KRAS
Gene Ontology Biological Process
- Fc-epsilon receptor signaling pathway [TAS]
- MAPK cascade [TAS]
- Ras protein signal transduction [TAS]
- activation of MAPKK activity [TAS]
- axon guidance [TAS]
- blood coagulation [TAS]
- epidermal growth factor receptor signaling pathway [TAS]
- fibroblast growth factor receptor signaling pathway [TAS]
- innate immune response [TAS]
- insulin receptor signaling pathway [TAS]
- leukocyte migration [TAS]
- neurotrophin TRK receptor signaling pathway [TAS]
- positive regulation of cell proliferation [IMP]
- positive regulation of gene expression [IMP]
- positive regulation of protein phosphorylation [IMP]
- small GTPase mediated signal transduction [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
SFPQ
Gene Ontology Biological Process
- RNA splicing [TAS]
- alternative mRNA splicing, via spliceosome [IMP]
- histone H3 deacetylation [ISS]
- mRNA processing [TAS]
- negative regulation of circadian rhythm [ISS]
- negative regulation of transcription from RNA polymerase II promoter [IDA, IGI, IMP]
- negative regulation of transcription, DNA-templated [ISS]
- positive regulation of oxidative stress-induced intrinsic apoptotic signaling pathway [IDA]
- regulation of circadian rhythm [ISS]
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
Integrative oncogene-dependency mapping identifies RIT1 vulnerabilities and synergies in lung cancer.
CRISPR-based cancer dependency maps are accelerating advances in cancer precision medicine, but adequate functional maps are limited to the most common oncogenes. To identify opportunities for therapeutic intervention in other rarer subsets of cancer, we investigate the oncogene-specific dependencies conferred by the lung cancer oncogene, RIT1. Here, genome-wide CRISPR screening in KRAS, EGFR, and RIT1-mutant isogenic lung cancer cells identifies ... [more]
Throughput
- High Throughput
Ontology Terms
- phenotype: growth abnormality (HP:0001507) [viability (PATO:0000169)]
Additional Notes
- CRISPR GI screen
- Cell Line: PC9-Cas9-KRASG12V
- Experimental Setup: Negative selection in the presence of 40 nM erlotinib
- GIST: A-phenotypic negative genetic interaction
- Library: Brunello Library
- Significance Threshold:
- CS
- >0.5 and p<0.05
Related interactions
| Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
|---|---|---|---|---|---|---|
| KRAS SFPQ | Synthetic Growth Defect Synthetic Growth Defect A genetic interaction is inferred when mutations in separate genes, each of which alone causes a minimal phenotype, result in a significant growth defect under a given condition when combined in the same cell. | High | - | BioGRID | 1278539 |
Curated By
- BioGRID