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Low expression level of BRCA1 is associated with triple negative breast cancer.
Data suggest that metabolic rewiring of the breast epithelium towards increased anabolism might constitute an unanticipated and inherited form of metabolic reprogramming linked to increased risk of oncogenesis in women bearing pathogenic germline BRCA1 mutations.
Pyrosequencing is a precise and efficient method to quantify BRCA1 promoter methylation level, with a high potential for future clinical implication, as it identifies subgroups of patients with poorer prognosis.
we show that this combined approach allows the rapid and reliable detection of both germline and somatic aberrations affecting BRCA1 and BRCA2 (zeige BRCA2 ELISA Kits) in DNA derived from FFPE OCs, enabling improved hereditary cancer risk assessment and clinical treatment of ovarian cancer patients.
BRCA1/2 mutation carriers who have been treated with PS have a substantially reduced breast cancer incidence and mortality.
Several lines of evidence suggest ID4 (zeige ID4 ELISA Kits) may suppress BRCA1 function in basal-like breast cancer (BLBC) and in doing so, define a subset of BLBC patients who may respond to therapies traditionally used in BRCA1-mutant cancers. This review highlights recent advances in our understanding of the requirement for ID4 (zeige ID4 ELISA Kits) in mammary lineage commitment and the role for ID4 (zeige ID4 ELISA Kits) in BLBC.
high-accuracy and low-cost testing for mutations in BRCA1 and BRCA2 (zeige BRCA2 ELISA Kits) by using small amounts of input DNA, is reported.
Of note is the recent U.S. Food and Drug Administration breakthrough therapy designation of olaparib for the treatment of BRCA1/2- or ATM (zeige ATM ELISA Kits)-mutated metastatic castration-resistant prostate cancer. The implications of this new knowledge for clinical practice now and in the future are discussed.
In this review, we will discuss the emerging importance of somatic and epigenetic alterations of BRCA- and BRCA-related genes(BRCA1 and BRCA2 (zeige BRCA2 ELISA Kits) ) in the management of ovarian cancer.
Cells redox environment mediated by NOX1 isozymes activation down-regulates BRCA1 expression and promotes DNA homologous recombination repair in cancer.
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 is necessary for hematopoietic stem cells maintenance and normal hematopoiesis and that distinct mutations lead to different degrees of hematopoietic dysfunction.
TGFbeta (zeige TGFB1 ELISA Kits) stabilized the abundance of BRCA1 by reducing the abundance of microRNA-182 (miR (zeige MLXIP ELISA Kits)-182). Ectopic expression of BRCA1 or antagonism of miR (zeige MLXIP ELISA Kits)-182 in cultured TGFbeta (zeige TGFB1 ELISA Kits)-deficient mammary epithelial cells restored luminal lineage commitment.
BRCA1 inactivation can increase expression of miR (zeige MLXIP ELISA Kits)-155, contributing to cardiac hypertrophy. And Rev produces their beneficial effects partially by down-regulating miR (zeige MLXIP ELISA Kits)-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 ELISA Kits), encoding the DNA damage response factor 53BP1 (zeige TP53BP1 ELISA Kits); mice expressing RING-less BRCA1 do not show an increased susceptibility to tumors in the absence of 53BP1 (zeige TP53BP1 ELISA Kits); Genomic instability in cells expressing RING-less BRCA1 correlates with loss of BARD1 (zeige BARD1 ELISA Kits) 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 ELISA Kits) 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.
Brca1-Wwox (zeige WWOX ELISA Kits) interaction supports non-homologous end-joining as the dominant DSB repair pathway in Wwox (zeige WWOX ELISA Kits)-sufficient cells
Structure-guided separation-of-function mutations show that the RNF8 E2 stimulating activity is essential for DSB signaling in mammalian cells and is necessary for downstream recruitment of 53BP1 and BRCA1.
MRN (Mre11 (zeige MRE11A ELISA Kits), Rad50 (zeige RAD50 ELISA Kits), and Nbs1 (zeige NLRP2 ELISA Kits)) complex, CtIP (zeige RBBP8 ELISA Kits), and BRCA1 are required for both the removal of Top2 (zeige TOP2 ELISA Kits)-DNA adducts and the subsequent resection of Top2 (zeige TOP2 ELISA Kits)-adducted DSB ends.
BRCA1-dependent helicase (zeige DNA2 ELISA Kits) 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