PI3K/Akt/mTOR · target hub

PIK3C2G

Phosphatidylinositol 4-phosphate 3-kinase catalytic subunit type 2 gamma (PI3K-C2γ)

PIK3C2G encodes class II PI3K γ with a more restricted expression profile; reported roles span secretory, neuronal/synaptic-like compartments, and epithelial polarity programs—together with C2α/C2β it parallel-regulates inositol lipid pools and trafficking networks.

Research notes

  • Primary tissue-derived models help capture lower-abundance γ expression windows.
  • Triple KD matrices with PIK3C2A/B can expose redundancy vs branch-specific phenotypes.
  • Secretory, ciliary, or junctional readouts can anchor functional assays (literature-guided).

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 PIK3C2G

  • Lipid side: PIP₃/PI(3,4)P₂ probes or PH-domain pulldowns—separate PIK3C2G 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.

PIK3C2G 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 PIK3C2G studies (examples)

  • Tool lines: HEK293T, MCF-7, HCT116, Jurkat, U937—screen by PIK3C2G expression and pathway context (CCLE/DepMap).
  • Combine with neighbors (PIK3C2A, PIK3C2B) 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 PIK3C2G 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 PIK3C2G 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 PIK3C2G immunoprecipitation

  • Tagged overexpression: HEK293T FLAG/HA-PIK3C2G 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 PIK3C2G can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.

Quick search presets

PIK3C2G-related antibodies (keyword-biased)

Adds PIK3C2G 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.