PRKDC
Gene Ontology Biological Process
- DNA repair [TAS]
- cellular protein modification process [TAS]
- cellular response to insulin stimulus [IMP]
- double-strand break repair [TAS]
- double-strand break repair via homologous recombination [IBA]
- double-strand break repair via nonhomologous end joining [TAS]
- innate immune response [TAS]
- negative regulation of protein phosphorylation [ISS]
- peptidyl-serine phosphorylation [IDA]
- positive regulation of transcription from RNA polymerase II promoter [IMP]
- positive regulation of type I interferon production [TAS]
- regulation of circadian rhythm [ISS]
- signal transduction involved in mitotic G1 DNA damage checkpoint [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
SFPQ
Gene Ontology Biological Process
- RNA splicing [TAS]
- alternative mRNA splicing, via spliceosome [IMP]
- histone H3 deacetylation [ISS]
- mRNA processing [TAS]
- negative regulation of circadian rhythm [ISS]
- negative regulation of transcription from RNA polymerase II promoter [IDA, IGI, IMP]
- negative regulation of transcription, DNA-templated [ISS]
- positive regulation of oxidative stress-induced intrinsic apoptotic signaling pathway [IDA]
- regulation of circadian rhythm [ISS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Affinity Capture-Western
An interaction is inferred when a bait protein is affinity captured from cell extracts by either polyclonal antibody or epitope tag and the associated interaction partner identified by Western blot with a specific polyclonal antibody or second epitope tag. This category is also used if an interacting protein is visualized directly by dye stain or radioactivity. Note that this differs from any co-purification experiment involving affinity capture in that the co-purification experiment involves at least one extra purification step to get rid of potential contaminating proteins.
Publication
IGFBP-3 interacts with NONO and SFPQ in PARP-dependent DNA damage repair in triple-negative breast cancer.
Women with triple-negative breast cancer (TNBC) are generally treated by chemotherapy but their responsiveness may be blunted by DNA double-strand break (DSB) repair. We previously reported that IGFBP-3 forms nuclear complexes with EGFR and DNA-dependent protein kinase (DNA-PKcs) to modulate DSB repair by non-homologous end-joining (NHEJ) in TNBC cells. To discover IGFBP-3 binding partners involved in chemoresistance through stimulation of ... [more]
Throughput
- Low Throughput
Curated By
- BioGRID