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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
Note of clarification of data in the paper entitled association between BRIP1 (BACH1) polymorphisms and breast cancer risk.
Wang et al., Zhengzhou, China. In Breast Cancer Res Treat, 18 Apr 2015
UNASSIGNED: With great interest, we read the recent article entitled "Association between BRIP1 (BACH1) polymorphisms and breast cancer risk: a meta-analysis" published online in Pabalan et al. (Breast Cancer Res Treat 137:553-558, 2013).
Evolutionary patterns of DNA base composition and correlation to polymorphisms in DNA repair systems.
Yu et al., Ames, United States. In Nucleic Acids Res, 12 Apr 2015
However, the evolutionary pattern of base composition and its potential causes have not been well understood.
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%).
[Structure and evolution of the eukaryotic FANCJ-like proteins].
Xuguang et al., Taiwan. In Yi Chuan, Feb 2015
The FANCJ-like protein family is a class of ATP-dependent helicases that can catalytically unwind duplex DNA along the 5'-3' direction.
Genetics of Breast Cancer: A Topic in Evolution.
Korde et al., Seattle, United States. In Ann Oncol, Feb 2015
An additional 2-3% of cases are due to a mutation in a rare, moderate-penetrance gene (e.g., CHEK2, BRIP1, ATM, and PALB2), each associated with a two-fold increase in risk.
FANCD2, FANCJ and BRCA2 cooperate to promote replication fork recovery independently of the Fanconi Anemia core complex.
Sobeck et al., Minneapolis, United States. In Cell Cycle, Dec 2014
In contrast, the downstream FA pathway members FANCJ and BRCA2 share FANCD2's role in replication fork restart and the suppression of new origin firing.
The spectrum of genetic mutations in breast cancer.
Al Tamimi et al., Karāchi, Pakistan. In Asian Pac J Cancer Prev, Dec 2014
However, the great majority of breast cancer cases are not related to a mutated gene of high penetrance, but to genes of low penetrance such as CHEK2, CDH1, NBS1, RAD50, BRIP1 and PALB2, which are frequently mutated in the general population.
[Current clinical issues and recent trends in hereditary breast and ovarian cancer in Japan-genetic testing for HBOC and risk-reducing surgery].
Takeshima et al., In Gan To Kagaku Ryoho, Nov 2014
The recognition of hereditary breast and ovarian cancer (HBOC) is gradually spreading in Japan after a famous American actress made it public that she underwent risk-reducing mastectomy (RRM) based on mutation of BRCA1.
Heme-mediated SPI-C induction promotes monocyte differentiation into iron-recycling macrophages.
Murphy et al., Saint Louis, United States. In Cell, 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.
Genetic and epigenetic control of RKIP transcription.
Yeung et al., Kuwait, Kuwait. In Crit Rev Oncog, 2013
We also review the genetic and epigenetic modulation of RKIP transcription through EZH2, a component of the polycomb repressive complex 2 (PRC2) and sequence specific transcription factors (TFs) BACH1 and Snail.
Molecular and cellular functions of the FANCJ DNA helicase defective in cancer and in Fanconi anemia.
Cantor et al., Baltimore, United States. In Front Genet, 2013
FANCJ also operates in the FA pathway of interstrand cross-link repair and contributes to homologous recombination.
Growing recognition of the role for rare missense substitutions in breast cancer susceptibility.
Chenevix-Trench et al., Salt Lake City, United States. In Biomark Med, 2013
Among genes that have been extensively evaluated, BRCA1, BRCA2, PALB2 and BRIP1 stand as examples where the majority of mutations lead to protein truncation;TP53 provides a counter example, where the majority of pathogenic variants are missense substitutions.
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.
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.
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)).
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.
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.
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