Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Using genetically modified mice to study apolipoprotein B

S G Young1

  • 1Gladstone Institute of Cardiovascular Disease, San Francisco, CA 94141-9100, USA.

Journal of Atherosclerosis and Thrombosis
|January 1, 1996
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Heterogeneity in the properties of mutant secreted lymphocyte antigen 6/urokinase receptor-related protein 1 (SLURP1) in Mal de Meleda.

The British journal of dermatology·2015
Same author

Stable isotope imaging of biological samples with high resolution secondary ion mass spectrometry and complementary techniques.

Methods (San Diego, Calif.)·2014
Same author

Glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 and the intravascular processing of triglyceride-rich lipoproteins.

Journal of internal medicine·2012
Same author

Genetic abnormalities in apolipoprotein B.

Trends in cardiovascular medicine·2011
Same author

Generation of transgenic mice from yeast artificial chromosome DNA that has been modified by gene targeting.

Trends in cardiovascular medicine·2011
Same author

Farnesylation of Pex19p is not essential for peroxisome biogenesis in yeast and mammalian cells.

Cellular and molecular life sciences : CMLS·2006
Same journal

Beyond Sinus Rhythm: Rhythm Control and Mechanism-Based Secondary Prevention in Atrial Fibrillation-Related Stroke.

Journal of atherosclerosis and thrombosis·2026
Same journal

Efficacy and Safety of Evinacumab in Japanese Patients with Homozygous Familial Hypercholesterolemia: Long-term Results from an Open-label, Single-arm, Phase 3 Trial.

Journal of atherosclerosis and thrombosis·2026
Same journal

Knowledge Gaps and Nonadherence Among Japanese Patients with Atherosclerotic Cardiovascular Disease.

Journal of atherosclerosis and thrombosis·2026
Same journal

Association of Multimodal Intracoronary Imaging-Derived Plaque Morphology with the Pathophysiological Disease Patterns Assessed by the Quantitative Flow Ratio-Pullback Pressure Gradient.

Journal of atherosclerosis and thrombosis·2026
Same journal

Prognostic Significance of Atrial Cardiopathy in Patients with Embolic Stroke of an Undetermined Source.

Journal of atherosclerosis and thrombosis·2026
Same journal

Two Sides of the Same Curve: Targets, Reduction, and LDL-C Burden.

Journal of atherosclerosis and thrombosis·2026
See all related articles

Genetically modified mice reveal apolipoprotein B

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry
  • Cardiovascular Research

Background:

  • Apolipoprotein B (apo-B) is crucial for lipoprotein metabolism and is linked to atherosclerosis.
  • Understanding apo-B's role requires precise genetic manipulation.
  • Existing knowledge on apo-B's function and regulation is incomplete.

Purpose of the Study:

  • To investigate apolipoprotein B biology using genetically modified mouse models.
  • To elucidate the roles of apo-B48 and apo-B100 in lipid transport and disease.
  • To explore the genetic regulation of apo-B expression and structure-function relationships.

Main Methods:

  • Gene targeting in mouse embryonic stem cells to create apo-B-deficient mice.

Related Experiment Videos

  • Generation of human apo-B transgenic mice with large genomic fragments.
  • Creation of apo B48-only and apo B100-only mice via gene targeting.

    • Main Results:

    • Apo-B deficiency led to embryonic lethality due to impaired lipid nutrient delivery.
    • Human apo-B transgenic mice showed elevated LDL cholesterol and increased atherosclerosis susceptibility.
    • Intestinal apo-B gene expression is regulated by distant DNA sequences.
    • A specific cysteine residue (Cys-4326) in apo-B100 is essential for forming lipoprotein (a).

    Conclusions:

    • Genetically engineered mice are powerful tools for studying apo-B metabolism and function.
    • Apo-B is essential for embryonic development and lipoprotein metabolism.
    • Specific structural features of apo-B100 are critical for lipoprotein (a) assembly and function.