KRAS
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
ERCC3
Gene Ontology Biological Process
- 7-methylguanosine mRNA capping [TAS]
- DNA repair [IMP, TAS]
- DNA topological change [IMP]
- apoptotic process [IMP]
- gene expression [TAS]
- hair cell differentiation [IMP]
- nucleotide-excision repair [IMP, TAS]
- nucleotide-excision repair, DNA damage removal [TAS]
- nucleotide-excision repair, DNA duplex unwinding [IMP]
- nucleotide-excision repair, DNA incision [IMP]
- positive regulation of apoptotic process [IDA]
- positive regulation of transcription from RNA polymerase II promoter [IDA]
- positive regulation of viral transcription [TAS]
- protein localization [IMP]
- regulation of mitotic cell cycle phase transition [IMP]
- response to UV [IMP]
- response to oxidative stress [IMP]
- termination of RNA polymerase I transcription [TAS]
- transcription elongation from RNA polymerase I promoter [TAS]
- transcription elongation from RNA polymerase II promoter [TAS]
- transcription from RNA polymerase I promoter [TAS]
- transcription from RNA polymerase II promoter [IDA, IMP, TAS]
- transcription initiation from RNA polymerase I promoter [TAS]
- transcription initiation from RNA polymerase II promoter [TAS]
- transcription-coupled nucleotide-excision repair [IDA, TAS]
- viral process [TAS]
Gene Ontology Molecular Function- 3'-5' DNA helicase activity [IDA, IMP]
- ATPase activity [IDA]
- DNA binding [TAS]
- DNA-dependent ATPase activity [IDA, IMP]
- RNA polymerase II carboxy-terminal domain kinase activity [IDA]
- damaged DNA binding [NAS]
- protein C-terminus binding [IPI]
- protein N-terminus binding [IPI]
- protein binding [IPI]
- protein kinase activity [IDA]
- transcription factor binding [IDA]
- 3'-5' DNA helicase activity [IDA, IMP]
- ATPase activity [IDA]
- DNA binding [TAS]
- DNA-dependent ATPase activity [IDA, IMP]
- RNA polymerase II carboxy-terminal domain kinase activity [IDA]
- damaged DNA binding [NAS]
- protein C-terminus binding [IPI]
- protein N-terminus binding [IPI]
- protein binding [IPI]
- protein kinase activity [IDA]
- transcription factor binding [IDA]
Gene Ontology Cellular Component
- holo TFIIH complex [IDA, TAS]
- nucleoplasm [IDA, TAS]
- nucleus [TAS]
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]
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.
Related interactions
| Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
|---|---|---|---|---|---|---|
| KRAS ERCC3 | Negative Genetic Negative Genetic Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores. | High | - | BioGRID | 3343156 |
Curated By
- BioGRID