Gene Ontology annotation through association of InterPro records with GO terms
Gene Ontology annotation based on Enzyme Commission mapping
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic Gene Ontology annotation based on Rhea mapping
Electronic Gene Ontology annotations created by ARBA machine learning models
BACH1, a novel helicase-like protein, interacts directly with BRCA1 and contributes to its DNA repair function.
Cadmium induces nuclear export of Bach1, a transcriptional repressor of heme oxygenase-1 gene.
The BRCT domain is a phospho-protein binding domain.
The BRCA1-associated protein BACH1 is a DNA helicase targeted by clinically relevant inactivating mutations.
Structure of the BRCT repeats of BRCA1 bound to a BACH1 phosphopeptide: implications for signaling.
Structure and mechanism of BRCA1 BRCT domain recognition of phosphorylated BACH1 with implications for cancer.
Analysis of the DNA substrate specificity of the human BACH1 helicase associated with breast cancer.
Multifactorial contributions to an acute DNA damage response by BRCA1/BARD1-containing complexes.
Abraxas and RAP80 form a BRCA1 protein complex required for the DNA damage response.
The FANCJ/MutLalpha interaction is required for correction of the cross-link response in FA-J cells.
FANCJ (BACH1) helicase forms DNA damage inducible foci with replication protein A and interacts physically and functionally with the single-stranded DNA-binding protein.
Pathogenicity of the BRCA1 missense variant M1775K is determined by the disruption of the BRCT phosphopeptide-binding pocket: a multi-modal approach.
FANCJ helicase defective in Fanconia anemia and breast cancer unwinds G-quadruplex DNA to defend genomic stability.
PALB2 is an integral component of the BRCA complex required for homologous recombination repair.
Fanconi anemia group J mutation abolishes its DNA repair function by uncoupling DNA translocation from helicase activity or disruption of protein-DNA complexes.
Interaction between the helicases genetically linked to Fanconi anemia group J and Bloom's syndrome.
BRCA1 tumor suppressor network: focusing on its tail.
FANCJ/BACH1 acetylation at lysine 1249 regulates the DNA damage response.
IOP1 protein is an external component of the human cytosolic iron-sulfur cluster assembly (CIA) machinery and functions in the MMS19 protein-dependent CIA pathway.
A massively parallel pipeline to clone DNA variants and examine molecular phenotypes of human disease mutations.
FancJ (Brip1) loss-of-function allele results in spermatogonial cell depletion during embryogenesis and altered processing of crossover sites during meiotic prophase I in mice.
DNA Repair Network Analysis Reveals Shieldin as a Key Regulator of NHEJ and PARP Inhibitor Sensitivity.
A reference map of the human binary protein interactome.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
A protein interaction landscape of breast cancer.
The FANCJ helicase unfolds DNA-protein crosslinks to promote their repair.
Multimodal cell maps as a foundation for structural and functional genomics.
Binding of ATR:ATRIP to RPA at resected DNA DSBs
CHEK1 is recruited to resected DNA DSBs
Activation of CHEK1 at resected DNA DSBs
ATR activation at DNA DSBs
BCDX2 complex stabilizes RAD51 filament
CX3 complex binds D-loop structures
EXO1 or DNA2 in complex with BLM or WRN binds initially resected DNA DSBs along with BRIP1 recruitment
Long-range resection of DNA DSBs by EXO1 or DNA2
BLM mediates dissolution of double Holliday junction
MUS81:EME1,EME2 cleaves D-loop
Resolution of D-loops cleaved by MUS81:EME1 or MUS81:EME2
Resolution of Holliday junctions cleaved by GEN1 or SLX1A:SLX4:MUS81:EME1,(MUS81:EME2)
RAD52 promotes single strand annealing at resected DNA DSBs
ERCC1:XPF cleaves flaps generated by SSA
Ligation of DNA and formation of Holliday structures following repair synthesis
Association of RPA complexes with ssDNA at resected DNA DSBs
RAD51 binds BRCA2 at resected DNA DSBs
Association of RAD51 with RAD52:DNA double-strand break ends
Association of RAD52 with the RPA complex at resected DNA DSBs
Cleavage of Holliday junctions by GEN1 or SLX1A:SLX4:MUS81:EME1,(MUS81:EME2)
D-loop dissociation and strand annealing
D-loop extension by DNA polymerases
D-loop formation mediated by PALB2, BRCA2 and RAD51
Defective D-loop formation mediated by PALB2, BRCA2 and RAD51 due to loss-of-function of BRCA1 in PALB2 binding
Defective D-loop formation mediated by PALB2, BRCA2 and RAD51 due to loss-of-function of PALB2 in BRCA1 binding
Defective D-loop formation mediated by PALB2, BRCA2 and RAD51 due to loss-of-function of PALB2 in binding to BRCA2/RAD51/RAD51C
BRCA2 mutants with BRC defects or a defect in the C-terminal RAD51 binding site do not bind RAD51
Defective recruitment of BRCA2 and RAD51 due to loss of BRCA2 function in PALB2 binding
ERCC1:XPF binds DNA DSBs with annealed 3' ssDNA overhangs and displaced flaps generated by SSA