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
PIN1
DOD, UBL5
peptidylprolyl cis/trans isomerase, NIMA-interacting 1
GO Process (13)
GO Function (6)
GO Component (3)
Gene Ontology Biological Process
- cytokine-mediated signaling pathway [TAS]
- innate immune response [TAS]
- negative regulation of ERK1 and ERK2 cascade [IDA]
- negative regulation of cell motility [IDA]
- negative regulation of transforming growth factor beta receptor signaling pathway [IDA]
- negative regulation of type I interferon production [TAS]
- positive regulation of Rho GTPase activity [IMP]
- positive regulation of protein phosphorylation [IGI]
- positive regulation of ubiquitin-protein transferase activity [IDA]
- protein peptidyl-prolyl isomerization [IDA]
- regulation of cytokinesis [IGI, IMP]
- regulation of mitosis [TAS]
- regulation of pathway-restricted SMAD protein phosphorylation [IDA]
Gene Ontology Molecular Function
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 genome-wide RNAi screen identifies multiple synthetic lethal interactions with the Ras oncogene.
Oncogenic mutations in the small GTPase Ras are highly prevalent in cancer, but an understanding of the vulnerabilities of these cancers is lacking. We undertook a genome-wide RNAi screen to identify synthetic lethal interactions with the KRAS oncogene. We discovered a diverse set of proteins whose depletion selectively impaired the viability of Ras mutant cells. Among these we observed a ... [more]
Cell May. 29, 2009; 137(5);835-48 [Pubmed: 19490893]
Throughput
- High Throughput
Ontology Terms
- phenotype: growth abnormality (HP:0001507)
Additional Notes
- RNAi screen
Curated By
- BioGRID