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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
Candidate gene analysis of BRCA1/2 mutation-negative high-risk Russian breast cancer patients.
New
Imyanitov et al., Saint Petersburg, Russia. In Cancer Lett, 10 May 2015
None of the studied cases carried germ-line defects in recently discovered hereditary BC genes, BRIP1, FANCC, MRE11A and RAD51C.
Structure and evolution of the eukaryotic FANCJ-like proteins.
New
Xuguang et al., Taiwan. In Yi Chuan, 20 Mar 2015
The FANCJ-like protein family is a class of ATP-dependent helicases that can catalytically unwind duplex DNA along the 5'-3' direction.
Aberrant recombination and repair during immunoglobulin class switching in BRCA1-deficient human B cells.
New
Pan-Hammarström et al., Stockholm, Sweden. In Proc Natl Acad Sci U S A, 17 Mar 2015
Furthermore, increased use of long microhomologies was found at recombination junctions derived from E3 ubiquitin-protein ligase RNF168-deficient, Fanconi anemia group J protein (FACJ, BRIP1)-deficient, or DNA endonuclease RBBP8 (CtIP)-compromised cells, whereas an increased frequency of S-region inversions was observed in breast cancer type 2 susceptibility protein (BRCA2)-deficient cells.
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, 01 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%).
FANCD2, FANCJ and BRCA2 cooperate to promote replication fork recovery independently of the Fanconi Anemia core complex.
New
Sobeck et al., Minneapolis, United States. In Cell Cycle, 28 Feb 2015
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.
Hereditary Predisposition to Ovarian Cancer, Looking Beyond BRCA1/BRCA2.
New
Monk et al., Aliso Viejo, United States. In Gynecol Oncol, 23 Feb 2015
With the advent of next generation sequencing, hereditary panel testing provides an efficient method for evaluating multiple genes simultaneously.
Genetics of Breast Cancer: A Topic in Evolution.
Review
New
Korde et al., Seattle, United States. In Ann Oncol, 20 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.
[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.
Growing recognition of the role for rare missense substitutions in breast cancer susceptibility.
Review
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.
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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