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Related Concept Videos

GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

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Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
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G Protein-coupled Receptors01:15

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G Protein-Coupled Receptors or GPCRs are membrane-bound receptors that transiently associate with heterotrimeric G proteins and induce an appropriate response to sensory stimuli such as light, odors, hormones, cytokines, or neurotransmitters.
GPCRs are also called heptahelical, 7TM, or serpentine receptors, and consist of seven (H1-H7) transmembrane alpha-helices that span the bilayer to form a cylindrical core. The transmembrane helices are connected by three extracellular loops and three...
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Activation and Inactivation of G Proteins01:22

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Heterotrimeric G proteins are guanine nucleotide-binding proteins. As the name suggests, heterotrimeric G proteins are composed of three subunits: alpha, beta, and gamma. They remain GDP-bound or GTP-bound inside the cells and switch between inactive/active states. The Gα subunit possesses the nucleotide-binding pocket that binds guanine nucleotides and switches between GDP or GTP-bound states. In contrast, the Gꞵ and Gγ subunits are always bound together with high...
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G-protein Coupled Receptors01:21

G-protein Coupled Receptors

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G-protein coupled receptors are ligand binding receptors that indirectly affect changes in the cell. The actual receptor is a single polypeptide that transverses the cell membrane seven times creating intracellular and extracellular loops. The extracellular loops create a ligand specific pocket which binds to neurotransmitters or hormones. The intracellular loops holds onto the G-protein.
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cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

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Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
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Transducer Mechanism: G Protein–Coupled Receptors01:30

Transducer Mechanism: G Protein–Coupled Receptors

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G Protein–Coupled Receptors (GPCRs) are membrane-bound receptors that transiently associate with heterotrimeric G proteins and induce an appropriate response to various stimuli. GPCRs regulate critical physiological pathways and are excellent drug targets for treating diseases such as diabetes, cancer, obesity, depression, or Alzheimer's. Nearly 35% of approved drugs implement their therapeutic effects by selectively interacting with specific GPCRs.
GPCRs are also called heptahelical,...
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Related Experiment Video

Updated: Dec 26, 2025

A Kinetic Fluorescence-based Ca2+ Mobilization Assay to Identify G Protein-coupled Receptor Agonists, Antagonists, and Allosteric Modulators
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A Kinetic Fluorescence-based Ca2+ Mobilization Assay to Identify G Protein-coupled Receptor Agonists, Antagonists, and Allosteric Modulators

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GPCRs, G Proteins, and Their Impact on β-cell Function.

Anjaneyulu Kowluru1

  • 1Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Center for Translational Research in Diabetes, Biomedical Research Service, John D. Dingell VA Medical Center, Wayne State University, Detroit, Michigan, USA.

Comprehensive Physiology
|March 13, 2020
PubMed
Summary
This summary is machine-generated.

G protein signaling regulates insulin secretion from islet beta cells. Dysfunctional G proteins contribute to diabetes, while GPCR agonists may offer therapeutic benefits for metabolic defects.

Keywords:
cell physiologydiabetesendocrinologyhormone receptorsintracellular signalingmetabolism

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Area of Science:

  • Endocrinology
  • Cell Biology
  • Metabolic Research

Background:

  • Insulin secretion involves complex intracellular signaling pathways.
  • G proteins play a critical role in regulating these signaling events within islet beta cells.
  • Understanding G protein function is crucial for comprehending beta cell physiology and pathology.

Purpose of the Study:

  • To review the role of G protein regulators in G protein-coupled receptor (GPCR)-G protein-effector coupling for beta cell function.
  • To explore novel, noncanonical, GPCR-independent mechanisms of G protein activation in islets.
  • To discuss the impact of G protein dysfunction on beta cell health in diabetes and the potential of GPCR agonists as therapeutics.

Main Methods:

  • Literature review and synthesis of existing research on GPCR-G protein signaling in islet beta cells.
  • Analysis of evidence for both canonical and noncanonical G protein activation pathways.
  • Examination of studies investigating the link between G protein dysfunction and diabetes-related beta cell pathology.

Main Results:

  • G protein regulators modulate GPCR-G protein-effector coupling essential for normal beta cell function.
  • Evidence supports GPCR-independent G protein activation mechanisms in islets.
  • Abnormal G protein function is implicated in islet beta cell dysregulation and demise during metabolic stress and diabetes.
  • GPCR agonists show potential in mitigating metabolic defects in beta cells under pathological conditions.

Conclusions:

  • G protein signaling is a key regulator of islet beta cell function, with both canonical and noncanonical pathways involved.
  • Dysregulation of G protein function contributes to diabetes pathogenesis.
  • Targeting GPCRs with agonists may represent a therapeutic strategy for metabolic disorders affecting the islet beta cell.