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anti-Human BRCA2 Anticorps:
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Human Polyclonal BRCA2 Primary Antibody pour 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. dans Oxidative medicine and cellular longevity 1970
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Human Monoclonal BRCA2 Primary Antibody pour IHC, IHC (p) - ABIN445491
Wu, Jiang, Thangaraju, Wu, Couch: Induction of the BRCA2 promoter by nuclear factor-kappa B. dans The Journal of biological chemistry 2000
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Human Monoclonal BRCA2 Primary Antibody pour 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. dans Breast cancer research : BCR 2001
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Frequency of BRCA2 breast cancer pathogenic mutations in the Mexican population.
oursplicing analysis performed in three independent carriers show thatBRCA2c.7976+5G>T alleles produce a major in-frame transcript Delta17 predicted to encode a non-functional protein, and that even though variable proportions of additional transcripts (Delta16-18, Delta17,18,Delta18 and 17q224) have been detected, none of them arepredicted to rescue BRCA2 functionality.
Knowing a patient's BRCA mutation status is important for prevention and treatment decision-making. Improving the characterization of mutations will lead to better management, treatment, and BCa prevention efforts in African Americans who are disproportionately affected with aggressive BCa and may inform future precision medicine genomic-based clinical studies.
Among ovarian cancer patients, BRCA2 carriers with mutations located in the RAD51-BD (exon 11) have prolonged PFS, PFI, and OS.
The BRCA2 is the most prevalent type mutation among hereditary breast and/or ovarian cancer patients in the Arab region, with an estimated prevalence was 17% with a higher pooled prevalence of BRCA mutations in the Levant Region 28%. When compared with studies from different parts of the world the Arab world appear to have different profiles with varying BRCA frequencies.[meta-analysis]
Among Korean women with the BRCA1/2 mutation, the location of the mutations may influence the risk of breast and ovarian cancers according to the putative functional domain regions
Carriers of BRCA1/BRCA2 mutation with sporadic Pancreatic Ductal Adenocarcinoma had a worse survival after pancreatectomy than their BRCA wild-type counterparts. However, platinum-based chemotherapy regimens were associated with markedly improved survival in patients with BRCA1/BRCA2 mutations, with survival differences no longer appreciated with wild-type patients.
Assessment of the clinical relevance of BRCA2 missense variants by functional and computational approaches has been presented.
Identified APEX2 and FEN1 as synthetic lethal genes with both BRCA1 and BRCA2 loss of function in tumor cell lines.
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.
14 had pathogenic variants in the BRCA1 gene and 5 had pathogenic variants in the BRCA2 gene
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.
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.
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.
These results suggest a modest association between BRCA1 and BRCA2 and Nonsyndromic cleft lip with or without cleft palate.
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.
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.
Our results did not provide evidence for elevated risks of invasivebreast cancer (BC) or epithelial ovarian cancer in BRCA1/BRCA2 predictive test negatives
These findings might be exploited to assess the relevance for cancer risk of other BRCA2 spliceogenic variants.
BRCA1/2 mutation prevalence in unselected breast cancer patients was 1.8%.
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