PI3K/Akt/mTOR · target hub

SHC2

SHC adaptor protein 2 (SHC2)

SHC2 is a Upstream RTK–Ras–MAPK node on the PI3K/Akt/mTOR axis. SHC2 participates in PI3K/Akt/mTOR signaling—see UniProt and primary literature for isoforms and tissue context. It is indexed under "Ras / MAPK & adaptors (RTK→PI3K bypass)" 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 SHC2.
  • 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)

Activating lesions & amplification (quick reference)

Type / exampleDomain / context (brief)
Kinase domainKinase-domain activating lesions (RTK-dependent)
Fusion / amplificationFusion or amplification (cohort-dependent)
CN gainCopy gain and overexpression

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

Assay readouts for SHC2

  • Receptor phosphorylation: p-RTK or p-Tyr blots—ligand time courses.
  • Downstream: p-AKT and p-ERK—partition PI3K vs MAPK dependence.
  • Genetics: KRAS/BRAF/PTEN context; bypass on resistance.
  • Inhibitor matrix: RTK/MEK/PI3K-selective agents.

SHC2 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 SHC2 studies (examples)

  • Tool lines: A549, HepG2, PC-9, Ba/F3, HEK293T—screen by SHC2 expression and pathway context (CCLE/DepMap).
  • Combine with neighbors (HRAS, KRAS, NRAS, MRAS) 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 SHC2 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 SHC2 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 SHC2 immunoprecipitation

  • Tagged overexpression: HEK293T FLAG/HA-SHC2 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 SHC2 can differ in dosage, splicing, and compartmentation—in organoids/PDX, record passage, matrix, and drug history.

Quick search presets

SHC2-related antibodies (keyword-biased)

Adds SHC2 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.