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
ACVRL1
ACVRLK1, ALK-1, ALK1, HHT, HHT2, ORW2, SKR3, TSR-I
activin A receptor type II-like 1
GO Process (37)
GO Function (11)
GO Component (2)
Gene Ontology Biological Process
- BMP signaling pathway [IMP]
- activin receptor signaling pathway [IDA]
- angiogenesis [IMP]
- artery development [ISS]
- blood circulation [IMP]
- blood vessel endothelial cell proliferation involved in sprouting angiogenesis [TAS]
- blood vessel maturation [TAS]
- blood vessel remodeling [ISS]
- cellular response to BMP stimulus [IMP]
- cellular response to transforming growth factor beta stimulus [IDA]
- endothelial tube morphogenesis [IMP]
- lymphangiogenesis [ISS]
- lymphatic endothelial cell differentiation [IMP]
- negative regulation of DNA biosynthetic process [IMP]
- negative regulation of blood vessel endothelial cell migration [IMP]
- negative regulation of cell adhesion [IMP]
- negative regulation of cell growth [IDA]
- negative regulation of cell migration [IMP]
- negative regulation of cell proliferation [IMP]
- negative regulation of endothelial cell migration [IDA]
- negative regulation of focal adhesion assembly [IMP]
- positive regulation of BMP signaling pathway [IDA]
- positive regulation of chondrocyte differentiation [TAS]
- positive regulation of pathway-restricted SMAD protein phosphorylation [IMP]
- positive regulation of transcription from RNA polymerase II promoter [IDA]
- positive regulation of transcription, DNA-templated [IDA]
- protein phosphorylation [IDA]
- regulation of DNA replication [TAS]
- regulation of blood pressure [IMP]
- regulation of blood vessel endothelial cell migration [TAS]
- regulation of endothelial cell proliferation [TAS]
- regulation of transcription, DNA-templated [IMP]
- retina vasculature development in camera-type eye [ISS]
- signal transduction [IDA]
- transforming growth factor beta receptor signaling pathway [IDA]
- venous blood vessel development [ISS]
- wound healing, spreading of epidermal cells [IMP]
Gene Ontology Molecular Function- ATP binding [IDA]
- SMAD binding [IDA]
- activin binding [IDA]
- activin receptor activity, type I [IDA, TAS]
- protein binding [IPI]
- protein kinase binding [IPI]
- protein serine/threonine kinase activity [IDA]
- transforming growth factor beta binding [IPI]
- transforming growth factor beta receptor activity, type I [IDA]
- transforming growth factor beta-activated receptor activity [IDA]
- transmembrane receptor protein serine/threonine kinase activity [NAS]
- ATP binding [IDA]
- SMAD binding [IDA]
- activin binding [IDA]
- activin receptor activity, type I [IDA, TAS]
- protein binding [IPI]
- protein kinase binding [IPI]
- protein serine/threonine kinase activity [IDA]
- transforming growth factor beta binding [IPI]
- transforming growth factor beta receptor activity, type I [IDA]
- transforming growth factor beta-activated receptor activity [IDA]
- transmembrane receptor protein serine/threonine kinase activity [NAS]
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