Localization of the domains involved in ligand binding and activation of the glucose-dependent insulinotropic polypeptide receptor

Endocrinology. 1997 Jun;138(6):2640-3. doi: 10.1210/endo.138.6.9104.

Abstract

The receptors for the two structurally related insulinotropic hormones Glucose-dependent Insulinotropic Polypeptide (GIP) and Glucagon-Like Peptide-1 (GLP-1) share approximately 40% sequence identity and demonstrate complete specificity for their endogenous ligands, while utilizing similar second messenger pathways. In the current study chimeric GIP-GLP-1 receptors were prepared, and the effect of domain-exchange on ligand binding and adenylyl cyclase activation examined. A chimera (CH-2) consisting of the first 132 amino acids of the external N-terminal (NT) domain bound 125I-GIP with high affinity (27.77 +/- 11.85 nM). However, for receptor coupling to cAMP production it was necessary to extend the NT into the first transmembrane (TM-1) region (CH-3: IC50 = 9.04 +/- 1.07 nM; EC50 = 17.1 +/- 3.5 nM). A chimera which included part of TM-3 (CH-4) demonstrated binding and signalling (IC50 = 8.33 +/- 0.14 nM; EC50 = 467.5 +/- 173.6 pM) similar to the wild type receptor (IC50 = 1.33 +/- 0.19 nM; EC50 = 497.9 +/- 211.7 pM). Surprisingly constructs CH-2 and CH-3, while devoid of detectable 125I-GLP-1 binding, were capable of eliciting GLP-1-specific cAMP production (EC50s CH-2 = 81.4 +/- 19.6 nM; CH-3 = 5.99 +/- 0.68 nM) suggesting that receptor activation is not completely dependent on high affinity receptor binding. These data clearly demonstrate that the NT domain of the GIP receptor acts as the ligand-specific binding domain and that the first transmembrane domain is important for receptor activation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenylyl Cyclases / metabolism
  • Animals
  • Binding Sites
  • Binding, Competitive
  • CHO Cells
  • COS Cells
  • Cloning, Molecular
  • Cricetinae
  • Cyclic AMP / metabolism
  • Gastric Inhibitory Polypeptide / metabolism
  • Gastric Inhibitory Polypeptide / pharmacology*
  • Glucagon / metabolism
  • Glucagon / pharmacology*
  • Glucagon-Like Peptide 1
  • Glucagon-Like Peptide-1 Receptor
  • Humans
  • Kinetics
  • Models, Structural
  • Peptide Fragments / metabolism
  • Peptide Fragments / pharmacology*
  • Protein Precursors / metabolism
  • Protein Precursors / pharmacology*
  • Protein Structure, Secondary
  • Rats
  • Receptors, Gastrointestinal Hormone / biosynthesis
  • Receptors, Gastrointestinal Hormone / chemistry*
  • Receptors, Gastrointestinal Hormone / metabolism*
  • Receptors, Glucagon / biosynthesis
  • Receptors, Glucagon / chemistry*
  • Receptors, Glucagon / metabolism*
  • Recombinant Fusion Proteins / biosynthesis
  • Recombinant Fusion Proteins / chemistry
  • Recombinant Fusion Proteins / metabolism
  • Signal Transduction
  • Transfection

Substances

  • GLP1R protein, human
  • Glp1r protein, rat
  • Glucagon-Like Peptide-1 Receptor
  • Peptide Fragments
  • Protein Precursors
  • Receptors, Gastrointestinal Hormone
  • Receptors, Glucagon
  • Recombinant Fusion Proteins
  • Gastric Inhibitory Polypeptide
  • Glucagon-Like Peptide 1
  • Glucagon
  • gastric inhibitory polypeptide receptor
  • Cyclic AMP
  • Adenylyl Cyclases