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

TRPC4 and TRPC4-deficient mice.

Marc Freichel1, Stephan Philipp, Adolfo Cavalié

  • 1Experimentelle und Klinische Pharmakologie und Toxikologie, Medizinische Fakultät der Universität des Saarlandes, D 66421 Homburg, Germany.

Novartis Foundation Symposium
|April 24, 2004
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

JPT2/HN1L functions as an NAADP-binding protein in a cell-type-specific manner.

Cell calcium·2026
Same author

Loss of erythrocyte arginase-1 impairs vasorelaxation due to endothelial GSNOR overexpression and denitrosylation of G protein subunits.

Redox biology·2026
Same author

Activation of IRF3 in cardiomyocytes impairs mitochondrial oxidative function through PGC-1α inhibition and drives heart failure.

Nature communications·2026
Same author

ABE9 fused to SpRY Cas9 nickase enables precise generation of bystander free mouse models.

Scientific reports·2026
Same author

Adenosine-Specific Transcriptional Programs in Murine Connective Tissue-Type Mast Cells.

ACS pharmacology & translational science·2026
Same author

T-Cell-Derived Exosomes From Multi Core Granules Exhibit Superior Caspase-3-Mediated Tumor-Suppressive Activity Compared to Those From Multivesicular Bodies.

Journal of extracellular vesicles·2026
Same journal

Genetic and therapeutic control of diabetogenic CD8+ T cells.

Novartis Foundation symposium·2009
Same journal

Translating mucosal antigen based prevention of autoimmune diabetes to human.

Novartis Foundation symposium·2009
Same journal

Re-establishing immune tolerance in type 1 diabetes via regulatory T cells.

Novartis Foundation symposium·2009
Same journal

Immune markers of disease and therapeutic intervention in type 1 diabetes.

Novartis Foundation symposium·2009
Same journal

Towards a curative therapy in type 1 diabetes: remission of autoimmunity, maintenance and augmentation of beta cell mass.

Novartis Foundation symposium·2009
Same journal

CD8 and cytotoxic T cells in type 1 diabetes.

Novartis Foundation symposium·2009
See all related articles

Transient Receptor Potential Canonical 4 (TRPC4) channels are crucial for calcium signaling in endothelial cells. TRPC4 knockout mice reveal its essential role in vascular function and signaling pathways.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Physiology

Background:

  • Transient Receptor Potential (TRP) proteins regulate localized calcium (Ca2+) increases for signal transduction.
  • TRP channels are activated by complex mechanisms involving phospholipase C and phosphatidylinositol pathways.
  • Several TRP channels, including TRPC4, are expressed in mouse endothelial cells.

Purpose of the Study:

  • To investigate the role of TRPC4 in endothelial cell function.
  • To determine if TRPC4 acts as a channel-forming subunit or an essential activator.
  • To provide insights into the biological functions of TRPC4 using a TRPC4 knockout mouse model.

Main Methods:

  • Review of heterologously expressed TRPC4.
  • Analysis of the phenotype of TRPC4 knockout (TRPC4-/-) mice.

Related Experiment Videos

  • Investigation of agonist-induced Ca2+ entry and vascular responses.

    • Main Results:

    • TRPC4 is indispensable for agonist-induced Ca2+ entry in endothelial cells.
    • TRPC4 contributes significantly to agonist-induced vessel relaxation and microvascular permeability.
    • The TRPC4 knockout mouse model provides insights into its in vivo functions.

    Conclusions:

    • TRPC4 plays a critical role in endothelial cell calcium signaling and vascular physiology.
    • Further research is needed to fully elucidate TRPC4's precise function as a channel subunit or activator.
    • TRPC4 knockout mice are a valuable tool for studying TRPC4's biological significance.