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
WRN
RECQ3, RECQL2, RECQL3
Werner syndrome, RecQ helicase-like
GO Process (21)
GO Function (17)
GO Component (4)
Gene Ontology Biological Process
- ATP catabolic process [IDA]
- DNA duplex unwinding [IDA, IMP]
- DNA metabolic process [IDA]
- DNA replication [IMP]
- DNA synthesis involved in DNA repair [IDA]
- aging [NAS]
- base-excision repair [IDA]
- cell aging [IMP]
- cellular response to DNA damage stimulus [IDA]
- cellular response to gamma radiation [IDA]
- cellular response to starvation [IDA]
- double-strand break repair [IMP]
- multicellular organismal aging [IMP]
- nucleic acid phosphodiester bond hydrolysis [IDA]
- nucleolus to nucleoplasm transport [IDA]
- positive regulation of hydrolase activity [IDA]
- regulation of apoptotic process [IGI]
- replication fork processing [IDA, IMP]
- response to UV-C [IDA]
- response to oxidative stress [IDA]
- telomere maintenance [IMP]
Gene Ontology Molecular Function- 3'-5' DNA helicase activity [IDA]
- 3'-5' exonuclease activity [IDA]
- ATP-dependent DNA helicase activity [IDA]
- ATPase activity [IDA]
- DNA binding [IDA]
- DNA helicase activity [IDA, IMP]
- G-quadruplex DNA binding [IDA]
- Y-form DNA binding [IDA]
- bubble DNA binding [IDA]
- exonuclease activity [IDA]
- four-way junction helicase activity [IDA]
- helicase activity [IDA]
- magnesium ion binding [IDA]
- manganese ion binding [IDA]
- protein binding [IPI]
- protein complex binding [IDA]
- protein homodimerization activity [IDA]
- 3'-5' DNA helicase activity [IDA]
- 3'-5' exonuclease activity [IDA]
- ATP-dependent DNA helicase activity [IDA]
- ATPase activity [IDA]
- DNA binding [IDA]
- DNA helicase activity [IDA, IMP]
- G-quadruplex DNA binding [IDA]
- Y-form DNA binding [IDA]
- bubble DNA binding [IDA]
- exonuclease activity [IDA]
- four-way junction helicase activity [IDA]
- helicase activity [IDA]
- magnesium ion binding [IDA]
- manganese ion binding [IDA]
- protein binding [IPI]
- protein complex binding [IDA]
- protein homodimerization activity [IDA]
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