Endocrine & hormone · target hub

INS

Insulin (INS)

INS is a Metabolic / incretin hormones on the endocrine & hormone axis. Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver It is indexed under "Insulin–glucagon–incretin axis" on our pathway page for antibodies, inhibitors, and assay guidance.

Back to pathway overviewSearch: INSUniProt (P01308)

Research notes

  • Combine with other genes in the same hub block via genetics or pharmacology to test non-redundant roles of INS.
  • For nuclear receptors pair ligands, co-regulators, and reporter assays; for membrane receptors note GPCR/RTK downstream and desensitization.
  • 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 INS

  • Islet/liver: INS with insulin secretion, gluconeogenesis, or lipid readouts.
  • Incretins: GLP-1/GIP stimulation and receptor agonists.
  • p-AKT / p-ERK: combined nutrient and hormone stimulation.
  • Metabolic disease models: tissue insulin sensitivity.

INS 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 INS studies (examples)

  • Tool lines: MIN6, INS-1, HepG2, 3T3-L1, HEK293T—screen by INS expression and pathway context (CCLE/DepMap).
  • Combine with neighbors (IGF1, IGF2, INSR, IGF1R) 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 INS 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 INS 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 INS immunoprecipitation

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

Quick search presets

INSINS antibodyINS ligand/agonisthormone/receptor antibody

INS-related antibodies (keyword-biased)

Adds INS keyword bias atop the 内分泌和激素 antibody pool—if sparse, use presets above or global search.

Neighboring targets (same hub)

IGF1IGF2INSRIGF1RINSRRIRS1IRS2IRS4

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 endocrine & hormone hub for neighboring targets—cross-check PI3K, MAPK, RTK, and metabolism pages as needed.

Endocrine & hormone·PI3K/Akt/mTOR·MAPK/ERK·Receptor tyrosine kinase·Metabolism