BAIT
EPHB4
HTK, MYK1, TYRO11
EPH receptor B4
GO Process (7)
GO Function (3)
GO Component (2)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
NTRK1
MTC, TRK, TRK1, TRKA, Trk-A, p140-TrkA
neurotrophic tyrosine kinase, receptor, type 1
GO Process (24)
GO Function (6)
GO Component (7)
Gene Ontology Biological Process
- Ras protein signal transduction [TAS]
- activation of MAPKK activity [TAS]
- activation of adenylate cyclase activity [TAS]
- activation of phospholipase C activity [TAS]
- axonogenesis involved in innervation [ISS]
- cellular response to nerve growth factor stimulus [ISS]
- developmental programmed cell death [ISS]
- negative regulation of cell proliferation [IDA]
- negative regulation of neuron apoptotic process [ISS]
- neurotrophin TRK receptor signaling pathway [IDA, TAS]
- peptidyl-tyrosine phosphorylation [IDA]
- phosphatidylinositol-mediated signaling [TAS]
- positive regulation of ERK1 and ERK2 cascade [IDA]
- positive regulation of NF-kappaB transcription factor activity [IDA]
- positive regulation of Ras GTPase activity [IDA]
- positive regulation of Ras protein signal transduction [IDA]
- positive regulation of angiogenesis [IDA]
- positive regulation of neuron projection development [IDA]
- positive regulation of programmed cell death [ISS]
- protein autophosphorylation [IDA]
- protein phosphorylation [IDA]
- small GTPase mediated signal transduction [TAS]
- sympathetic nervous system development [ISS]
- transmembrane receptor protein tyrosine kinase signaling pathway [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
Negative Genetic
Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores.
Publication
Synergistic drug combinations for cancer identified in a CRISPR screen for pairwise genetic interactions.
Identification of effective combination therapies is critical to address the emergence of drug-resistant cancers, but direct screening of all possible drug combinations is infeasible. Here we introduce a CRISPR-based double knockout (CDKO) system that improves the efficiency of combinatorial genetic screening using an effective strategy for cloning and sequencing paired single guide RNA (sgRNA) libraries and a robust statistical scoring ... [more]
Nat. Biotechnol. Mar. 20, 2017; 0(); [Pubmed: 28319085]
Quantitative Score
- -2.702 [Confidence Score]
Throughput
- High Throughput
Ontology Terms
- phenotype: growth abnormality (HP:0001507)
Additional Notes
- CRISPR GI screen
- Cell Line:K562 (EFO:0002067)
- Experimental Setup:Timecourse
- GIST: A-phenotypic negative genetic interaction
- Library:Drug Target-CDKO CRISPRn library
- Significance Threshold: q-value<0.05
Curated By
- BioGRID