Associated Papers
FANCJ promotes PARP1 activity during DNA replication that is essential in BRCA1 deficient cells.
Cong K et al.
Nature Communications, 2024
MutSβ-MutLβ-FANCJ axis mediates the restart of DNA replication after fork stalling at cotranscriptional G4/R-loops.
Isik E et al.
Science Advances, 2024
FANCJ DNA helicase is recruited to the replisome by AND-1 to ensure genome stability.
Boavida A et al.
Embo Reports, 2024
Purification and biochemical characterization of the G4 resolvase and DNA helicase FANCJ.
Kulikowicz T et al.
Methods in Enzymology, 2024
Genome-scale mapping of DNA damage suppressors through phenotypic CRISPR-Cas9 screens.
Zhao Y et al.
Molecular Cell, 2023
Comprehensive Mutational Analysis of the BRCA1-Associated DNA Helicase and Tumor-Suppressor FANCJ/BACH1/BRIP1.
Calvo JA et al.
Molecular Cancer Research : Mcr, 2021
Single-molecule imaging reveals replication fork coupled formation of G-quadruplex structures hinders local replication stress signaling.
Lee WTC et al.
Nature Communications, 2021
Targeted Therapy of Papillary Thyroid Cancer: A Comprehensive Genomic Analysis.
Hescheler DA et al.
Frontiers in Endocrinology, 2021
FANCJ compensates for RAP80 deficiency and suppresses genomic instability induced by interstrand cross-links.
Awate S et al.
Nucleic Acids Research, 2020
Timeless couples G-quadruplex detection with processing by DDX11 helicase during DNA replication.
Lerner LK et al.
The Embo Journal, 2020
Cancer-associated mutations in the iron-sulfur domain of FANCJ affect G-quadruplex metabolism.
Odermatt DC et al.
Plos Genetics, 2020
FANCJ helicase promotes DNA end resection by facilitating CtIP recruitment to DNA double-strand breaks.
Nath S et al.
Plos Genetics, 2020
Rare BRIP1 Missense Alleles Confer Risk for Ovarian and Breast Cancer.
Moyer CL et al.
Cancer Research, 2020
Opposing Roles of FANCJ and HLTF Protect Forks and Restrain Replication during Stress.
Peng M et al.
Cell Reports, 2018
BRIP1 overexpression is correlated with clinical features and survival outcome of luminal breast cancer subtypes.
Gupta I et al.
Endocrine Connections, 2018
FANCJ helicase controls the balance between short- and long-tract gene conversions between sister chromatids.
Nath S et al.
Nucleic Acids Research, 2017
Mutational analysis of FANCJ helicase.
Guo M et al.
Methods (san Diego, Calif.), 2016
Crosstalk between BRCA-Fanconi anemia and mismatch repair pathways prevents MSH2-dependent aberrant DNA damage responses.
Peng M et al.
The Embo Journal, 2014
Insight into the roles of helicase motif Ia by characterizing Fanconi anemia group J protein (FANCJ) patient mutations.
Guo M et al.
The Journal of Biological Chemistry, 2014
FANCJ localization by mismatch repair is vital to maintain genomic integrity after UV irradiation.
Guillemette S et al.
Cancer Research, 2014
Germline variation in cancer-susceptibility genes in a healthy, ancestrally diverse cohort: implications for individual genome sequencing.
Bodian DL et al.
Plos One, 2014
Specialization among iron-sulfur cluster helicases to resolve G-quadruplex DNA structures that threaten genomic stability.
Bharti SK et al.
The Journal of Biological Chemistry, 2013
FANCJ couples replication past natural fork barriers with maintenance of chromatin structure.
Schwab RA et al.
The Journal of Cell Biology, 2013
The Q motif of Fanconi anemia group J protein (FANCJ) DNA helicase regulates its dimerization, DNA binding, and DNA repair function.
Wu Y et al.
The Journal of Biological Chemistry, 2012
Interaction between the helicases genetically linked to Fanconi anemia group J and Bloom's syndrome.
Suhasini AN et al.
The Embo Journal, 2011
Hereditary breast cancer and the BRCA1-associated FANCJ/BACH1/BRIP1.
Cantor SB et al.
Future Oncology (london, England), 2011
FANCJ/BRIP1 recruitment and regulation of FANCD2 in DNA damage responses.
Zhang F et al.
Chromosoma, 2010
Fanconi anemia group J mutation abolishes its DNA repair function by uncoupling DNA translocation from helicase activity or disruption of protein-DNA complexes.
Wu Y et al.
Blood, 2010
An MLH1 mutation links BACH1/FANCJ to colon cancer, signaling, and insight toward directed therapy.
Xie J et al.
Cancer Prevention Research (philadelphia, Pa.), 2010
Helicase-inactivating mutations as a basis for dominant negative phenotypes.
Wu Y et al.
Cell Cycle (georgetown, Tex.), 2010
Assessing the link between BACH1/FANCJ and MLH1 in DNA crosslink repair.
Cantor SB et al.
Environmental and Molecular Mutagenesis, 2010
Targeting the FANCJ-BRCA1 interaction promotes a switch from recombination to poleta-dependent bypass.
Xie J et al.
Oncogene, 2010
FANCM-FAAP24 and FANCJ: FA proteins that metabolize DNA.
Ali AM et al.
Mutation Research, 2009
FANCJ helicase operates in the Fanconi Anemia DNA repair pathway and the response to replicational stress.
Wu Y et al.
Current Molecular Medicine, 2009
FANCJ uses its motor ATPase to destabilize protein-DNA complexes, unwind triplexes, and inhibit RAD51 strand exchange.
Sommers JA et al.
The Journal of Biological Chemistry, 2009
FANCJ is a structure-specific DNA helicase associated with the maintenance of genomic G/C tracts.
London TB et al.
The Journal of Biological Chemistry, 2008
FANCJ helicase defective in Fanconia anemia and breast cancer unwinds G-quadruplex DNA to defend genomic stability.
Wu Y et al.
Molecular and Cellular Biology, 2008
The FANCJ/MutLalpha interaction is required for correction of the cross-link response in FA-J cells.
Peng M et al.
The Embo Journal, 2007
Inhibition of BACH1 (FANCJ) helicase by backbone discontinuity is overcome by increased motor ATPase or length of loading strand.
Gupta R et al.
Nucleic Acids Research, 2006