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Smooth-muscle contraction without smooth-muscle myosin
TLDR
It is proposed that, in neonatal smooth muscle phase 1 is generated by recruitment of smooth-muscles myosin heavy chain, whereas phase 2 can be generated by activation of non-muscle myos in heavy chain. Expand
Small Molecule AKAP-Protein Kinase A (PKA) Interaction Disruptors That Activate PKA Interfere with Compartmentalized cAMP Signaling in Cardiac Myocytes*
TLDR
FMP-API-1 represents not only a novel means to study compartmentalized cAMP/PKA signaling but, due to its effects on cardiac myocytes and intact hearts, provides the basis for a new concept in the treatment of chronic heart failure. Expand
The carboxyl‐terminal region of ahnak provides a link between cardiac L‐type Ca2+ channels and the actinbased cytoskeleton
TLDR
The results suggest that ahnak provides a structural basis for the subsarcolemmal cytoarchitecture and confers the regulatory role of the actin‐based cytoskeleton to the L‐type Ca2+ channel. Expand
L‐type calcium channel expression depends on the differentiated state of vascular smooth muscle cells
TLDR
The data suggest that regulation of ion channel expression during differentiation may have physiological importance for normal smooth muscle function and may influence VSMC behavior under pathophysiological conditions. Expand
Regulation of human heart contractility by essential myosin light chain isoforms.
TLDR
The expression of ALC-1 in the human heart modulates cross-bridge cycling kinetics accelerating shortening velocity and isometric tension production. Expand
Molecular mechanisms of early electrical remodeling: transcriptional downregulation of ion channel subunits reduces I(Ca,L) and I(to) in rapid atrial pacing in rabbits.
TLDR
L-type calcium current and I(to) are reduced in early phases of electrical remodeling, a major mechanism appears to be transcriptional downregulation of underlying ion channels, which partially preceded ion current changes. Expand
L-type calcium channels in insulin-secreting cells: biochemical characterization and phosphorylation in RINm5F cells.
TLDR
It is concluded that alpha1C is a major constituent of dihydropyridine-labeled LTCCs in RINm5F cells, its long form serving as a substrate for cAMP-dependent protein kinase. Expand
The carboxyl‐terminal ahnak domain induces actin bundling and stabilizes muscle contraction
TLDR
The results suggest that the carboxyl‐terminal ahnak domain exerts a stabilizing effect on muscle contractility via its interaction with actin of thin filaments. Expand
Atrial Glutathione Content, Calcium Current, and Contractility*
TLDR
S-Nitrosylation may contribute to the glutathione-sensitive attenuation of ICa,L observed in AF, and the biotin switch technique was used to evaluate S-nitrosylated of calcium channels. Expand
Modulation of the smooth-muscle L-type Ca2+ channel alpha1 subunit (alpha1C-b) by the beta2a subunit: a peptide which inhibits binding of beta to the I-II linker of alpha1 induces functional
TLDR
The results demonstrate that the beta2a subunit controls fast gating ofalpha1C-b channels, and suggest the alpha1-beta interaction domain in the cytoplasmic I-II linker of alpha1C (AID) as a possible target of modulation of the channel. Expand
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