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
CYP11B1
CPN1, CYP11B, FHI, P450C11
cytochrome P450, family 11, subfamily B, polypeptide 1
GO Process (14)
GO Function (2)
GO Component (2)
Gene Ontology Biological Process
- C21-steroid hormone biosynthetic process [IDA]
- aldosterone biosynthetic process [IDA, IMP]
- cellular response to hormone stimulus [IEP]
- cellular response to potassium ion [IEP]
- cortisol biosynthetic process [IDA, IMP]
- glucocorticoid biosynthetic process [TAS]
- glucose homeostasis [TAS]
- immune response [TAS]
- mineralocorticoid biosynthetic process [TAS]
- regulation of blood pressure [IMP]
- small molecule metabolic process [TAS]
- steroid metabolic process [TAS]
- sterol metabolic process [TAS]
- xenobiotic metabolic 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 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