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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)
Top mentioned proteins: Iris, PALB2, CAN, Atm, Chk2
Papers on Bach1
Germline Mutations in the BRIP1, BARD1, PALB2, and NBN Genes in Women With Ovarian Cancer.
New
Gayther et al., Los Angeles, United States. In J Natl Cancer Inst, 30 Nov 2015
METHODS: Next generation sequencing was used to identify germline mutations in the coding regions of four candidate susceptibility genes-BRIP1, BARD1, PALB2 and NBN-in 3236 invasive EOC case patients and 3431 control patients of European origin, and in 2000 unaffected high-risk women from a clinical screening trial of ovarian cancer (UKFOCSS).
Protein-truncating variants in moderate-risk breast cancer susceptibility genes: A meta-analysis of high-risk case-control screening studies.
New
Geraghty et al., Dublin, Ireland. In Cancer Genet, 30 Sep 2015
An electronic search was conducted to identify studies that sequenced the full coding regions of ATM, CHEK2, BRIP1, PALB2, NBS1, and RAD50 in a general and gene-targeted approach.
Fanconi anemia: a model disease for studies on human genetics and advanced therapeutics.
New
Surrallés et al., Spain. In Curr Opin Genet Dev, 06 Sep 2015
We review the recent discovery of FA genes and efforts to develop genetic therapies for FA in the last five years.
hMSH5 Facilitates the Repair of Camptothecin-induced Double-strand Breaks through an Interaction with FANCJ.
New
Her et al., Pullman, United States. In J Biol Chem, 24 Aug 2015
Furthermore, the hMSH5-FANCJ chromatin recruitment underlies the effects of hMSH5 on homologous recombination and Chk1 activation.
Genetics of breast cancer: a topic in evolution.
Review
New
Korde et al., Seattle, United States. In Ann Oncol, Jul 2015
However, in patients with a suggestive personal and/or family history, a specific predisposing gene is identified in <30% of cases.
Inherited mutations in 17 breast cancer susceptibility genes among a large triple-negative breast cancer cohort unselected for family history of breast cancer.
New
Impact
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%).
Hereditary ovarian cancer: not only BRCA 1 and 2 genes.
Review
New
Cortesi et al., Modena, Italy. In Biomed Res Int, Dec 2014
More than one-fifth of ovarian tumors have hereditary susceptibility and, in about 65-85% of these cases, the genetic abnormality is a germline mutation in BRCA genes.
Serine/arginine-rich splicing factor 3 (SRSF3) regulates homologous recombination-mediated DNA repair.
New
Zhang et al., Rockford, United States. In Mol Cancer, Dec 2014
We demonstrated that the downregulation of BRCA1, BRIP1 and RAD51 expression was caused by decreased transcription and not due to increased nonsense-mediated mRNA decay.
[Current clinical issues and recent trends in hereditary breast and ovarian cancer in Japan-genetic testing for HBOC and risk-reducing surgery].
Review
New
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.
New
Impact
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.
Review
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.
Review
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.
FANCJ/BACH1 acetylation at lysine 1249 regulates the DNA damage response.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
Impact
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.
Impact
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.
Impact
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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