GoPubMed Proteins lists recent and important papers and reviews for
proteins. Page last changed on 14 Mar 2013.
BRCA1 interacting protein C-terminal helicase 1
Bach1, BRIP1, FANCJ
The protein encoded by this gene is a member of the RecQ DEAH helicase family and interacts with the BRCT repeats of breast cancer, type 1 (BRCA1). The bound complex is important in the normal double-strand break repair function of breast cancer, type 1 (BRCA1). This gene may be a target of germline cancer-inducing mutations. [provided by RefSeq, Jul 2008] (from
NCBI)
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Papers on
Bach1
BRIP1 variations analysis reveals their relative importance as genetic susceptibility factor for cervical cancer.
New
Xi'an, China. In Biochem Biophys Res Commun, 06 Apr 2013
To evaluate the association between gene variations in BRIP1 (BRCA1-interacting protein 1) and the risk of cervical cancer, we examined eight single nucleotide polymorphisms (SNPs: rs2048718, rs12937080, rs4988344, rs6504074, rs4988345, rs4986764, rs4986763, and rs11079454) in the BRIP1 gene in cervical tissue from a Chinese population using the MassARRAY system.
Microarray gene expression profiling analysis combined with bioinformatics in multiple sclerosis.
New
Shanghai, China. In Mol Biol Rep, 01 Apr 2013
Furthermore, the RIF result suggested that IKZF1, BACH1, CEBPB, EGR1, FOS may play central regulatory roles in controlling gene expression in the pathogenesis of MS.
Haplotype analysis of eight genes of the monoubiquitinated FANCD2-DNA damage-repair pathway in breast cancer patients.
New
Changsha, China. In Cancer Epidemiol, 25 Feb 2013
Among these, four haplotypes (ATC in block 1 of NBS1, GCCCC and GCCCT in block 2 of NBS1, and GCT in block 2 of BRIP1) were correlated with breast cancer risk in sporadic cases (OR (95% CI) 1.350(1.124-1.623),
[Molecular basis of gynecological oncology--TopBP1 protein and its participation in the transcription process].
Review
New
Poland. In Ginekol Pol, May 2012
However currently known susceptibility genes including BRCA1, BRCA2, ATM, Chk2, PALB2, and BRIP1 explain less than 25% of familial breast and/ovarian cancers.
Translational advances regarding hereditary breast cancer syndromes.
Review
New
Bethesda, United States. In J Surg Oncol, May 2012
Approximately 5-10% of breast cancers may be inheritable, up to 90% of which are due to mutations in BRCA1 and BRCA2.
Hereditary ovarian cancer: beyond the usual suspects.
Review
New
Seattle, United States. In Gynecol Oncol, Feb 2012
Recently, three new ovarian cancer susceptibility genes have been identified: RAD51C, RAD51D, and BRIP1.
Oxidative stress in Fanconi anaemia: from cells and molecules towards prospects in clinical management.
Review
Napoli, Italy. In Biol Chem, 2012
Some FA gene products involved in redox homeostasis can be summarized as follows: (a) FANCA, FANCC, and FANCG interact with cytochrome P450-related activities and/or respond to oxidative damage; (b) FANCD2 in OS response interacts with forkhead box O3 and ataxia telangiectasia mutated protein; (c) FANCG is found in mitochondria and interacts with PRDX3, and FA-G cells display distorted mitochondria and decreased peroxidase activity; (d) FANCJ (BACH1/BRIP1) is a repressor of haeme oxygenase-1 gene and senses oxidative base damage; (e) antioxidants, such as tempol and resveratrol decrease cancer incidence and haematopoietic defects in Fancd2(-/-) mice.
Oncogenic RAS regulates BRIP1 expression to induce dissociation of BRCA1 from chromatin, inhibit DNA repair, and promote senescence.
GeneRIF
Philadelphia, United States. In Dev Cell, 2012
Downregulation of BRIP1, a physiological partner of BRCA1 in the DNA repair pathway, triggers BRCA1 chromatin dissociation.
Novel insights into the regulation of antioxidant-response-element-mediated gene expression by electrophiles: induction of the transcriptional repressor BACH1 by Nrf2.
GeneRIF
Kuopio, Finland. In Biochem J, 2012
We conclude that BACH1 is a bona fide Nrf2 target gene and that induction of BACH1 by Nrf2 may serve as a feedback-inhibitory mechanism for antioxidant-response-element-mediated gene regulation.
RAD51 and breast cancer susceptibility: no evidence for rare variant association in the Breast Cancer Family Registry study.
Lyon, France. In Plos One, 2011
BACKGROUND: Although inherited breast cancer has been associated with germline mutations in genes that are functionally involved in the DNA homologous recombination repair (HRR) pathway, including BRCA1, BRCA2, TP53, ATM, BRIP1, CHEK2 and PALB2, about 70% of breast cancer heritability remains unexplained.
Genotyping of fanconi anemia patients by whole exome sequencing: advantages and challenges.
Würzburg, Germany. In Plos One, 2011
Disease-causing are biallelic mutations in any one of at least 15 genes encoding members of the FA/BRCA pathway of DNA-interstrand crosslink repair.
Mutations in BRIP1 confer high risk of ovarian cancer.
Impact
Reykjavík, Iceland. In Nat Genet, 2011
We discovered a rare (0.41% allelic frequency) frameshift mutation, c.2040_2041insTT, in the BRIP1 (FANCJ) gene that confers an increase in ovarian cancer risk (odds ratio (OR) = 8.13, P = 2.8 × 10(-14)).
The BTB and CNC homology 1 (BACH1) target genes are involved in the oxidative stress response and in control of the cell cycle.
GeneRIF
Berlin, Germany. In J Biol Chem, 2011
The BTB and CNC homology 1 (BACH1) target genes are involved in the oxidative stress response and in control of the cell cycle.
BRIP1, PALB2, and RAD51C mutation analysis reveals their relative importance as genetic susceptibility factors for breast cancer.
GeneRIF
Newcastle, Australia. In Breast Cancer Res Treat, 2011
six missense variants predicted to be causative were detected, one in BRIP1 and five in PALB2
Inherited mutations in breast cancer genes--risk and response.
Review
Montréal, Canada. In J Mammary Gland Biol Neoplasia, 2011
Meanwhile, an understanding of the function of BRCA1 and BRCA2 in the DNA damage response pathway has lead to the identification of a number of breast cancer susceptibility genes including PALB2, CHEK2, ATM and BRIP1, all of which interact directly or indirectly with BRCA1 or BRCA2.
Interaction between the helicases genetically linked to Fanconi anemia group J and Bloom's syndrome.
GeneRIF
Baltimore, United States. In Embo J, 2011
FANCJ catalytic activity and its effect on BLM protein stability contribute to preservation of genomic stability and a normal response to replication stress.
XPD helicase structures and activities: insights into the cancer and aging phenotypes from XPD mutations.
Impact
Los Angeles, United States. In Cell, 2008
These results provide a foundation for understanding disease consequences of mutations in XPD and related 4Fe-4S helicases including FancJ.
Structure of the DNA repair helicase XPD.
Impact
Saint Andrews, United Kingdom. In Cell, 2008
The XPD helicase (Rad3 in Saccharomyces cerevisiae) is a component of transcription factor IIH (TFIIH), which functions in transcription initiation and Nucleotide Excision Repair in eukaryotes, catalyzing DNA duplex opening localized to the transcription start site or site of DNA damage, respectively.
Emergence of a DNA-damage response network consisting of Fanconi anaemia and BRCA proteins.
Review
Impact
Baltimore, United States. In Nat Rev Genet, 2007
Fanconi anaemia (FA) has recently become an attractive model to study breast cancer susceptibility (BRCA) genes, as three FA genes, FANCD1, FANCN and FANCJ, are identical to the BRCA genes BRCA2, PALB2 and BRIP1.
Abraxas and RAP80 form a BRCA1 protein complex required for the DNA damage response.
Impact
Boston, United States. In Science, 2007
Abraxas binds BRCA1 to the mutual exclusion of BACH1 (BRCA1-associated C-terminal helicase) and CtIP (CtBP-interacting protein), forming a third type of BRCA1 complex.
