BAIT
BRD4
CAP, HUNK1, HUNKI, MCAP
bromodomain containing 4
GO Process (10)
GO Function (4)
GO Component (5)
Gene Ontology Biological Process
- cellular response to DNA damage stimulus [IMP]
- chromatin remodeling [IDA]
- negative regulation of DNA damage checkpoint [IMP]
- positive regulation of G2/M transition of mitotic cell cycle [IMP]
- positive regulation of I-kappaB kinase/NF-kappaB signaling [IDA]
- positive regulation of transcription elongation from RNA polymerase II promoter [IDA, IMP]
- positive regulation of transcription from RNA polymerase II promoter [IDA]
- regulation of inflammatory response [IDA]
- regulation of phosphorylation of RNA polymerase II C-terminal domain [IDA]
- regulation of transcription involved in G1/S transition of mitotic cell cycle [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
CRK
CRKII, p38
v-crk avian sarcoma virus CT10 oncogene homolog
GO Process (11)
GO Function (3)
GO Component (4)
Gene Ontology Biological Process
- Fc-gamma receptor signaling pathway involved in phagocytosis [TAS]
- activation of MAPKK activity [TAS]
- blood coagulation [TAS]
- ephrin receptor signaling pathway [IDA]
- innate immune response [TAS]
- insulin receptor signaling pathway [TAS]
- neurotrophin TRK receptor signaling pathway [TAS]
- platelet activation [TAS]
- regulation of Rho GTPase activity [IDA]
- regulation of actin cytoskeleton organization [IDA]
- regulation of transcription from RNA polymerase II promoter [TAS]
Gene Ontology Molecular Function
Homo sapiens
Affinity Capture-MS
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 is identified by mass spectrometric methods.
Publication
Synthetic Lethal and Resistance Interactions with BET Bromodomain Inhibitors in Triple-Negative Breast Cancer.
BET bromodomain inhibitors (BBDIs) are candidate therapeutic agents for triple-negative breast cancer (TNBC) and other cancer types, but inherent and acquired resistance to BBDIs limits their potential clinical use. Using CRISPR and small-molecule inhibitor screens combined with comprehensive molecular profiling of BBDI response and resistance, we identified synthetic lethal interactions with BBDIs and genes that, when deleted, confer resistance. We ... [more]
Mol Cell Dec. 18, 2019; 78(6);1096-1113.e8 [Pubmed: 32416067]
Throughput
- High Throughput
Curated By
- BioGRID