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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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Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...
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Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
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In-vitro Mutagenesis

To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.

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Related Experiment Video

Updated: May 9, 2026

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer
06:01

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer

Published on: July 6, 2017

Mitochondrial gene polymorphisms that protect mice from colitis.

Florian Bär1, Wiebke Bochmann, Andrea Widok

  • 1Medical Department I, University Hospital Schleswig-Holstein, Lübeck, Germany; Institute of Anatomy, University of Lübeck, Lübeck, Germany.

Gastroenterology
|July 23, 2013
PubMed
Summary
This summary is machine-generated.

Mitochondrial DNA variants that boost intestinal ATP levels protect mice from colitis. Enhancing mitochondrial ATP synthesis in gut cells may offer a new therapy for ulcerative colitis (UC).

Keywords:
2,4-dinitrophenolADPATPCSConplastic Inbred MiceDNPDSSEnergy MetabolismIBDIBD ModelIcam-1Mitochondrial DysfunctionNF-κBOXPHOSTNBSUCadenosine diphosphateadenosine triphosphateconplastic inbred straindextran sodium sulfateinflammatory bowel diseaseintercellular adhesion molekule 1mDAImitochondrialmodified disease activity indexmtnuclear factor-κBoxidative phosphorylationtrinitrobenzene sulfonateulcerative colitis

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Murine Distal Colostomy, A Novel Model of Diversion Colitis in C57BL/6 Mice
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Murine Distal Colostomy, A Novel Model of Diversion Colitis in C57BL/6 Mice

Published on: July 12, 2018

Area of Science:

  • Mitochondrial biology
  • Gastroenterology
  • Immunology

Background:

  • Ulcerative colitis (UC) is linked to disrupted energy balance in the gut lining.
  • Reduced mitochondrial oxidative phosphorylation (OXPHOS) activity is seen in UC patients, suggesting a role in disease development.
  • Mechanisms altering OXPHOS activity in UC remain unclear.

Purpose of the Study:

  • To investigate the role of mitochondrial genomes in OXPHOS activity and colitis susceptibility.
  • To use conplastic mice (identical nuclear, different mitochondrial genomes) to study OXPHOS complex activity.

Main Methods:

  • Induced colitis in wild-type and conplastic mice using dextran sodium sulfate or trinitrobenzene sulfonate.
  • Analyzed colon tissues for histopathology, protein expression, ATP levels, reactive oxygen species, OXPHOS activity, and cell proliferation/apoptosis.

Main Results:

  • Mice with higher mucosal OXPHOS activity and ATP levels showed reduced colitis severity.
  • These mice exhibited increased enterocyte proliferation and nuclear factor-κB activity, associated with mucosal barrier protection.
  • Defects in these processes are linked to inflammatory bowel disease.

Conclusions:

  • Mitochondrial DNA variations increasing mucosal ATP levels confer protection against colitis in mice.
  • Boosting mitochondrial ATP synthesis in intestinal epithelial cells presents a potential therapeutic strategy for UC.