Endocrine & hormone · target hub

GCGR

Glucagon receptor (GCGR)

GCGR is a Membrane hormone receptor (RTK/GPCR) on the endocrine & hormone axis. G-protein coupled receptor for glucagon that plays a central role in the regulation of blood glucose levels and glucose homeostasis. Regulates the rate of hepatic glucose production by promoting glycogen hydrolysis and gluconeogenesis. Plays an important role in mediating the res… It is indexed under "Insulin–glucagon–incretin axis" on our pathway page for antibodies, inhibitors, and assay guidance.

Back to pathway overviewSearch: GCGRUniProt (P47871)

Research notes

  • Combine with other genes in the same hub block via genetics or pharmacology to test non-redundant roles of GCGR.
  • 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)
Ligand stimulationLigand-dependent phosphorylation
GPCR desensitizationβ-arrestin / internalization control
CN / expressionCopy number & tissue expression

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

Assay readouts for GCGR

  • Receptor activation: GCGR ligand-induced p-Tyr / p-AKT / cAMP.
  • GPCR: β-arrestin recruitment and internalization; second-messenger reporters.
  • RTK: insulin/IGF IRS–PI3K axis where applicable.
  • Pharmacology: peptide hormones or small-molecule agonist/antagonist matrices.

GCGR 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 GCGR studies (examples)

  • Tool lines: HEK293T, CHO, MIN6, MCF-7, Ba/F3—screen by GCGR expression and pathway context (CCLE/DepMap).
  • Combine with neighbors (INS, IGF1, IGF2, INSR) 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 GCGR 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 GCGR 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 GCGR immunoprecipitation

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

Quick search presets

GCGRGCGR antibodyGCGR ligand/agonisthormone/receptor antibody

GCGR-related antibodies (keyword-biased)

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

Neighboring targets (same hub)

PTH1RPTH2RCALCRCALCRLGLP1RGLP2RGIPRVIPR1

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