BAIT
KRAS
C-K-RAS, CFC2, K-RAS2A, K-RAS2B, K-RAS4A, K-RAS4B, KI-RAS, KRAS1, KRAS2, NS, NS3, RASK2
Kirsten rat sarcoma viral oncogene homolog
GO Process (16)
GO Function (2)
GO Component (5)
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
Homo sapiens
PREY
PPP1CC
PP-1G, PP1C, PPP1G
protein phosphatase 1, catalytic subunit, gamma isozyme
GO Process (9)
GO Function (6)
GO Component (9)
Gene Ontology Biological Process
- circadian regulation of gene expression [ISS]
- entrainment of circadian clock by photoperiod [ISS]
- mitotic cell cycle [TAS]
- negative regulation of transforming growth factor beta receptor signaling pathway [TAS]
- protein dephosphorylation [IMP, ISS]
- regulation of circadian rhythm [IMP]
- small molecule metabolic process [TAS]
- transforming growth factor beta receptor signaling pathway [TAS]
- triglyceride catabolic process [TAS]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
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.
Publication
A Role for Mitochondrial Translation in Promotion of Viability in K-Ras Mutant Cells.
Activating mutations in the KRAS oncogene are highly prevalent in tumors, especially those of the colon, lung, and pancreas. To better understand the genetic dependencies that K-Ras mutant cells rely upon for their growth, we employed whole-genome CRISPR loss-of-function screens in two isogenic pairs of cell lines. Since loss of essential genes is uniformly toxic in CRISPR-based screens, we also ... [more]
Cell Rep Jul. 11, 2017; 20(2);427-438 [Pubmed: 28700943]
Throughput
- High Throughput
Additional Notes
- CRISPR screen analysis showed synthetic lethality with K-Ras mutant in DLD1 cells.
- Gene loss results in the selective reduction of K-Ras mutant cell growth.
- Synthetic lethality score > 1.0.
Curated By
- BioGRID