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
RPTOR
Gene Ontology Biological Process
- TOR signaling [IDA]
- cell cycle arrest [TAS]
- cell growth [IMP]
- cellular response to amino acid stimulus [IMP]
- cellular response to nutrient levels [IMP]
- insulin receptor signaling pathway [TAS]
- positive regulation of TOR signaling [IDA]
- positive regulation of protein serine/threonine kinase activity [IDA]
- positive regulation of transcription from RNA polymerase III promoter [IMP]
- regulation of cell size [IMP]
Gene Ontology Molecular Function- 14-3-3 protein binding [IDA]
- RNA polymerase III type 1 promoter DNA binding [IDA]
- RNA polymerase III type 2 promoter DNA binding [IDA]
- RNA polymerase III type 3 promoter DNA binding [IDA]
- TFIIIC-class transcription factor binding [IDA]
- protein binding [IPI]
- protein complex binding [IPI]
- protein kinase binding [IPI]
- 14-3-3 protein binding [IDA]
- RNA polymerase III type 1 promoter DNA binding [IDA]
- RNA polymerase III type 2 promoter DNA binding [IDA]
- RNA polymerase III type 3 promoter DNA binding [IDA]
- TFIIIC-class transcription factor binding [IDA]
- protein binding [IPI]
- protein complex 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
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
- 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 RPTOR | Synthetic Lethality Synthetic Lethality A genetic interaction is inferred when mutations or deletions in separate genes, each of which alone causes a minimal phenotype, result in lethality when combined in the same cell under a given condition. | High | - | BioGRID | 2619668 |
Curated By
- BioGRID