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Related Concept Videos

GPCR Desensitization01:12

GPCR Desensitization

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...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
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Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
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Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...

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A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
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Platelet GP IIIa Pl(A) polymorphisms display different sensitivities to agonists.

A D Michelson1, M I Furman, P Goldschmidt-Clermont

  • 1Departments of Medicine and Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

Circulation
|March 7, 2000
PubMed
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The Pl(A2) gene variant in platelets increases their reactivity and activation. This genetic difference in platelet function may explain inherited predisposition to coronary events.

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Last Updated: Jul 15, 2026

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
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Published on: June 5, 2019

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Analyzing Platelet Subpopulations by Multi-color Flow Cytometry

Published on: June 10, 2025

Area of Science:

  • Cardiovascular Genetics
  • Hematology
  • Molecular Biology

Background:

  • Inherited predisposition and platelet hyperreactivity are linked to ischemic coronary events.
  • Mechanisms underlying genetic differences in platelet function remain unclear.
  • The Pl(A2) polymorphism of glycoprotein IIIa (GP IIIa) is associated with coronary syndromes, prompting investigation into its role in platelet hyperreactivity.

Purpose of the Study:

  • To characterize functional parameters of platelets with the Pl(A) (HPA-1) polymorphism.
  • To investigate the impact of the Leu (Pl(A1)) to Pro (Pl(A2)) substitution in GP IIIa on platelet activation and function.
  • To determine if the Pl(A2) variant contributes to platelet hyperreactivity and influences response to antiplatelet agents.

Main Methods:

  • Studied 56 healthy donors genotyped for the Pl(A) polymorphism (Pl(A1,A1), Pl(A1,A2), Pl(A2,A2)).
  • Assessed surface-expressed P-selectin, GP IIb/IIIa-bound fibrinogen, and activated GP IIb/IIIa in response to adenosine diphosphate (ADP).
  • Evaluated platelet aggregation sensitivity to aspirin and abciximab.

Main Results:

  • Pl(A2)-positive platelets exhibited a gene dosage effect with significantly greater P-selectin, fibrinogen binding, and GP IIb/IIIa activation upon low-dose ADP stimulation compared to Pl(A1,A1) platelets.
  • ADP-stimulated GP IIb/IIIa expression was significantly higher in Pl(A2,A2) platelets.
  • Platelets heterozygous for Pl(A) alleles (Pl(A1,A2)) showed increased sensitivity to aspirin and abciximab inhibition of aggregation.

Conclusions:

  • Pl(A2)-positive platelets demonstrate a reduced threshold for activation.
  • Heterozygous Pl(A) platelets exhibit heightened sensitivity to common antiplatelet drugs.
  • These in vitro findings suggest potential relevance for understanding in vivo thrombotic conditions and personalized antiplatelet therapy.