PI3K/Akt/mTOR · target hub
Phosphoinositide 3-kinase regulatory subunit 1 (p85α)
PIK3R1 encodes p85α, a principal class IA PI3K regulatory subunit with SH2/SH3 modules that recognize phosphotyrosine motifs on RTKs or IRS scaffolds, stabilizing catalytic subunits and tuning membrane recruitment and lipid kinase output. KO/dominant-negative contexts blunt insulin/growth-factor–driven PIP3 generation; splice isoforms and expression imbalance can be meaningful in select cancers.
| Type / example | Domain / context (brief) |
|---|---|
| Expression context | Tissue/cell-type–dependent expression |
| Rare variants | Sporadic variants—require functional validation |
| Pathway coupling | Co-occurs with neighboring nodes on the hub |
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 PIK3R1 can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.
Adds PIK3R1 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.