PI3K/Akt/mTOR · target hub
Muscle RAS oncogene homolog (MRAS)
MRAS is a Upstream RTK–Ras–MAPK node on the PI3K/Akt/mTOR axis. MRAS participates in PI3K/Akt/mTOR signaling—see UniProt and primary literature for isoforms and tissue context. It is indexed under "Ras / MAPK & adaptors (RTK→PI3K bypass)" on our pathway page for antibodies, inhibitors, and assay guidance.
| Type / example | Domain / context (brief) |
|---|---|
| Kinase domain | Kinase-domain activating lesions (RTK-dependent) |
| Fusion / amplification | Fusion or amplification (cohort-dependent) |
| CN gain | Copy gain and overexpression |
Naming and prevalence vary by cohort and assay—annotate clinically with COSMIC, ClinVar, OncoKB, and datasheets; research context only.
Examples below reflect common literature and public resources (e.g., CCLE, DepMap)—validate genotypes, expression, and passage in your own stocks before committing assays.
Human tissues and primary cells require ethics/IRB approval; tumors are heterogeneous—record histotype, site, and preservation conditions.
Overexpression vs endogenous MRAS can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.
Adds MRAS keyword bias atop the PI3K/Akt/mTOR antibody pool—if sparse, use presets above or global search.
This content supports research reagents and pathway education—not medical advice. Annotate mutations, drug indications, and protocols with authoritative databases, datasheets, and institutional oversight.
Last reviewed: 2026-05-18
See the PI3K/Akt/mTOR hub for neighboring nodes and assay guidance—cross-check MAPK, RTK, metabolism, and autophagy pages as needed.