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

Mouse models for extracellular matrix diseases

A Aszódi1, A Pfeifer, M Wendel

  • 1Max-Planck Institut für Biochemie, Martinsried, Germany.

Journal of Molecular Medicine (Berlin, Germany)
|April 16, 1998
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

Calcific aortic valve disease augments vesicular microRNA-145-5p to regulate the calcification of valvular interstitial cells via cellular crosstalk.

Basic research in cardiology·2025
Same author

Human and porcine aortic valve endothelial and interstitial cell isolation and characterization.

Frontiers in cardiovascular medicine·2023
Same author

An amyloid beta vaccine that safely drives immunity to a key pathological species in Alzheimer's disease: pyroglutamate amyloid beta.

Brain communications·2022
Same author

Optical analysis of glutamate spread in the neuropil.

Cerebral cortex (New York, N.Y. : 1991)·2022
Same author

Rescuing lethal phenotypes induced by disruption of genes in mice: a review of novel strategies.

Physiological research·2021
Same author

The Matrilin-3 T298M mutation predisposes for post-traumatic osteoarthritis in a knock-in mouse model.

Osteoarthritis and cartilage·2020
Same journal

Beyond the target: implications of Wnt pathway inhibitors on bone health.

Journal of molecular medicine (Berlin, Germany)·2026
Same journal

Proteomic analysis reveals divergent inflammatory mechanisms of COVID-associated Guillain-Barré syndrome.

Journal of molecular medicine (Berlin, Germany)·2026
Same journal

Integrative genetic and functional analysis of autosomal dominant hearing loss in 108 multigenerational families.

Journal of molecular medicine (Berlin, Germany)·2026
Same journal

Preclinical evaluation of cysteine protease-inhibitor aloxistatin (E64d) for heart failure therapy.

Journal of molecular medicine (Berlin, Germany)·2026
Same journal

Zinc-binding protein metallothionein 3 protects vascular smooth muscle cells from ferroptosis via blocking lysosomal degradation of GPX4.

Journal of molecular medicine (Berlin, Germany)·2026
Same journal

Clinical utility of cerebrospinal fluid interleukin-10 in central nervous system lymphoma: a molecular neuropathology-informed diagnostic meta-analysis.

Journal of molecular medicine (Berlin, Germany)·2026
See all related articles

Mouse models with mutations in extracellular matrix (ECM) genes offer insights into development and disease. Studying these ECM gene mutations in mice aids in understanding human conditions and discovering novel protein functions.

Area of Science:

  • Biochemistry
  • Genetics
  • Developmental Biology

Background:

  • Extracellular matrix (ECM) proteins are crucial for tissue structure and function.
  • Genetic mutations in ECM proteins can lead to various developmental abnormalities and diseases.
  • Mouse models are valuable tools for studying gene function and disease mechanisms.

Purpose of the Study:

  • To compile and review all known mouse strains with spontaneous and induced mutations in ECM genes.
  • To analyze the phenotypes of these mutant mice and compare them to human diseases.
  • To highlight the insights gained regarding the roles of ECM proteins in development and disease.

Main Methods:

  • Literature review of spontaneous and experimentally induced mutations in ECM genes in mice.

Related Experiment Videos

  • Phenotypic analysis of described mouse models.
  • Comparative analysis of mouse phenotypes and human diseases associated with ECM gene mutations.

    • Main Results:

    • Various mouse strains with ECM gene mutations have elucidated ECM protein roles in development.
    • Some mutations confirmed links between ECM genes and human diseases.
    • Unexpected phenotypes in certain mouse models revealed novel ECM protein functions.
    • Null mutations in some ECM genes resulted in no observable phenotype, posing challenges for function discovery.

    Conclusions:

    • Mouse models of ECM gene mutations are instrumental in understanding ECM protein functions.
    • These models aid in validating human disease links and identifying new therapeutic targets.
    • Further research is needed to elucidate the functions of ECM genes with no apparent phenotypic alterations in mice.