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Three of 32 tumors had pathogenic BRCA1 gene alterations: two of these pathogenic variants exhibited deletions leading to frameshift mutations, and the remaining single-nucleotid-variant resulted in premature STOP codon.
In this study, we evaluated this novel mechanism of drug resistance in newly diagnosed, early-stage BRCA1/2-mutant breast cancer patients who had a poor response to platinum-based neoadjuvant chemotherapy.We report a BRCA1 reversion mutation in a patient newly diagnosed with triple-negative breast cancer that developed over 18 weeks of platinum-based neoadjuvant therapy.
These data demonstrate the added benefit of combining Topo I inhibition mediated by IMMU-132 with synthetic lethality provided by PARPi in triple-negative breast cancer, regardless of BRCA1/2 status, thus supporting the rationale for such a combination clinically
In the olaparib LT group, 244 genetic alterations were detected, with TP53, BRCA1, and BRCA2 mutations being most common (90%, 25%, and 35%, respectively). BRCA2 mutations were enriched among the LT responders. BRCA methylation was not associated with response duration. High myriad HRD score (>42) and/or BRCA1/2 mutation was associated with LT response to olaparib
Rucaparib was tolerable and had activity in patients with platinum-sensitive germline BRCA1/2-mutated high-grade ovarian carcinoma
BRCA1- and BRCA2- (BRCA)-associated tumors respond to both platinum compounds and PARP inhibitors (PARPi). Potential synergism for carboplatin and the PARPi veliparib was demonstrated in preclinical studies. In a companion phase II trial, veliparib was demonstrated to be active as a single agent in both BRCA1- and BRCA2-associated MBC patients
Findings reveal a previously unknown effect of BRCA1 suppression on mechanisms that regulate the cell division axis in proliferating, non-transformed human mammary epithelial cells and consequent downstream effects on the mitotic integrity and phenotype control of their progeny.
BRCA1 role in homologous recombination repair, replication, involvement in checkpoint regulation, transcription, chromatin remodeling, and cytoplasmic function (centrosome regulation, apoptosis, selective autophagy), also BRCA1 role in ovarian and breast cancer.[review]
Findings indicate a transcriptional axis of FOXP3 (zeige FOXP3 Proteine)-BRCA1-miR (zeige MLXIP Proteine)-155 in breast cancer cells and show that plasma miR (zeige MLXIP Proteine)-155 may serve as a non-invasive biomarker for detection of early stage breast cancer.
Lack-of-function mutations in EDC4 were detected in BRCA1/2-mutation-negative breast cancer cases, suggesting a role in breast cancer susceptibility.
Investigation on BRCA1 SNPs and its effects on mastitis in Chinese commercial cattle.
The gene-specific SNP marker analysis showed a significant association of BRCA1 C28300A with milk somatic cell scores.
In general, OC use, childbearing and breastfeeding do not differ between BRCA1/2 carriers and non-carriers with ovarian cancer. However, the effects of tubal ligation may differ between BRCA1 carriers and non-carriers.
Bovine BRCA1 was phosphorylated and nuclear speckling was enhanced in response to DNA-damaging agents.These results provide evidence that phosphorylation and nuclear relocalization are highly conserved features of the BRCA1 response to genotoxic stress.
Consensus-based recombinant adeno-associated virus-BRCA1 knock out virus vectors failed to induce BRCA1 knockout in Gottingen fibroblasts.
BRCA1, but not BRCA2, suppresses the formation of tandem duplications at a site-specific chromosomal replication fork barrier imposed by the binding of Tus proteins to an array of Ter sites. BRCA1 has no equivalent role at chromosomal double-stranded DNA breaks, indicating that tandem duplications form specifically at stalled forks.
Loss of p16INK4 protein (p16) transforms breast cancer 1 (Brca1)-deficient mammary epithelial cell (MEC (zeige CCL28 Proteine)) and induces mammary tumors.
Brca1 is necessary for hematopoietic stem cells maintenance and normal hematopoiesis and that distinct mutations lead to different degrees of hematopoietic dysfunction.
TGFbeta (zeige TGFB1 Proteine) stabilized the abundance of BRCA1 by reducing the abundance of microRNA-182 (miR (zeige MLXIP Proteine)-182). Ectopic expression of BRCA1 or antagonism of miR (zeige MLXIP Proteine)-182 in cultured TGFbeta (zeige TGFB1 Proteine)-deficient mammary epithelial cells restored luminal lineage commitment.
BRCA1 inactivation can increase expression of miR (zeige MLXIP Proteine)-155, contributing to cardiac hypertrophy. And Rev produces their beneficial effects partially by down-regulating miR (zeige MLXIP Proteine)-155 expression, which might be a novel strategy for treatment of cardiac hypertrophy.
both murine Brca1185stop tumors and human BRCA1185delAG breast cancer cells express a new gene domain-less (RING-less) BRCA1 protein that mediated resistance to homologous recombination deficient-targeted therapies
Genomic instability can be rescued by deletion of Trp53bp1 (zeige TP53BP1 Proteine), encoding the DNA damage response factor 53BP1 (zeige TP53BP1 Proteine); mice expressing RING-less BRCA1 do not show an increased susceptibility to tumors in the absence of 53BP1 (zeige TP53BP1 Proteine); Genomic instability in cells expressing RING-less BRCA1 correlates with loss of BARD1 (zeige BARD1 Proteine) and a defect in restart of replication forks after hydroxyurea treatment
the aberrant proliferative capacity of Brca1(-/-) luminal progenitor cells is linked to the replication-associated DNA damage response, where proliferation of mammary progenitors is perpetuated by damage-induced, autologous NF-kappaB (zeige NFKB1 Proteine) signaling.
We report here elevated recombination rates at telomeres in cells from human BRCA1 mutation carriers and in mouse embryonic stem cells lacking both copies of functional Brca1.
loss of Brca1, a tumor suppressor that functions in DNA damage repair, in the mammary epithelium induced senescence with induction of p16 and a decline of stem cell function, which was rescued by p16 loss.
MRN (Mre11 (zeige MRE11A Proteine), Rad50 (zeige RAD50 Proteine), and Nbs1 (zeige NLRP2 Proteine)) complex, CtIP (zeige RBBP8 Proteine), and BRCA1 are required for both the removal of Top2 (zeige TOP2 Proteine)-DNA adducts and the subsequent resection of Top2 (zeige TOP2 Proteine)-adducted DSB ends.
BRCA1-dependent helicase unloading is a critical, early event in DNA interstrand crosslink repair.
This gene encodes a nuclear phosphoprotein that plays a role in maintaining genomic stability, and it also acts as a tumor suppressor. The encoded protein combines with other tumor suppressors, DNA damage sensors, and signal transducers to form a large multi-subunit protein complex known as the BRCA1-associated genome surveillance complex (BASC). This gene product associates with RNA polymerase II, and through the C-terminal domain, also interacts with histone deacetylase complexes. This protein thus plays a role in transcription, DNA repair of double-stranded breaks, and recombination. Mutations in this gene are responsible for approximately 40% of inherited breast cancers and more than 80% of inherited breast and ovarian cancers. Alternative splicing plays a role in modulating the subcellular localization and physiological function of this gene. Many alternatively spliced transcript variants, some of which are disease-associated mutations, have been described for this gene, but the full-length natures of only some of these variants has been described. A related pseudogene, which is also located on chromosome 17, has been identified.
BRCA1/BRCA2-containing complex, subunit 1
, RING finger protein 53
, breast and ovarian cancer susceptibility protein 1
, breast and ovarian cancer sususceptibility protein 1
, breast cancer type 1 susceptibility protein
, protein phosphatase 1, regulatory subunit 53
, BRCA1 homologue
, breast cancer type 1 susceptibility protein homolog
, breast cancer 1, early onset
, BRCA1 homolog
, breast and ovarian cancer susceptibility protein
, breast cancer associated 1