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prostate carcinoma cell proliferation is enhanced by the down-regulation of BRCA2 expression when interacting with COL1, a major component of the ECM (显示 MMRN1 ELISA试剂盒) at osseous metastatic sites
Study have shown that mutations in BRCA1, BRCA2, and PALB2 (显示 PALB2 ELISA试剂盒) account for more than 10 % of breast cancer in Trinidad and Tobago. 25 different mutations identified; of these, four mutations were seen in two patients each.
evidence on the role of BRCA2 as a modulator of cancer cell growth and elucidation of the molecular mechanisms involved in its down-regulation in cancer cells when interacting with basement membranes
The heterogeneity of the detected mutations confirms the necessity of simultaneous analysis of BRCA1/2 genes in all patients diagnosed with serous ovarian carcinoma. Moreover, the use of tumor tissue for mutational analysis allowed the detection of both somatic and germline BRCA1/2 mutations.
We demonstrated an association between six previously published single nucleotide polymorphisms (rs15869 [ BRCA2], rs1805389 [ LIG4 (显示 LIG4 ELISA试剂盒)], rs8079544 [ TP53 (显示 TP53 ELISA试剂盒)], rs25489 [ XRCC1 (显示 XRCC1 ELISA试剂盒)], rs1673041 [ POLD1 (显示 POLD1 ELISA试剂盒)], and rs11615 [ ERCC1 (显示 ERCC1 ELISA试剂盒)]) and subsequent CNS tumors in survivors of childhood cancer treated by radiation therapy.
Results show the overall prevalence of BRCA1/2 mutations at 3.9 % in the current large cohort of Chinese women with breast cancer, which is comparable with previous findings. Also, 41 % of the BRCA1/2 mutations detected have not been previously reported, suggesting that these mutations could be specific for Chinese women.
Patients with Fanconi anemia (显示 PALB2 ELISA试剂盒) have higher incidences of ectopic neurohypophysis, adenohypophysis hypoplasia, platybasia and other midline central nervous system skull base posterior fossa abnormalities than age- and sex-matched controls. Patients with posterior fossa abnormalities, including pontocerebellar hypoplasia, are more likely to have biallelic BRCA2 mutations.
CDNA representing BRCA2 alternate splice sites was amplified.
Pre-test genetic counselling prior to BRCA1/2 testing.
have confirmed previous reports of an association between breast, ovarian, and pancreatic cancers with BRCA1 and 2 mutations
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 (显示 TP53 ELISA试剂盒) 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
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 (显示 PALB2 ELISA试剂盒) 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 (显示 PALB2 ELISA试剂盒) and Trp53 (显示 TP53 ELISA试剂盒) heterozygosity .
Merit40 (显示 BABAM1 ELISA试剂盒) mutation exacerbated ICL-induced chromosome instability in the context of concomitant Brca2 deficiency but not in conjunction with Fancd2 (显示 FANCD2 ELISA试剂盒) 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 (显示 PARP1 ELISA试剂盒) inhibition.
BRCA2-mediated sequestration of nuclear RAD51 (显示 RAD51 ELISA试剂盒) 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.
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