Browse our anti-BRCA2 (BRCA2) Antibodies

Human Breast Cancer 2, Early Onset (BRCA2) interaction partners

1. Assessment of the clinical relevance of BRCA2 missense variants by functional and computational approaches has been presented.

2. Identified APEX2 and FEN1 as synthetic lethal genes with both BRCA1 and BRCA2 loss of function in tumor cell lines.

3. BRCA2 expression is highly sensitive to promoter variations as most of them induced relevant changes. Moreover, we mapped critical regions of the BRCA2 promoter that may constitute potential targets for regulatory variants.

4. 14 had pathogenic variants in the BRCA1 gene and 5 had pathogenic variants in the BRCA2 gene

5. Different mechanisms inactivating the wild type allele are present within the same tumor sample at various extents. Results indicate that BRCA1/2-linked breast and ovarian cancer cells are predominantly characterized by LOH, but harbor a complex combination of second hits at various frequencies.

6. BRCA carriers with and without malignancy exhibit comparable ovarian reserve and responses to ovarian stimulation compared with women with BRCA-negative cancers and cancer-free controls.

7. homologous recombination deficiency (HRD), tumor BRCA1/2 mutations, and absence of CCNE1 amplification are associated with improved survival of ovarian cancer patients treated with platinum monotherapy and HRD-positive patients may benefit from platinum dose intensification.

8. These results suggest a modest association between BRCA1 and BRCA2 and Nonsyndromic cleft lip with or without cleft palate.

9. This study comprehensively describes the characteristics of the 1,650 unique BRCA1 and 1,731 unique BRCA2 deleterious (disease-associated) mutations identified in the CIMBA database.

10. Study shows that BRCA1, PALB2 and BRCA2 can all play a significant role in both checkpoint activation and checkpoint maintenance, depending on cell type and context, and that PALB2 links BRCA1 and BRCA2 in the checkpoint response. The BRCA1-PALB2 interaction can be important for checkpoint activation, whereas PALB2-BRCA2 complex appears to be more critical for checkpoint maintenance.

11. Our results did not provide evidence for elevated risks of invasivebreast cancer (BC) or epithelial ovarian cancer in BRCA1/BRCA2 predictive test negatives

12. These findings might be exploited to assess the relevance for cancer risk of other BRCA2 spliceogenic variants.

13. BRCA1/2 mutation prevalence in unselected breast cancer patients was 1.8%.

14. RAD51 can dissociate the very D-loops they create if in stoichiometric excess. BRCA2 regulates HR at a post-synaptic stage by modulating RAD51-mediated D-loop dissociation. Provides a biochemical mechanistic underpinning of homeostasis between RAD51 and BRCA2 previously reported in cellular experiments.

15. The prevalence of germline BRCA1/2 mutations in patients with peritoneal carcinoma or fallopian tube carcinoma is comparable to that of BRCA1/2 mutations in epithelial ovarian cancer patients.

16. Prevalence of BRCA1/2 germline pathogenic (P) and likely pathogenic (LP) variants is slightly higher than previously described by the largest occidental studies, with a high prevalence of variant c.5266dupC (p.Gln1756Profs*74) in BRCA1 observed. Moreover, we identified a new LP variant.

17. Population-Based BRCA1/2 Testing in Ashkenazi Jews: Ready for Prime Time.

18. We identified a speculative association of germ-line BRCA1/2 alterations with brain metastases in pancreas ductal adenocarcinoma

19. the study included all BRCA1/2 germline missense mutations identified in breast and ovarian cancer patients; the Asian population was the most affected by BRCA2 mutant patterns (Systematic Review)

20. Applying established referral criteria for genetic testing in Serbia will help identify BRCA1/2 mutation carriers but will not help identify mutations in other cancer susceptibility genes. Until better predictors emerge we should be performing wider genetic testing of EOC in order to identify all mutation carriers.

Fruit Fly (Drosophila melanogaster) Breast Cancer 2, Early Onset (BRCA2) interaction partners

1. 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.

2. A mutation in Cyp6d2, a cytochrome P450 gene, when combined with a brca2 mutation, resulted in synergistic hypersensitivity to camptothecin.

3. DNA repair by homologous recombination is dramatically decreased in CG30169 (brca2 homolog) mutants.

Zebrafish Breast Cancer 2, Early Onset (BRCA2) interaction partners

1. the data suggest for the first time that brca2/fancd1 is essential for vertebrate kidney ontogeny.

2. Carcinogenesis in zebrafish with combined mutations in tp53 and brca2 typically requires biallelic mutation or loss of at least one of these genes.

3. The novel role of Brca2 in organizing the vertebrate egg nucleus may provide new insights into the origin of ovarian cancer

4. critical roles for brca2 in ovarian development and tumorigenesis in reproductive tissues

Mouse (Murine) Breast Cancer 2, Early Onset (BRCA2) interaction partners

1. BRCA2-proficient and deficient cells are radiosensitised by HT, indicating that HT does not exclusively act by inhibition of HR.

2. 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.

3. The functional consequence of Parp1 heterozygosity on BRCA2 loss is demonstrated by a significant increase in tumorigenesis in Brca2 knockout mice.

4. 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.

5. 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.

6. 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 .

7. Merit40 mutation exacerbated ICL-induced chromosome instability in the context of concomitant Brca2 deficiency but not in conjunction with Fancd2 mutation.

8. Heterozygous and homozygous Brca2 mutation may lead to dysfunction in T cell populations.

9. 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.

10. 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.

11. BRCA2-mediated sequestration of nuclear RAD51 serves to prevent inappropriate DNA interactions.

12. BRCA2 directly represses the expression of IFN-related genes

13. the models reveal novel aspects of cancer evolution in carriers of germline BRCA2 mutations, provide new insights into the tumour suppressive role of BRCA2

14. 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.

15. 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

16. BRCA2 accumulates DNA damage, which triggers checkpoint signalling and ARF activation

17. 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

18. BRCA2 is required for telomere homeostasis and may be particularly important for the replication of G-rich telomeric lagging strands.

19. 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

20. FANCD1/BRCA2 played notably important roles in the repair of TMZ-induced DNA damage.