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
ATR
FCTCS, FRP1, MEC1, SCKL, SCKL1
ATR serine/threonine kinase
GO Process (14)
GO Function (6)
GO Component (4)
Gene Ontology Biological Process
- DNA damage checkpoint [IDA]
- DNA repair [TAS]
- DNA replication [TAS]
- cell cycle [TAS]
- cellular response to DNA damage stimulus [TAS]
- cellular response to UV [IMP]
- cellular response to gamma radiation [IDA]
- double-strand break repair via homologous recombination [IBA]
- multicellular organismal development [TAS]
- negative regulation of DNA replication [IMP]
- peptidyl-serine phosphorylation [IDA]
- positive regulation of DNA damage response, signal transduction by p53 class mediator [IMP]
- protein autophosphorylation [IDA]
- replicative senescence [IMP]
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 HCT116 cells.
- Gene loss results in the selective reduction of K-Ras mutant cell growth.
- Synthetic lethality score > 1.0.
Curated By
- BioGRID