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
PSEN1
Gene Ontology Biological Process
- Notch receptor processing [IBA, TAS]
- amyloid precursor protein catabolic process [IBA, TAS]
- beta-amyloid metabolic process [IBA]
- calcium ion transmembrane transport [IMP]
- canonical Wnt signaling pathway [IBA]
- endoplasmic reticulum calcium ion homeostasis [IDA, IGI]
- extracellular matrix disassembly [TAS]
- extracellular matrix organization [TAS]
- membrane protein ectodomain proteolysis [IDA]
- negative regulation of apoptotic process [IDA]
- positive regulation of catalytic activity [IDA]
- protein processing [IDA]
- regulation of phosphorylation [IDA]
- single organismal cell-cell adhesion [IMP]
- smooth endoplasmic reticulum calcium ion homeostasis [IBA]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
- Golgi apparatus [IDA]
- Z disc [IBA]
- apical plasma membrane [IBA]
- axon [IBA]
- cell cortex [IBA]
- cell surface [IBA]
- centrosome [IDA]
- ciliary rootlet [IBA]
- dendritic shaft [IBA]
- endoplasmic reticulum [IDA]
- gamma-secretase complex [IDA]
- growth cone [IBA]
- integral component of membrane [TAS]
- integral component of plasma membrane [IDA]
- kinetochore [IDA]
- lysosomal membrane [IBA]
- membrane [IDA]
- membrane raft [IBA, IDA]
- mitochondrial inner membrane [IBA]
- mitochondrion [IDA]
- neuromuscular junction [IBA]
- neuronal cell body [IBA]
- nuclear membrane [IDA]
- nuclear outer membrane [IDA]
- perinuclear region of cytoplasm [IBA]
- rough endoplasmic reticulum [IDA]
- smooth endoplasmic reticulum [IDA]
Proximity Label-MS
An interaction is inferred when a bait-enzyme fusion protein selectively modifies a vicinal protein with a diffusible reactive product, followed by affinity capture of the modified protein and identification by mass spectrometric methods.
Publication
Interrogating the protein interactomes of RAS isoforms identifies PIP5K1A as a KRAS-specific vulnerability.
In human cancers, oncogenic mutations commonly occur in the RAS genes KRAS, NRAS, or HRAS, but there are no clinical RAS inhibitors. Mutations are more prevalent in KRAS, possibly suggesting a unique oncogenic activity mediated by KRAS-specific interaction partners, which might be targeted. Here, we determine the specific protein interactomes of each RAS isoform by BirA proximity-dependent biotin identification. The ... [more]
Quantitative Score
- 38.6212754 [Confidence Score]
Throughput
- High Throughput
Additional Notes
- BioID system:Biotin-labled proteins with at least a 2-fold enrichment and p-value < 0.05 were considered significant.
Related interactions
Interaction | Experimental Evidence Code | Dataset | Throughput | Score | Curated By | Notes |
---|---|---|---|---|---|---|
KRAS PSEN1 | Proximity Label-MS Proximity Label-MS An interaction is inferred when a bait-enzyme fusion protein selectively modifies a vicinal protein with a diffusible reactive product, followed by affinity capture of the modified protein and identification by mass spectrometric methods. | High | 25 | BioGRID | 2991795 | |
KRAS PSEN1 | Synthetic Lethality 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. | High | - | BioGRID | 1414683 |
Curated By
- BioGRID