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
RPS3
S3, OK/SW-cl.26
ribosomal protein S3
GO Process (20)
GO Function (12)
GO Component (10)
Gene Ontology Biological Process
- DNA catabolic process, endonucleolytic [IBA, IDA]
- RNA metabolic process [TAS]
- SRP-dependent cotranslational protein targeting to membrane [TAS]
- cellular protein metabolic process [TAS]
- cellular response to DNA damage stimulus [IEP]
- cytoplasmic translation [IBA]
- gene expression [TAS]
- mRNA metabolic process [TAS]
- negative regulation of DNA repair [IMP]
- nuclear-transcribed mRNA catabolic process, nonsense-mediated decay [TAS]
- positive regulation of DNA N-glycosylase activity [IDA]
- positive regulation of NF-kappaB transcription factor activity [IMP]
- positive regulation of apoptotic signaling pathway [IDA]
- translation [IC, NAS, TAS]
- translational elongation [TAS]
- translational initiation [NAS, TAS]
- translational termination [TAS]
- viral life cycle [TAS]
- viral process [TAS]
- viral transcription [TAS]
Gene Ontology Molecular Function- DNA-(apurinic or apyrimidinic site) lyase activity [IDA]
- NF-kappaB binding [IPI]
- damaged DNA binding [IDA]
- enzyme binding [IPI]
- iron-sulfur cluster binding [NAS]
- mRNA binding [IDA]
- oxidized purine nucleobase lesion DNA N-glycosylase activity [IBA]
- poly(A) RNA binding [IDA]
- protein binding [IPI]
- protein kinase A binding [IPI]
- protein kinase binding [IPI]
- structural constituent of ribosome [IDA, NAS]
- DNA-(apurinic or apyrimidinic site) lyase activity [IDA]
- NF-kappaB binding [IPI]
- damaged DNA binding [IDA]
- enzyme binding [IPI]
- iron-sulfur cluster binding [NAS]
- mRNA binding [IDA]
- oxidized purine nucleobase lesion DNA N-glycosylase activity [IBA]
- poly(A) RNA binding [IDA]
- protein binding [IPI]
- protein kinase A binding [IPI]
- protein kinase binding [IPI]
- structural constituent of ribosome [IDA, 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 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