Use your antibodies-online credentials, if available.
observations indicate that nascent DNA degradation in BRCA1/2-deficient cells occurs as a consequence of MRE11 (显示 MRE11A 蛋白)-dependent nucleolytic processing of reversed forks generated by fork remodelers
We report that CTSO (显示 CTSK 蛋白) reduces the protein levels of BRCA1 and ZNF423 through cysteine proteinase-mediated degradation. We also have identified a series of transcription factors of BRCA1 that are regulated by CTSO (显示 CTSK 蛋白) at the protein level.
BRCA1 downregulation combined with CHK1 (显示 CHEK1 蛋白) inhibition induced excessive amounts of DNA damage, resulting in an inability to complete the S-phase. Therefore, we suggest CHK1 (显示 CHEK1 蛋白) inhibition as a strategy for targeting BRCA1- or CDK12 (显示 CRKRS 蛋白)-deficient tumors.
BRCA1(185delAG) results in expression of mutant BRCA1 lacking the RING domain, promoting resistance; expression of RING-less BRCA1 may serve as a biomarker to predict response to therapy in patients with BRCA1-mutant tumors
Evidence does not support routine risk-reducing hysterectomy for BRCA1 and BRCA2 (显示 BRCA2 蛋白) mutation carriers.
pol beta and BRCA1 appeared to have a functional interaction, observed in both DT40 and human cell lines, in protecting cells against alkylating MMS-induced cytotoxicity; but pol beta had no protective effect in the absence of BRCA1. In vivo and in vitro assays for a base excision repair role of BRCA1 were negative.
BRCA1 p.His1673del is a pathogenic mutation associated with ovarian cancer.
the BRCA1-dependent translation of mRNAs participating in unexpected functions such as cellular movement, nucleic acid metabolism or protein trafficking is indicative of novel functions for BRCA1.
BRCA1-dysfunctional tumors are hypersensitive to DNA damaging chemotherapeutic agents.
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
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.
Genomic instability can be rescued by deletion of Trp53bp1 (显示 TP53BP1 蛋白), encoding the DNA damage response factor 53BP1 (显示 TP53BP1 蛋白); mice expressing RING-less BRCA1 do not show an increased susceptibility to tumors in the absence of 53BP1 (显示 TP53BP1 蛋白); Genomic instability in cells expressing RING-less BRCA1 correlates with loss of BARD1 (显示 BARD1 蛋白) 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 (显示 NFKB1 蛋白) 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 (显示 WWOX 蛋白) interaction supports non-homologous end-joining as the dominant DSB repair pathway in Wwox (显示 WWOX 蛋白)-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.
Results reveal a broader biological role for BRCA1 in protecting the developing embryo from oxidative stress, and corroborate a role for DNA damage in the mechanism of ethanol embryotoxicity.
This study uncovers a previously unappreciated, DNA repair-independent function of BRCA1 in antagonizing COBRA1 (显示 COBRA1 蛋白)-dependent transcription program during mammary gland development.
loss of Brca1 in murine BM causes hematopoietic defects similar to those seen in people with FA, which provides strong evidence that Brca1 is critical for normal hematopoiesis and that Brca1 is a bona fide FA-like gene.
MRN (Mre11 (显示 MRE11A 蛋白), Rad50 (显示 RAD50 蛋白), and Nbs1 (显示 NLRP2 蛋白)) complex, CtIP (显示 RBBP8 蛋白), and BRCA1 are required for both the removal of Top2 (显示 TOP2 蛋白)-DNA adducts and the subsequent resection of Top2 (显示 TOP2 蛋白)-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