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Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

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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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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Abnormal Proliferation

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The pharmacogenetics of drug transporters is increasingly recognized as a critical factor influencing interindividual variability in drug absorption, distribution, and elimination. These membrane-bound proteins regulate drugs' movement across cellular barriers by actively pumping them out (efflux) or facilitating their uptake (influx). Among the major transporter families, ATP-binding cassette (ABC) and solute carrier (SLC) transporters play particularly prominent roles. Genetic polymorphisms...
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Phase II biotransformation reactions are essential for detoxifying and eliminating xenobiotics, including many pharmaceutical compounds. These reactions typically involve conjugation, the covalent attachment of polar endogenous groups such as glucuronic acid, sulfate, methyl, or acetyl moieties to functional groups introduced during Phase I metabolism. The resulting conjugates are more water-soluble, enabling efficient renal or biliary excretion.The major classes of Phase II enzymes include...
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Principles of Pharmacogenetics: Types of Genetic Variants

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Yeast As a Chassis for Developing Functional Assays to Study Human P53
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Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

The human Tp53 Arg72Pro polymorphism explains different functional prognosis in stroke.

Jose C Gomez-Sanchez1, Maria Delgado-Esteban, Irene Rodriguez-Hernandez

  • 1Department of Neurology, University Hospital of Salamanca, 37007 Salamanca, Spain.

The Journal of Experimental Medicine
|March 2, 2011
PubMed
Summary
This summary is machine-generated.

The Arg/Arg genotype of the p53 tumor suppressor protein is linked to poor stroke outcomes and increased neuronal apoptosis. This finding suggests it could serve as a genetic marker for predicting stroke prognosis.

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Last Updated: Jun 4, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

Targeted Next-generation Sequencing and Bioinformatics Pipeline to Evaluate Genetic Determinants of Constitutional Disease
09:34

Targeted Next-generation Sequencing and Bioinformatics Pipeline to Evaluate Genetic Determinants of Constitutional Disease

Published on: April 4, 2018

Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Stroke outcomes are unpredictable and not accurately predicted by initial clinical assessments.
  • Neuronal apoptosis in affected brain areas may contribute to poor prognosis after stroke.
  • Genetic factors influencing apoptosis susceptibility could explain variable stroke outcomes.

Purpose of the Study:

  • To investigate the role of p53 variants in stroke outcome.
  • To determine if p53 genotypes are associated with functional recovery after stroke.
  • To explore the mechanism by which p53 variants affect neuronal vulnerability to apoptosis.

Main Methods:

  • Genotyping patients for p53 Arg72Pro single nucleotide polymorphisms.
  • Correlating p53 genotypes with functional outcomes and clinical parameters post-stroke.
  • Investigating the interaction of Arg(72)-p53 and Pro(72)-p53 with mitochondrial proteins in cultured neurons.

Main Results:

  • The Arg/Arg genotype of p53 was significantly associated with poor functional outcomes in both ischemic and hemorrhagic stroke.
  • This genotype correlated with early neurological deterioration in ischemic stroke and larger residual cavity volumes in intracerebral hemorrhage.
  • Arg(72)-p53, unlike Pro(72)-p53, directly interacted with mitochondrial Bcl-xL and promoted apoptosis in neurons subjected to ischemic conditions.

Conclusions:

  • The Tp53 Arg/Arg genotype influences neuronal vulnerability to apoptosis.
  • This genotype is a potential genetic marker for predicting poor functional outcomes after stroke.
  • Understanding p53's role in apoptosis may lead to novel therapeutic strategies for stroke.