ANKRD1 activates the Wnt signaling pathway by modulating CAV3 expression and thus promotes BMSC osteogenic differentiation and bone formation in ovariectomized mice.
Nitrative Modification of Caveolin-3: A Novel Mechanism of Cardiac Insulin Resistance and a Potential Therapeutic Target Against Ischemic Heart Failure in Prediabetic Animals.
Cardiac myocyte specific overexpression of caveolin-3 (Cav-3) provides better cardiac contractile responses and less corrected QT prolongation during adrenergic stress in a cirrhotic cardiomyopathy model.
Caveolin-3 KO disrupts t-tubule structure and decreases t-tubular ICa density in mouse ventricular myocytes leading to cardiac hypertrophy and dysfunction.
Results provide evidence that cav-3 differentially organizes serotonergic and cholinergic signaling in airway smooth muscle through mechanisms that are specific for airways of certain caliber and anatomical position.
Data show that caveolin-3 binds to low glycosylated extracellular matrix metalloproteinase inducer (LG-EMMPRIN) in cardiac cells and in the hearts of healthy mice.
Data show increased expression of T-type Ca(2+) current and association of protein kinase C alpha (PKCalpha) with caveolin-3 (Cav-3)was disrupted in the hypertrophic ventricular myocyte.
We'd like to inform you that we have updated our Privacy Notice to comply with Europe’s new General Data Protection Regulation (GDPR) that applies since 25 May 2018.