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HRAS proto-oncogene GTPase (mutated) (HRAS)
- Target
- HRAS
- Molecular classification
- Small GTPase, Ras superfamily
01
Overview
HRAS is a small GTPase proto-oncogene in the Ras family that cycles between GTP-bound (active, signaling via Raf/MEK/ERK or PI3K/Akt) and GDP-bound (inactive) states, regulated by GEFs and GAPs. Mutated HRAS, such as G12D (oncogenic, transforming) or G12P (non-transforming with retained intrinsic GTPase activity), alters dynamics in Switch I/II regions and nucleotide pocket, leading to persistent signaling in cancers like bladder, thyroid, and head/neck squamous cell carcinoma. The G12P mutant stabilizes the pocket, allows GTP hydrolysis without GAP, and serves as a model for GAP-independent activity, with Y32 dynamics proposed as a therapeutic target to restore GTPase in oncogenic mutants.
- Other names
- H-RASHarvey rat sarcoma viral oncogene homologRASH1p21rasC-H-RASHAMSV
02
Biological functions
Signal transductionCell proliferationCell differentiationCell survival
03
Disease associations
Cancer
04
Safety considerations
Oncogenic activation due to mutations locking protein in GTP-bound active state, impairing GTPase activitychallenges in targeting due to loss of GAP binding in mutants
05
Biomarkers
HRAS mutations (e.g., for head and neck squamous cell carcinoma, bladder cancer)
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