PI3K/Akt/mTOR · target hub

SH3GLB1

Endophilin-B1 (SH3GLB1)

SH3GLB1 is a PI3K lipid kinase / regulatory module on the PI3K/Akt/mTOR axis. SH3GLB1 participates in PI3K/Akt/mTOR signaling—see UniProt and primary literature for isoforms and tissue context. It is indexed under "Class III PI3K (Vps34 complex; autophagy/endosome crosstalk)" 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 SH3GLB1.
  • 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 SH3GLB1

  • Lipid side: PIP₃/PI(3,4)P₂ probes or PH-domain pulldowns—separate SH3GLB1 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.

SH3GLB1 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 SH3GLB1 studies (examples)

  • Tool lines: HEK293T, MCF-7, HCT116, Jurkat, U937—screen by SH3GLB1 expression and pathway context (CCLE/DepMap).
  • Combine with neighbors (PIK3C3, VPS15, NRBF2, BECN1) 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 SH3GLB1 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 SH3GLB1 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 SH3GLB1 immunoprecipitation

  • Tagged overexpression: HEK293T FLAG/HA-SH3GLB1 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 SH3GLB1 can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.

Quick search presets

SH3GLB1-related antibodies (keyword-biased)

Adds SH3GLB1 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.