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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, Chk2, Atm
Papers on Bach1
Genetics of breast cancer: a topic in evolution.
Review
New
Korde et al., Seattle, United States. In Ann Oncol, 31 Jul 2015
However, in patients with a suggestive personal and/or family history, a specific predisposing gene is identified in <30% of cases.
hMSH5 facilitates the repair of camptothecin-induced double-strand breaks through an interaction with FANCJ.
New
Her et al., Washington, D.C., United States. In J Biol Chem, 08 Jul 2015
Furthermore, hMSH5 mediates chromatin recruitment of FANCJ, which underlies the effects of hMSH5 on HR and Chk1 activation.
Note of clarification of data in the paper entitled association between BRIP1 (BACH1) polymorphisms and breast cancer risk.
New
Wang et al., Zhengzhou, China. In Breast Cancer Res Treat, Apr 2015
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).
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%).
The spectrum of genetic mutations in breast cancer.
New
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.
Hereditary Ovarian Cancer: Not Only BRCA 1 and 2 Genes.
Review
New
Cortesi et al., Modena, Italy. In Biomed Res Int, Dec 2014
UNASSIGNED: 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.
Kaposi Sarcoma Herpesvirus Induces HO-1 during De Novo Infection of Endothelial Cells via Viral miRNA-Dependent and -Independent Mechanisms.
New
Moses et al., Beaverton, United States. In Mbio, Dec 2014
In fact, in KSHV-infected LEC, the BACH1 message level is reduced, BACH1 subcellular localization is altered, and miR-K12-11 mediates the inverse regulation of HO-1 and BACH1 during viral latency.
Spectrum of variations in dog-1/FANCJ and mdf-1/MAD1 defective Caenorhabditis elegans strains after long-term propagation.
New
Chen et al., Canada. In Bmc Genomics, Dec 2014
In Caenorhabditis elegans, faithful transmission of G-rich DNA is ensured by the DOG-1/FANCJ deadbox helicase.
[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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