PI3K/Akt/mTOR · target hub

INPP4B

Inositol polyphosphate-4-phosphatase type II B (INPP4B)

INPP4B is a PIP₃ / Akt phosphatase or PP2A regulation on the PI3K/Akt/mTOR axis. INPP4B participates in PI3K/Akt/mTOR signaling—see UniProt and primary literature for isoforms and tissue context. It is indexed under "PIP₃ / inositol lipid phosphatases (negative regulation)" on our pathway page for antibodies, inhibitors, and assay guidance.

Research notes

  • Combine with other genes in the same hub block via genetics or pharmacology to test non-redundant roles of INPP4B.
  • Annotate PIK3CA/PTEN and upstream RTK–Ras context when reading p-AKT, mTORC1/2, or lipid outputs.
  • Verify antibody clone, phospho-site, and stimulation; include KD/KO or inhibitor controls.

On the pathway hub (sections)

Tumor suppressor & inactivation context (quick reference)

Type / exampleDomain / context (brief)
Loss-of-functionLoss/truncation; frequent in tumors
CN lossCopy loss or promoter methylation
Rare missenseValidate dominant-negative vs hypomorph

Naming and prevalence vary by cohort and assay—annotate clinically with COSMIC, ClinVar, OncoKB, and datasheets; research context only.

Assay readouts for INPP4B

  • Lipid pools: PIP₃, PI(3,4)P₂, or substrates relevant to INPP4B.
  • Loss-of-function: CRISPR/siRNA often elevates p-AKT and growth readouts (context-dependent).
  • Tumor specimens: matched tumor/adjacent with mutation/expression annotation.
  • Inhibitor controls: PI3K/mTOR inhibitors to test phenotypic reversibility.

INPP4B 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 INPP4B studies (examples)

  • Tool lines: MCF-7, U87, PC-3, HEK293T, A549—screen by INPP4B expression and pathway context (CCLE/DepMap).
  • Combine with neighbors (PTEN, TPTE, TPTE2, INPP4A) 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 INPP4B 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 INPP4B 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 INPP4B immunoprecipitation

  • Tagged overexpression: HEK293T FLAG/HA-INPP4B 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 INPP4B can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.

Quick search presets

INPP4B-related antibodies (keyword-biased)

Adds INPP4B 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.