PI3K/Akt/mTOR · target hub

INPPL1

Phosphatidylinositol 3,4,5-trisphosphate 5-phosphatase 2 (INPPL1)

INPPL1 is a PIP₃ / Akt phosphatase or PP2A regulation on the PI3K/Akt/mTOR axis. Phosphatidylinositol (PtdIns) phosphatase that specifically hydrolyzes the 5-phosphate of phosphatidylinositol-3,4,5-trisphosphate (PtdIns(3,4,5)P3) to produce PtdIns(3,4)P2, thereby negatively regulating the PI3K (phosphoinositide 3-kinase) pathways (PubMed:16824732). Required f… It is indexed under "PIP₃ / inositol lipid phosphatases (negative regulation)" on our pathway page for antibodies, inhibitors, and assay guidance.

Back to pathway overviewSearch: INPPL1UniProt (O15357)

Research notes

  • Combine with other genes in the same hub block via genetics or pharmacology to test non-redundant roles of INPPL1.
  • 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)

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 INPPL1

  • Lipid pools: PIP₃, PI(3,4)P₂, or substrates relevant to INPPL1.
  • 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.

INPPL1 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 INPPL1 studies (examples)

  • Tool lines: MCF-7, U87, PC-3, HEK293T, A549—screen by INPPL1 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 INPPL1 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 INPPL1 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 INPPL1 immunoprecipitation

  • Tagged overexpression: HEK293T FLAG/HA-INPPL1 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 INPPL1 can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.

Quick search presets

INPPL1INPPL1 antibodyPI3K inhibitormTOR inhibitor

INPPL1-related antibodies (keyword-biased)

Adds INPPL1 keyword bias atop the PI3K/Akt/mTOR antibody pool—if sparse, use presets above or global search.

Neighboring targets (same hub)

PTENTPTETPTE2INPP4AINPP4BINPP5DINPP5EINPP5F

External databases & resources

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.

PI3K/Akt/mTOR·MAPK/ERK·Receptor tyrosine kinase·Metabolism