PI3K/Akt/mTOR · target hub

PIK3R2

Phosphoinositide 3-kinase regulatory subunit 2 (p85β)

PIK3R2 encodes p85β, partnering with p85α as major class IA regulatory subunits that assemble RTK/IRS-dependent holoenzymes and participate in feedback control. Tissue distribution and developmental expression differ from p85α; mouse genetics highlight partially non-redundant roles in metabolic homeostasis and organ-specific signaling.

Research notes

  • In metabolic liver/muscle models, compare/contrast with PIK3R1.
  • Use interaction databases to infer preferred pairing with p110 isoforms.
  • In insulin resistance, reconcile literature on p85 abundance vs inhibitory scaffolding.

On the pathway hub (sections)

Genetic lesions & expression context (quick reference)

Type / exampleDomain / context (brief)
Expression contextTissue/cell-type–dependent expression
Rare variantsSporadic variants—require functional validation
Pathway couplingCo-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.

Assay readouts for PIK3R2

  • Lipid side: PIP₃/PI(3,4)P₂ probes or PH-domain pulldowns—separate PIK3R2 from class II/III compartments.
  • Biochemistry: IP–kinase or membrane recruitment; co-IP regulatory partners.
  • Downstream: p-AKT Thr308/Ser473, p-S6K, p-4E-BP1—pair totals and inhibitor titrations.
  • Genetics: PTEN/INPP4 status; NGS/ddPCR for lesions and copy number.

PIK3R2 experimental notes

Examples below reflect common literature and public resources (e.g., CCLE, DepMap)—validate genotypes, expression, and passage in your own stocks before committing assays.

[1] Cell lines commonly used for PIK3R2 studies (examples)

  • Tool lines: HEK293T, MCF-7, HCT116, Jurkat, U937—screen by PIK3R2 expression and pathway context (CCLE/DepMap).
  • Combine with neighbors (PIK3CA, PIK3CB, PIK3CD, PIK3CG) via KD/pharmacology to test non-redundancy.
  • Overexpression/rescue in HEK293T supports mechanism and IP workflows.
  • Isogenic/CRISPR models separate pathway dependency from bypass survival.

[2] Cell samples for PIK3R2 Western blot

  • Whole-cell lysates—optimize RIPA/NP-40 per antibody; phosphatase inhibitors for phospho blots.
  • Stimulation: serum starvation ± insulin/EGF or amino-acid withdrawal/refeed as relevant.
  • Controls: siRNA/shRNA, CRISPR KO, or inhibitors to validate band specificity.
  • Loading: BCA normalization; subcellular fractionation when needed.

[3] Tissue samples for PIK3R2 Western blot

  • Matched tumor/adjacent frozen tissues after pathology review.
  • Mouse GEMM or xenografts—mind species antibody cross-reactivity.
  • Primary cells/PDCs when ethically approved.
  • FFPE needs specialized extraction; frozen tissue preferred for phospho work.

[4] Cell samples for PIK3R2 immunoprecipitation

  • Tagged overexpression: HEK293T FLAG/HA-PIK3R2 for complex capture.
  • Endogenous IP: high-expression lines; often ≥1–5×10⁶ cells per IP.
  • Stimulation: ligand or nutrient treatments enrich interactions—pilot time courses.
  • Controls: isotype IgG, empty vector, KD/KO negatives.

Human tissues and primary cells require ethics/IRB approval; tumors are heterogeneous—record histotype, site, and preservation conditions.

Bypass & related pathways

Models & genetics note

Overexpression vs endogenous PIK3R2 can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.

Quick search presets

PIK3R2-related antibodies (keyword-biased)

Adds PIK3R2 keyword bias atop the PI3K/Akt/mTOR antibody pool—if sparse, use presets above or global search.

FAQ

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

Related on this site

See the PI3K/Akt/mTOR hub for neighboring nodes and assay guidance—cross-check MAPK, RTK, metabolism, and autophagy pages as needed.