KRAS
KRAS proto-oncogene, GTPase
- Ensembl:
- ENSG00000133703
- UniProt:
- P01116
- OMIM:
- 190070
- Synonyms:
- K-RAS4B, KRAS1, KRAS2
Cilia effects upon perturbation of KRAS
- Cilia number / % ciliated:
- Decreased cilia number
- Loss-of-function effect:
- Incrased cilia number
Ciliogenesis screen results (3 screens)
- Wheway et al. 2015 (siRNA) [siRNA]: Ciliogenesis Defect (z=-6.08) PMID:26167766
- Breslow et al. 2018 (CRISPR) [CRISPR]: Positive Regulator (Hh signaling, casTLE effect=-1.02) PMID:29459680
- Elliott et al. 2025 (CRISPRa) [CRISPRa]: Disassembly Trigger (casTLE Effect=-2.90) PMID:41160700
Subcellular localization
cilia associated gene, lysosomes
Functional category
- Ciliary assembly/disassembly
- Trafficking (BBSome, small GTPases, vesicular transport, ATPases)
- Actin & cytoskeleton regulation
- Neurogenesis & migration
- Signaling (Hedgehog, GPCRs, ion channels)
- Cardiac & muscle development
- Transcription regulation
Function
Inhibition of Kras effector pathways restored ciliogenesis in a mouse pancreatic cancer cell line, raising the possibility that ciliogenesis may be actively repressed by oncogenic Kras ( 19147554). Constitutive activation of KRAS promotes acinar-to-ductal metaplasia (ADM) but is associated with fewer primary cilia, and KRAS knockdown significantly increased cilia formation, suggesting that KRAS signalling suppresses ciliogenesis during ADM. (32571902)
Model organism evidence
Mutations in the Kras oncogene are present in approximately 25% of tumors, while defective primary cilium can either promote or suppress specific cancer types.
BET inhibition rescues ciliogenesis and ameliorates pancreatitis-driven phenotypic changes in mice with Par3 loss.