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Related Concept Videos

G Protein-coupled Receptors01:15

G Protein-coupled Receptors

13.9K
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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G Protein-coupled Receptors01:15

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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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G-protein Coupled Receptors01:21

G-protein Coupled Receptors

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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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GPCR Desensitization01:12

GPCR Desensitization

6.1K
G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
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Related Experiment Video

Updated: Apr 23, 2026

Identification and Classification of Position-specific GABAA Receptor Subunit Missense Variants for Their Role In Hippocampal Pyramidal Neurons
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Rare platelet GPCR variants: what can we learn?

S P Nisar1, M L Jones2, M R Cunningham1

  • 1School of Physiology and Pharmacology, University of Bristol, Bristol, UK.

British Journal of Pharmacology
|September 19, 2014
PubMed
Summary
This summary is machine-generated.

Understanding platelet G-protein coupled receptors (GPCRs) is key to improving anti-thrombotic therapies. Studying rare mutations reveals crucial structure-function insights for purinergic and thromboxane A2 receptors.

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Area of Science:

  • Molecular biology
  • Pharmacology
  • Hematology

Background:

  • Platelet G-protein coupled receptors (GPCRs) are vital for regulating platelet activity.
  • Targeting platelet GPCRs is a cornerstone of anti-thrombotic therapy for cardiovascular and cerebrovascular diseases.
  • Current anti-platelet drug efficacy varies significantly between patients, and bleeding complications are a concern.

Purpose of the Study:

  • To elucidate molecular mechanisms governing GPCRs and platelet function.
  • To optimize existing anti-platelet drug use and guide the development of novel therapeutics.
  • To investigate the role of genetic variations in platelet GPCRs and their link to bleeding disorders.

Main Methods:

  • Integrated functional genomics strategy.
  • Identification of rare, function-disrupting mutations in key platelet proteins.
  • Structure-function analysis of platelet GPCRs, focusing on purinergic and thromboxane A2 receptors.

Main Results:

  • Functional genomics approach yielded significant structure-function insights into platelet GPCRs.
  • Specific emphasis on purinergic and thromboxane A2 receptors provided detailed molecular understanding.
  • Findings contribute to understanding the genetic basis of mild bleeding disorders.

Conclusions:

  • Detailed knowledge of GPCR regulation in platelets is essential for therapeutic advancement.
  • Insights gained have direct implications for anti-platelet pharmacotherapy and patient treatment.
  • This research enhances understanding of the molecular underpinnings of bleeding disorders.