Human BRCA2 Antikörper:
anti-Rat (Rattus) BRCA2 Antikörper:
anti-Mouse (Murine) BRCA2 Antikörper:
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Human Polyclonal BRCA2 Primary Antibody für ICC, IF - ABIN4285198
Sergeeva, Ershova, Veiko, Malinovskaya, Kalyanov, Kameneva, Stukalov, Dolgikh, Konkova, Ermakov, Veiko, Izhevskaya, Kutsev, Kostyuk: Low-Dose Ionizing Radiation Affects Mesenchymal Stem Cells via Extracellular Oxidized Cell-Free DNA: A Possible Mediator of Bystander Effect and Adaptive Response. in Oxidative medicine and cellular longevity 1970
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Human Monoclonal BRCA2 Primary Antibody für IHC, IHC (p) - ABIN445491
Wu, Jiang, Thangaraju, Wu, Couch: Induction of the BRCA2 promoter by nuclear factor-kappa B. in The Journal of biological chemistry 2000
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Human Monoclonal BRCA2 Primary Antibody für IHC, IHC (fro) - ABIN445493
Bernard-Gallon, Déchelotte, Vissac, Aunoble, Cravello, Malpuech, Bignon: BRCA1 and BRCA2 protein expressions in an ovotestis of a 46, XX true hermaphrodite. in Breast cancer research : BCR 2001
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two novel heterozygous pathogenic variants in exons 18 and 11 of the BRCA2 gene in two Lebanese families, are reported.
FoxM1 activation occurs secondary to FoxO3a suppression in Idiopathic pulmonary fibrosis (IPF) fibroblasts while restoration of FoxO3a function sensitizes IPF fibroblasts to radiation-induced cell death and downregulates FoxM1, RAD51, and BRCA2.
The germline mutational landscape of BRCA1 and BRCA2 in Brazil.
Study identified rare single nucleotide variants and small indels mapping to the 5' non-coding region of BRCA2 through targeted sequencing of over 6000 early onset/familial breast cancer patients. Four variants in minimal promoter regions seem to alter gene activity; two others disrupt the binding with PAX5.
Mutations in BRCA1, BRCA2, and PALB2, and a panel of 50 cancer-associated genes in pancreatic ductal adenocarcinoma
The meta-analysis results provide clinicians and health-care regulatory agencies with evidence of the increased risk of colorectal cancer in BRCA1 mutation carriers, but not in BRCA2.
our study shows that the K3326* variant in BRCA2 associates primarily with cancer types that have strong environmental genotoxic risk factors. We report for the first time an association between the variant and risk of SCLC and SQCSC.
BRCA1/2 genes are the most commonly mutated pancreatic cancer susceptibility genes that should be considered in all pancreatic cancer cases with young age at onset or a family history of cancer.
Detection of disease-associated variants in the BRCA1 and BRCA2 (BRCA1/2) genes allows for cancer prevention and early diagnosis in high-risk individuals.
All patients in our centre were tested using next-generation sequencing (NGS) panels that included full gene sequencing as well as coverage for large deletions/duplications in BRCA1/2. We calculated MSS1-3 scores for index patients between 2014 and 2017 who had undergone BRCA1/2 genetic testing and recorded their genetic test results
The estimated penetrance of breast cancer to age 80 years was 60.8% for BRCA1 and 63.1% for BRCA2. For all BRCA carriers, the penetrance of breast cancer to age 80 for those with no first-degree relative with breast cancer was 60.4% and 63.3% for those with at least 1 first-degree relative with breast cancer
Five per cent of unselected Asian patients with breast cancer carry deleterious variants in BRCA2 in Malaysia.
BRCA2 variant (rs80359182, 319T/C) is significantly associated with high breast cancer risk in the Pakistani population. BRCA2-tryptophan > arginine substitutions result in altered interaction of BRCA1/PALB2/BRCA2/protein complex and impaired homology-directed DNA repair pathway.
Data found higher BRCA1/2 mRNA-expression in ovarian cancer (OC). BRCA1 mutated OCs exhibited lower BRCA1 but higher BRCA2 mRNA-expression. Low BRCA1-expression was associated with favorable overall survival and low BRCA2-expression with better progression-free and overall survival.
This is the largest study to date comparing outcomes in patients with EOC and BM by mutation status. mBRCA1 and mBCRA2 patients were more likely to have isolated BM, which may be a factor in their long survival.
RAD52 protein, just as BRCA2, interacts with pCHK1 checkpoint protein and helps maintain the checkpoint control in BRCA2 deficient cells during DNA damage response
BRCA 1/2 mutations are associated with a higher hematologic toxicity in patients with ovarian cancer who underwent platinum-based chemotherapy.
BRCA1/2 mutation testing thus has important and expanding roles in treatment planning for subsets of patients with breast cancer..Determining BRCA1/2 mutation status in this breast cancer subgroup could potentially expand treatment options beyond the current standard of taxane and anthracycline-based chemotherapy.
we believe we are the first to describe this germline mutation of BRCA2 (c.4211C>G, p.Ser1404Ter) in a patient with PCa, which was effectively treated with ADT and radiotherapy.
Protein truncating variants (PTVs) in specific DNA repair genes were significantly overrepresented among patients with the aggressive phenotype, with BRCA2, ATM and NBN the most frequently mutated genes.
persistent meiotic DNA double-strand breaks might correspond to crossovers, which are mobilized to the nuclear envelope for their repair; Brca2-Pds5 complexes may be key mediators of this process.
A mutation in Cyp6d2, a cytochrome P450 gene, when combined with a brca2 mutation, resulted in synergistic hypersensitivity to camptothecin.
DNA repair by homologous recombination is dramatically decreased in CG30169 (brca2 homolog) mutants.
the data suggest for the first time that brca2/fancd1 is essential for vertebrate kidney ontogeny.
Carcinogenesis in zebrafish with combined mutations in tp53 and brca2 typically requires biallelic mutation or loss of at least one of these genes.
The novel role of Brca2 in organizing the vertebrate egg nucleus may provide new insights into the origin of ovarian cancer
critical roles for brca2 in ovarian development and tumorigenesis in reproductive tissues
BRCA2-proficient and deficient cells are radiosensitised by HT, indicating that HT does not exclusively act by inhibition of HR.
Results suggest that the greater reliance on homology-directed repair (HDR) in the proliferating mammary gland, rather than a specific dependence on breast cancer 2 protein (BRCA2), may increase its susceptibility to tumorigenesis incurred by BRCA2 mutation.
The functional consequence of Parp1 heterozygosity on BRCA2 loss is demonstrated by a significant increase in tumorigenesis in Brca2 knockout mice.
Data indicate the importance of breast cancer 1 protein (BRCA1)/breast cancer 2 protein (BRCA2) function in cranial neural crest cells (CNCCs) during craniofacial skeletal formation.
we generated a Brca2 knock-in mouse model lacking exons 4-7 and demonstrated that these exons are dispensable for viability as well as tumor-free survival. This study provides the first in vivo evidence of the functional significance of a minor transcript of BRCA2 that can play a major role in the survival of humans who are homozygous for a clearly pathogenic mutation.
we describe a genetic approach to examine the functional significance of the interaction between BRCA2 and PALB2 by generating a knock-in mouse model of Brca2 carrying a single amino acid change (Gly25Arg, Brca2G25R) that disrupts this interaction. In addition, we have combined Brca2G25R homozygosity as well as hemizygosity with Palb2 and Trp53 heterozygosity .
Merit40 mutation exacerbated ICL-induced chromosome instability in the context of concomitant Brca2 deficiency but not in conjunction with Fancd2 mutation.
Heterozygous and homozygous Brca2 mutation may lead to dysfunction in T cell populations.
BRCA2 exon 27 domain maintains chromosomal integrity at both stalled and collapsed replication forks consistent with involvement in both replication fork maintenance and double strand break repair.
we use a genetically engineered mouse model of BRCA2-associated hereditary breast cancer to study drug resistance to several types of chemotherapy and PARP inhibition.
BRCA2-mediated sequestration of nuclear RAD51 serves to prevent inappropriate DNA interactions.
BRCA2 directly represses the expression of IFN-related genes
the models reveal novel aspects of cancer evolution in carriers of germline BRCA2 mutations, provide new insights into the tumour suppressive role of BRCA2
genetic stability, and hematopoietic differentiation potential of gene-corrected Brca2(Delta) (27/) (Delta) (27) iPSCs, achievements and limitations in the application of current reprogramming approaches in hematopoietic stem cell therapy are also discussed.
Results suggest that cellular levels of Brca2 and Rad51 are mutually dependent on each other, and that low levels of these proteins provide selective pressure for reduction of p53, which permits cell growth
BRCA2 accumulates DNA damage, which triggers checkpoint signalling and ARF activation
data showed that silencing of BRCA2 promoted cell proliferation, migration and invasion in vitro; data reported here demonstrate that BRCA2 may be a promising therapeutic targets for pancreatic ductal adenocarcinoma progression
BRCA2 is required for telomere homeostasis and may be particularly important for the replication of G-rich telomeric lagging strands.
Loss of Brca2 function predisposes the exocrine pancreas to profound DNA damage, and the frequency of invasive neoplasia is accentuated by the concomitant deregulation of p53
FANCD1/BRCA2 played notably important roles in the repair of TMZ-induced DNA damage.
Inherited mutations in BRCA1 and this gene, BRCA2, confer increased lifetime risk of developing breast or ovarian cancer. Both BRCA1 and BRCA2 are involved in maintenance of genome stability, specifically the homologous recombination pathway for double-strand DNA repair. The BRCA2 protein contains several copies of a 70 aa motif called the BRC motif, and these motifs mediate binding to the RAD51 recombinase which functions in DNA repair. BRCA2 is considered a tumor suppressor gene, as tumors with BRCA2 mutations generally exhibit loss of heterozygosity (LOH) of the wild-type allele.
BRCA1/BRCA2-containing complex, subunit 2
, breast and ovarian cancer susceptibility gene, early onset
, breast cancer 2 tumor suppressor
, breast cancer type 2 susceptibility protein
, fanconi anemia group D1 protein
, truncated breast and ovarian cancer susceptibility protein 2
, breast cancer 2, early onset homolog
, breast cancer 2, mutation 1, University of Wisconsin-Madison
, breast cancer susceptibility protein 2
, breast cancer type 2 susceptibility protein homolog
, fanconi anemia group D1 protein homolog
, breast and ovarian cancer susceptibility protein 2
, breast cancer 2, early onset
, breast cancer type 2 susceptibility protein-like