Aims L-type Ca2+ channels (LTCCs) in adult cardiomyocytes are localized to t-tubules
where they initiate excitation-contraction coupling. Our recent work has shown that a …

Rationale: The source of Ca2+ to activate pathological cardiac hypertrophy is not clearly
defined. Ca2+ influx through the L-type Ca2+ channels (LTCCs) determines “contractile” …

Activation of CaMKII induces a myriad of biological processes and plays dominant roles in
cardiac hypertrophy. Caveolar microdomain contains many calcium/calmodulin-dependent …

Cardiac hypertrophy is a major risk for the progression of heart failure; however, the
underlying molecular mechanisms contributing to this process remain elusive. The caveolae …

Objective: Caveolae, flask shaped invaginations of the cell membrane, influence signalling
cascades in many cell types. We have tested the hypothesis that caveolae modulate …

L-type Ca channels (LTCC), which play a key role in cardiac excitation–contraction coupling,
are located predominantly at the transverse (t-) tubules in ventricular myocytes. Caveolae …

Caveolins are important components of caveolae, which have been implicated in vesicular
trafficking and signal transduction. To investigate the in vivo significance of Caveolins in …

L-type Ca2+ channels play a critical role in regulating Ca2+-dependent signaling in cardiac
myocytes, including excitation-contraction coupling; however, the subcellular localization of …

Caveolin, a major protein component of caveolae, directly interacts with multiple signaling
molecules, such as Ras and growth factor receptors, and inhibits their function. However, the …

Pathological cardiac hypertrophy is characterized by subcellular remodeling of the
ventricular myocyte with a reduction in the scaffolding protein caveolin-3 (Cav-3), altered Ca …