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BRCA1 interacting protein C-terminal helicase 1

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)
Top mentioned proteins: Iris, PALB2, CAN, Atm, Chk2
Papers on Bach1
Heme-Mediated SPI-C Induction Promotes Monocyte Differentiation into Iron-Recycling Macrophages.
Murphy et al., Saint Louis, United States. In Cell, 13 Apr 2014
Here, we report that Spic also regulated the development of F4/80(+)VCAM1(+) bone marrow macrophages (BMM) and that Spic expression in BMM and RPM development was induced by heme, a metabolite of erythrocyte degradation.
Insight into the Roles of Helicase Motif Ia by Characterizing Fanconi Anemia Group J Protein (FANCJ) Patient Mutations.
Wu et al., Canada. In J Biol Chem, 25 Mar 2014
Our genetic complementation analysis revealed that both the R251C and Q255H alleles failed to rescue cisplatin sensitivity of a FANCJ null cell line as detected by cell survival or gamma-H2AX foci formation.
Two steps forward, one step back: Determining XPD helicase mechanism by single-molecule fluorescence and high-resolution optical tweezers.
Spies, United States. In Dna Repair (amst), 20 Mar 2014
The current model of the XPD unwinding mechanism will be discussed along with possible modifications to this mechanism by the helicase interacting partners and unique features of such bio-medically important XPD-like helicases as FANCJ (BACH1), RTEL1 and CHLR1 (DDX11).
Construction of pancreatic cancer double-factor regulatory network based on chip data on the transcriptional level.
Zhuang et al., Harbin, China. In Mol Biol Rep, 28 Feb 2014
However, the effect of TFs and miRNAs in pancreatic cancer pathogenesis remains vague.
Network of mutually repressive metastasis regulators can promote cell heterogeneity and metastatic transitions.
Rosner et al., Chicago, United States. In Proc Natl Acad Sci U S A, 21 Feb 2014
Analysis of the BACH1 network reveals the existence of an inverse relationship between BACH1 and RKIP involving both monostable and bistable transitions that can potentially give rise to nongenetic variability.
Common breast cancer risk variants in the post-COGS era: a comprehensive review.
Nathanson et al., Philadelphia, United States. In Breast Cancer Res, Jan 2014
In addition, a number of mutant alleles have been identified in genes such as CHEK2, PALB2, ATM and BRIP1, which often display incomplete penetrance and confer moderate lifetime risks of breast cancer.
Breast cancer genes: beyond BRCA1 and BRCA2.
Vega et al., Spain. In Front Biosci, 2012
Moreover, a combination of family-based and population-based approaches indicated that genes involved in DNA repair, such as CHEK2, ATM, BRIP1 (FANCJ), PALB2 (FANCN) and RAD51C (FANCO), are associated with moderate BC risk.
Hereditary breast cancer: the era of new susceptibility genes.
Fostira et al., Athens, Greece. In Biomed Res Int, 2012
5%-10% of breast cancer cases are hereditary and are caused by pathogenic mutations in the considered reference BRCA1 and BRCA2 genes.
Hereditary genes and SNPs associated with breast cancer.
Nasiri et al., Mashhad, Iran. In Asian Pac J Cancer Prev, 2012
Breast cancer is the most common cancer among women affecting up to one third of tehm during their lifespans.
FANCJ/BACH1 acetylation at lysine 1249 regulates the DNA damage response.
Cantor et al., Worcester, United States. In Plos Genet, 2012
We show that acetylation at lysine 1249 is a critical regulator of FANCJ function during cellular DNA repair.
The Q motif of Fanconi anemia group J protein (FANCJ) DNA helicase regulates its dimerization, DNA binding, and DNA repair function.
Brosh et al., Baltimore, United States. In J Biol Chem, 2012
the Q motif is essential for FANCJ enzymatic activity in vitro and DNA repair function in vivo
Bach1-mediated suppression of p53 is inhibited by p19(ARF) independently of MDM2.
Igarashi et al., Sendai, Japan. In Cancer Sci, 2012
The p19(ARF)-Bach1 interaction constitutes a regulatory pathway of p53 in parallel with the p19(ARF)-MDM2 pathway.
[Molecular basis of gynecological oncology--TopBP1 protein and its participation in the transcription process].
Bryś et al., Poland. In Ginekol Pol, 2012
However currently known susceptibility genes including BRCA1, BRCA2, ATM, Chk2, PALB2, and BRIP1 explain less than 25% of familial breast and/ovarian cancers.
microRNA-155 silencing inhibits proliferation and migration and induces apoptosis by upregulating BACH1 in renal cancer cells.
Zhao et al., Changsha, China. In Mol Med Report, 2012
miR-155 may function as an oncogene by targeting BACH1
Transcription-independent role of Bach1 in mitosis through a nuclear exporter Crm1-dependent mechanism.
Igarashi et al., Sendai, Japan. In Febs Lett, 2012
Bach1 depletion resulted in disordered mitotic chromosome alignment, which was rescued by Bach1 mutants lacking the BTB or DNA binding domains, suggesting its transcription-independent mechanism.
Oxidative stress in Fanconi anaemia: from cells and molecules towards prospects in clinical management.
Degan et al., 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.
Mutations in BRIP1 confer high risk of ovarian cancer.
Stefansson et al., 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)).
Structure of the DNA repair helicase XPD.
White et al., 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.
XPD helicase structures and activities: insights into the cancer and aging phenotypes from XPD mutations.
Tainer et al., 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.
Emergence of a DNA-damage response network consisting of Fanconi anaemia and BRCA proteins.
Wang, 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.
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