PRKAR1A
Gene Ontology Biological Process
- activation of phospholipase C activity [TAS]
- activation of protein kinase A activity [TAS]
- blood coagulation [TAS]
- cellular response to glucagon stimulus [TAS]
- energy reserve metabolic process [TAS]
- epidermal growth factor receptor signaling pathway [TAS]
- fibroblast growth factor receptor signaling pathway [TAS]
- innate immune response [TAS]
- intracellular signal transduction [TAS]
- negative regulation of cAMP-dependent protein kinase activity [IDA]
- neurotrophin TRK receptor signaling pathway [TAS]
- regulation of insulin secretion [TAS]
- regulation of transcription from RNA polymerase II promoter [TAS]
- signal transduction [TAS]
- small molecule metabolic process [TAS]
- transmembrane transport [TAS]
- water transport [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
PRKAR2A
Gene Ontology Biological Process
- activation of phospholipase C activity [TAS]
- activation of protein kinase A activity [TAS]
- blood coagulation [TAS]
- cellular response to glucagon stimulus [TAS]
- energy reserve metabolic process [TAS]
- epidermal growth factor receptor signaling pathway [TAS]
- fibroblast growth factor receptor signaling pathway [TAS]
- innate immune response [TAS]
- intracellular signal transduction [TAS]
- negative regulation of cAMP-dependent protein kinase activity [IDA]
- neurotrophin TRK receptor signaling pathway [TAS]
- regulation of insulin secretion [TAS]
- signal transduction [TAS]
- small molecule metabolic process [TAS]
- transmembrane transport [TAS]
- water transport [TAS]
Gene Ontology Molecular Function
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
- 0.02066018 [Confidence Score]
Throughput
- High Throughput
Additional Notes
- CRISPR GI screen
- Cell Line: HS936T_SKIN score (0.0206601799984393)
- 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