RPS6KA1
Gene Ontology Biological Process
- MyD88-dependent toll-like receptor signaling pathway [TAS]
- MyD88-independent toll-like receptor signaling pathway [TAS]
- TRIF-dependent toll-like receptor signaling pathway [TAS]
- axon guidance [TAS]
- innate immune response [TAS]
- negative regulation of apoptotic process [IMP]
- negative regulation of cysteine-type endopeptidase activity involved in apoptotic process [IDA]
- neurotrophin TRK receptor signaling pathway [TAS]
- positive regulation of cell differentiation [TAS]
- positive regulation of cell growth [TAS]
- positive regulation of hepatic stellate cell activation [IMP]
- positive regulation of transcription from RNA polymerase II promoter [IMP]
- regulation of DNA-templated transcription in response to stress [TAS]
- regulation of translation in response to stress [TAS]
- signal transduction [TAS]
- stress-activated MAPK cascade [TAS]
- synaptic transmission [TAS]
- toll-like receptor 10 signaling pathway [TAS]
- toll-like receptor 2 signaling pathway [TAS]
- toll-like receptor 3 signaling pathway [TAS]
- toll-like receptor 4 signaling pathway [TAS]
- toll-like receptor 5 signaling pathway [TAS]
- toll-like receptor 9 signaling pathway [TAS]
- toll-like receptor TLR1:TLR2 signaling pathway [TAS]
- toll-like receptor TLR6:TLR2 signaling pathway [TAS]
- toll-like receptor signaling pathway [TAS]
Gene Ontology Molecular Function
SGK2
Gene Ontology Biological Process
Gene Ontology Molecular Function
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
- 0.004686365 [Confidence Score]
Throughput
- High Throughput
Additional Notes
- CRISPR GI screen
- Cell Line: PK1_PANCREAS score (0.0005851086427053)
- Cell Line: HSC5_SKIN score (0.0046863649027028)
- Cell Line: IPC298_SKIN score (0.0151335628389681)
- Cell Line: MEL202_UVEA score (0.0412845136843711)
- 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