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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 09 Dec 2014.

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
Biallelic Mutations in BRCA1 Cause a New Fanconi Anemia Subtype.
New
Moilanen et al., Oulu, Finland. In Cancer Discov, 03 Jan 2015
Bona fide FA proteins, BRCA2 (FANCD1), PALB2 (FANCN), and BRIP1 (FANCJ) interact with BRCA1 during ICL repair.
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 Jan 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%).
Let-7c overexpression inhibits dengue virus replication in human hepatoma Huh-7 cells.
New
Yocupicio-Monroy et al., Mexico. In Virus Res, 20 Dec 2014
In accordance with this finding, HO-1, the main responsive factor of BACH1 was found up-regulated.
[Current Clinical Issues and Recent Trends in Hereditary Breast and Ovarian Cancer in Japan-Genetic Testing for HBOC and Risk-Reducing Surgery].
New
Takeshima et al., In Gan To Kagaku Ryoho, 30 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.
Cyclin B3 and dynein heavy chain cooperate to increase fitness in the absence of mdf-1/MAD1 in Caenorhabditis elegans.
New
Chen et al., Canada. In Cell Cycle, Nov 2014
Previously, in a dog-1(gk10)/FANCJ mutator background, we isolated a suppressor of mdf-1(gk2) sterility (such-4) which allowed indefinite propagation in the absence of MDF-1.
BRCA1 and FancJ cooperatively promote interstrand crosslinker induced centrosome amplification through the activation of polo-like kinase 1.
New
Zhang et al., United States. In Cell Cycle, Oct 2014
FancJ is a key component of the BRCA1 B-complex.
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.
Etiology of familial breast cancer with undetected BRCA1 and BRCA2 mutations: clinical implications.
Review
New
Yiannakopoulou, Athens, Greece. In Cell Oncol (dordr), Feb 2014
RESULTS: After excluding BRCA1 and BRCA2 mutations, factors proposed to contribute to familial breast cancer include: chance clustering of apparently sporadic cases, shared lifestyle, monogenic inheritance, i.e., dominant gene mutations associated with a high risk (TP53, PTEN, STK11), dominant gene mutations associated with a relatively low risk (ATM, BRIP1, RLB2), recessive gene mutations associated with horizontal inheritance patterns (sister-sister), and polygenic inheritance where susceptibility to familial breast cancer is thought to be conferred by a large number of low risk alleles.
Molecular and cellular functions of the FANCJ DNA helicase defective in cancer and in Fanconi anemia.
Review
New
Cantor et al., Baltimore, United States. In Front Genet, Dec 2013
FANCJ also operates in the FA pathway of interstrand cross-link repair and contributes to homologous recombination.
Hereditary genes and SNPs associated with breast cancer.
Review
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.
Breast cancer genes: beyond BRCA1 and BRCA2.
Review
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.
Review
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.
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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