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Study show that damage-induced long non-coding RNAs (dilncRNAs) play a role in DNA double-strand breaks (DSBs) repair by homologous recombination (HR) by contributing to the recruitment of the HR proteins BRCA1, BRCA2, and RAD51, without affecting DNA-end resection. BRCA2 directly interacts with RNase H2, mediates its localization to DSBs in the S/G2 cell-cycle phase, and controls DNA:RNA hybrid levels at DSBs.
The overall yield of comprehensive BRCA1/2 testing in ethnically diverse high-risk Israeli individuals is 3.3%. This is lower than expected by probability models. A slightly higher rate of BRCA1/2 carriers was seen among ovarian cancer cases. These data should guide BRCA1/2 optimal testing strategy in Israel.
The 2 identified likely pathogenic Unclassified variants in BRCA1 and BRCA2 require further verification with clinical evidence.
The total number of Ovarian Cancer patients captured was 802; of these, 53 and five families carry 22 mutations in BRCA1/2 genes. Of these, eight mutations were unique to the Arab populations, and five mutations were commonly circulated among Arabs (BRCA1: c.5266dupC, c.5095C>T, c.68_69delAG, and c.4041_4042delAG; BRCA 2 c.1310_1313delAAGA).
We conclude that BRCA1 and BRCA2 could be used as clinicopathological biomarkers to evaluate the prognosis of digestive system cancers.
Neither the patients tested nor the control subjects showed germline hypermethylation of the BRCA1 and BRCA2 promoter regions analyzed
Male carrying BRCA mutations have significantly lower QMAX than healthy men. BRCA1 patients have on average larger prostate glands and higher PSA than BRCA2 patients.
Evidence has been provided that the majority of the Cas9-induced single nicks at the target DNA strand rely on RAD51 and BRCA2 for efficient and scar-less DNA repair.
It has been shown that BRCA2-mutant prostate cancer cells harbor increased genomic instability and a mutational profile that more closely resembles metastatic than localized disease.
Both BRCA1 and BRCA2 mutations are associated with an increased risk for Prostate cancer(PC). BRCA2 in particular confers a more aggressive PC phenotype with a higher probability of locally advanced and metastatic disease, and should be considered a prognostic marker associated with poorer survival
Among BRCA mutation( BRCA1 or BRCA2) carriers, the mortality benefit of preventive mastectomy at age 25 is substantial, but the expected benefit declines rapidly with increasing age at surgery.
The present study demonstrates a clear protective effect of early first pregnancy on breast cancer risk in both BRCA1 and BRCA2 mutation carriers.
Overall, 5152 oncogenetic tests were reviewed in the present study, of which 4452 had no a priori known familial mutation. The majority of participants (68.6%) were genotyped because of personal history of cancer; 20.6% were tested because of family history of cancer, and details for the remaining 10.7% were missing. Overall, 256/4452 (5.8%) carriers were detected, 141 BRCA1 and 115 BRCA2 mutation carriers.
The present study aimed to clarify the clinicopathological features, including the level of p53 protein expression and BRCA mutations, of primary fallopian tube cancer (PFTC) in Japanese women.
Germline mutations involving the Fanconi anemia pathway, such as BRCA2 are often implicated in Invasive Pancreatic Ductal Adenocarcinoma.
Authors found that BRCA1/2 germline mutations in China exhibit distinct characteristics compared to those in Western populations.
We show a strong association between Triple Negative Breast Cancer and mutations in BRCA1/2 genes and the poor outcome of these patients. The survival curve analysis showed that the presence of AKT1, TP53, KDR, KIT, BRCA1 and BRCA2 mutations is correlated with a poor prognosis.
Letter: BRCA2- and ATM-mutated prostate cancer sensitive to high dose testosterone.
The authors propose that BRCA2 antagonizes 53BP1, RIF1, and Artemis-dependent c-nonhomologous end-joining and alt-nonhomologous end-joining to prevent gross genomic instability in a RAD51-independent manner.
region in the N terminus exhibits DNA binding activity and promotes RAD51-mediated homologous recombination
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