GRAP
Gene Ontology Biological Process
Gene Ontology Molecular Function
GRB2
Gene Ontology Biological Process
- Fc-epsilon receptor signaling pathway [TAS]
- Fc-gamma receptor signaling pathway involved in phagocytosis [TAS]
- Ras protein signal transduction [TAS]
- T cell costimulation [TAS]
- axon guidance [TAS]
- blood coagulation [TAS]
- cell-cell signaling [TAS]
- cellular response to ionizing radiation [IMP]
- epidermal growth factor receptor signaling pathway [TAS]
- fibroblast growth factor receptor signaling pathway [TAS]
- innate immune response [TAS]
- insulin receptor signaling pathway [IPI, TAS]
- leukocyte migration [TAS]
- negative regulation of epidermal growth factor receptor signaling pathway [TAS]
- neurotrophin TRK receptor signaling pathway [TAS]
- phosphatidylinositol-mediated signaling [TAS]
- platelet activation [TAS]
- positive regulation of reactive oxygen species metabolic process [IMP]
- receptor internalization [IMP]
- signal transduction in response to DNA damage [IMP]
Gene Ontology Molecular Function- SH3 domain binding [IDA]
- SH3/SH2 adaptor activity [TAS]
- ephrin receptor binding [IPI]
- epidermal growth factor receptor binding [IPI]
- identical protein binding [IPI]
- insulin receptor substrate binding [IPI]
- neurotrophin TRKA receptor binding [IPI]
- poly(A) RNA binding [IDA]
- protein binding [IPI]
- protein kinase binding [IPI]
- SH3 domain binding [IDA]
- SH3/SH2 adaptor activity [TAS]
- ephrin receptor binding [IPI]
- epidermal growth factor receptor binding [IPI]
- identical protein binding [IPI]
- insulin receptor substrate binding [IPI]
- neurotrophin TRKA receptor binding [IPI]
- poly(A) RNA binding [IDA]
- protein binding [IPI]
- protein kinase binding [IPI]
Gene Ontology Cellular Component
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
Paralog knockout profiling identifies DUSP4 and DUSP6 as a digenic dependence in MAPK pathway-driven cancers.
Although single-gene perturbation screens have revealed a number of new targets, vulnerabilities specific to frequently altered drivers have not been uncovered. An important question is whether the compensatory relationship between functionally redundant genes masks potential therapeutic targets in single-gene perturbation studies. To identify digenic dependencies, we developed a CRISPR paralog targeting library to investigate the viability effects of disrupting 3,284 ... [more]
Quantitative Score
- 0.000195053 [Confidence Score]
Throughput
- High Throughput
Additional Notes
- CRISPR GI screen
- Cell Line: PATU8988S_PANCREAS score (0.0001950530276662)
- Experimental Setup: Timecourse-Synthetic Lethality
- GIST: A-phenotypic negative genetic interaction
- Library: Digenic Paralog CRISPR library
- Significance Threshold: GEMINI FDR < 0.05
Curated By
- BioGRID