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BRCA1 associated RING domain 1

This gene encodes a protein which interacts with the N-terminal region of BRCA1. In addition to its ability to bind BRCA1 in vivo and in vitro, it shares homology with the 2 most conserved regions of BRCA1: the N-terminal RING motif and the C-terminal BRCT domain. The RING motif is a cysteine-rich sequence found in a variety of proteins that regulate cell growth, including the products of tumor suppressor genes and dominant protooncogenes. This protein also contains 3 tandem ankyrin repeats. The BARD1/BRCA1 interaction is disrupted by tumorigenic amino acid substitutions in BRCA1, implying that the formation of a stable complex between these proteins may be an essential aspect of BRCA1 tumor suppression. This protein may be the target of oncogenic mutations in breast or ovarian cancer. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Iris, Ubiquitin, CAN, p53, Atm
Papers on BARD1
Multigene testing of moderate-risk genes: be mindful of the missense.
Tavtigian et al., Salt Lake City, United States. In J Med Genet, Feb 2016
METHODS: We evaluated rare missense substitutions identified from a mutation screen of ATM, CHEK2, MRE11A, RAD50, NBN, RAD51, RINT1, XRCC2 and BARD1 in 1297 cases of early-onset breast cancer and 1121 controls via scores from Align-Grantham Variation Grantham Deviation (GVGD), combined annotation dependent depletion (CADD), multivariate analysis of protein polymorphism (MAPP) and PolyPhen-2.
Identification of germline alterations in breast cancer predisposition genes among Malaysian breast cancer patients using panel testing.
Teo et al., Kuala Selangor, Malaysia. In Clin Genet, Feb 2016
Twenty patients (19%) were identified to carry deleterious mutations, of whom thirteen (12%) were in the BRCA1 or BRCA2, six (6%) were in 5 other known breast cancer predisposition genes and one patient had a mutation in both BRCA2 and BARD1.
Inherited Mutations in Women With Ovarian Carcinoma.
Birrer et al., Providence, United States. In Jama Oncol, Jan 2016
Mutations in BRIP1 (n = 26), RAD51C (n = 11), RAD51D (n = 11), PALB2 (n = 12), and BARD1 (n = 4) were significantly more common in patients with OC than in the ESP or ExAC, present in 3.3%.
New concepts on BARD1: regulator of BRCA pathways and beyond.
Pilyugin et al., Genève, Switzerland. In Int J Biochem Cell Biol, Jan 2016
UNASSIGNED: For nearly two decades most research on BARD1 was closely linked to research on BRCA1, the breast cancer predisposition gene.
Genetic characterization of early onset ovarian carcinoma.
Swisher et al., Seattle, United States. In Gynecol Oncol, Jan 2016
We evaluated 11 genes associated with ovarian carcinoma (BARD1, BRCA1, BRCA2, BRIP1, MLH1, MSH2, MSH6, PALB2, PMS2, RAD51D, and RAD51C) and additional candidate genes in DNA repair (ATM, BAP1, CHEK2, MRE11A, NBN, PTEN, TP53).
Functional link between BRCA1 and BAP1 through histone H2A, heterochromatin and DNA damage response.
Ohta et al., Kawasaki, Japan. In Curr Cancer Drug Targets, Nov 2015
BRCA1 interacts with BARD1 to constitute a RING heterodimer-type E3 ubiquitin ligase.
Ubiquitin in regulation of spindle apparatus and its positioning: implications in development and disease.
Chakrabarti et al., Calcutta, India. In Biochem Cell Biol, Aug 2015
Some of the ubiquitin ligases regulating these proteins include PARK2, BRCA1/BARD1, MGRN1, SMURF2, and SIAH1; these play a pivotal role in the correct positioning of the spindle apparatus.
Inherited mutations in 17 breast cancer susceptibility genes among a large triple-negative breast cancer cohort unselected for family history of breast cancer.
Fasching et al., Rochester, United States. In J Clin Oncol, Mar 2015
Deleterious mutations in 15 other predisposition genes were detected in 3.7% of patients, with the majority observed in genes involved in homologous recombination, including PALB2 (1.2%) and BARD1, RAD51D, RAD51C, and BRIP1 (0.3% to 0.5%).
Alternative splicing in cancer: implications for biology and therapy.
Weiss et al., San Francisco, United States. In Oncogene, Feb 2015
Here, we review the splicing landscape of TP53, BARD1 and AR to illuminate roles for alternative splicing in cancer.
Clinicopathological values of NBS1 and DNA damage response genes in epithelial ovarian cancers.
Lee et al., Seoul, South Korea. In Exp Mol Med, 2014
As ovarian cancers frequently respond to DNA-damaging agents, we assessed the clinicopathological significance of key double-strand DNA break (DSB) repair genes, including BRCA1, BRCA2, BARD1, ATM, RAD51 and NBS1 in EOC cell lines and paraffin-embedded tissue sections from 140 EOC patients treated with cytoreductive surgery, followed by platinum-based chemotherapy.
OLA1 in centrosome biology alongside the BRCA1/BARD1 complex: looking beyond centrosomes.
Hergovich et al., London, United Kingdom. In Mol Cell, 2014
In this issue of Molecular Cell, Chiba and colleagues (Matsuzawa et al., 2014) identify Obg-like ATPase 1 (OLA1) as an additional member of the BRCA1/BARD1/γ-tubulin complex that is critically involved in centrosome amplification and microtubule aster formation.
Luring BRCA1 to the scene of the crime.
Baer, New York City, United States. In Cancer Cell, 2013
In this issue of Cancer Cell, Li and Yu report that BRCA1 recruitment involves a novel interaction between its partner protein BARD1 and poly(ADP-ribose) chains at the DSB.
Function of BRCA1 in the DNA damage response is mediated by ADP-ribosylation.
Yu et al., Ann Arbor, United States. In Cancer Cell, 2013
BRCA1 forms a Ring-domain heterodimer with BARD1, a major partner of BRCA1 that contains tandem BRCA1 C-terminus (BRCT) motifs.
The genetic landscape of high-risk neuroblastoma.
Maris et al., Cambridge, United States. In Nat Genet, 2013
Rare, potentially pathogenic germline variants were significantly enriched in ALK, CHEK2, PINK1 and BARD1.
53BP1 regulates DSB repair using Rif1 to control 5' end resection.
de Lange et al., New York City, United States. In Science, 2013
Rif1 inhibits resection involving CtIP, BLM, and Exo1; limits accumulation of BRCA1/BARD1 complexes at sites of DNA damage; and defines one of the mechanisms by which 53BP1 causes chromosomal abnormalities in Brca1-deficient cells.
The BARD1 Cys557Ser variant and risk of familial breast cancer in a South-American population.
Jara et al., Santiago, Chile. In Mol Biol Rep, 2012
Our results suggest that BARD1 557Ser and XRCC3 241Met may play roles in BC risk in women with a strong family history of breast cancer (BC).
BARD1: an independent predictor of survival in non-small cell lung cancer.
Irminger-Finger et al., Genève, Switzerland. In Int J Cancer, 2012
BARD1 isoforms might be involved in tumor initiation and invasive progression and might represent a novel prognostic marker for non-small cell lung cancer.
Common variation at BARD1 results in the expression of an oncogenic isoform that influences neuroblastoma susceptibility and oncogenicity.
Maris et al., Philadelphia, United States. In Cancer Res, 2012
our findings identify BARD1beta as an oncogenic driver of high-risk neuroblastoma tumorigenesis
Replication of neuroblastoma SNP association at the BARD1 locus in African-Americans.
Devoto et al., Philadelphia, United States. In Cancer Epidemiol Biomarkers Prev, 2012
Single-nucleotide polymorphisms in BARD1 gene is associated to neuroblastoma.
Quantitative proteomic identification of the BRCA1 ubiquitination substrates.
Shiio et al., San Antonio, United States. In J Proteome Res, 2011
the BRCA1/BARD1 ubiquitin ligase complex was found to enhance SAFB protein expression and induce Tel2 nuclear translocation
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