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Article
Moradeke A. Bamgboye, Kevin G. Herold, Daiana C.O. Vieira, Maria K. Traficante, Philippa J. Rogers, Manu Ben-Johny, Ivy E. Dick
Human mutations in CaV1.2 underlie life-threatening arrhythmias and neurodevelopmental disorders. Through in-depth biophysical analysis, this study identifies divergent mechanistic alterations linked to CaV1.2 channelopathies and reveals an association between changes in channel function and patient phenotypes.
Article | Excitation–Contraction Coupling
Pompeo Volpe, Alessandra Bosutti, Alessandra Nori, Riccardo Filadi, Gaia Gherardi, Gabor Trautmann, Sandra Furlan, Gabriele Massaria, Marina Sciancalepore, Aram Megighian, Paola Caccin, Annalisa Bernareggi, Michele Salanova, Roberta Sacchetto, Dorianna Sandonà, Paola Pizzo, Paola Lorenzon
The present study reports on a novel effect of denervation at the neuromuscular junction level. It shows that the absence of nerve causes a reduction in the subsynaptic type 1 inositol 1,4,5-trisphosphate-stained region likely involved in the stabilization of the endplate.
Article | Mechanotransduction by Membrane Proteins
Jamison L. Nourse, Vivian M. Leung, Hamid Abuwarda, Elizabeth L. Evans, Esmeralda Izquierdo-Ortiz, Alan T. Ly, Nguyen Truong, Samantha Smith, Harsh Bhavsar, Gabriella Bertaccini, Edwin S. Monuki, Mitradas M. Panicker, Medha M. Pathak
PIEZO1, a mechanically gated ion channel, transduces mechanical cues in neural stem cells. Here, we show the impact of Piezo1 knockout on neural development in vivo and find that cholesterol biosynthesis and lipid membrane composition are regulated by Piezo1.
Article
Jennifer Osten, Maral Mohebbi, Petra Uta, Faramarz Matinmehr, Tianbang Wang, Theresia Kraft, Mamta Amrute-Nayak, Tim Scholz
Compared to the “ventricular” essential myosin light chain MLC1sb/v, the longer and more positively charged MLC1sa present in slow-twitch M. soleus fibers decelerates actin filament gliding on β-myosin molecules presumably by a decreased dissociation rate from actin filaments.
Article
Megan Jean Hammell, Linda Kachmar, Zsombor Balassy, Gijs IJpma, Anne-Marie Lauzon
Using a novel assay chamber to inject myosin light chain phosphatase during laser trap measurements, tonic smooth muscle force maintenance is observed at the myosin molecular level, marking an important step toward elucidating the underlying mechanisms of the latch state.
Article | Excitation–Contraction Coupling
Anna V. Maltsev, Michael D. Stern, Victor A. Maltsev
The present numerical modeling study shows that disorder in locations of Ca release units in cardiac pacemaker cells has substantial functional impact by creating release clusters, similar to Poisson clumping, and opportunity of Ca release to propagate within the clusters.
Article | Excitation–Contraction Coupling
Maricela García-Castañeda, Antonio Michelucci, Nan Zhao, Sundeep Malik, Robert T. Dirksen
Postdevelopmental, muscle-specific ablation of Orai1 in mdx mice abolishes excessive constitutive and store-operated Ca2+ entry, improves muscular dystrophy pathology, and promotes sarcolemmal integrity, thus demonstrating an important role of enhanced Orai1-mediated Ca2+ entry in exacerbating the dystrophic phenotype.

Related Articles from Rockefeller University Press

Issue Cover
Current Issue
Volume 154,
Issue 10,
3 October 2022
Reviews & Opinions
Viewpoint
Lawrence G. Palmer
The kidneys regulate transport of Na+ and K+ in complex ways to maintain the overall economies of both ions simultaneously.
Editorial | Excitation–Contraction Coupling
Robert T. Dirksen, David A. Eisner, Eduardo Ríos, Karin R. Sipido
The term “excitation–contraction (EC) coupling” was introduced by Alexander Sandow ( Sandow, 1952 ) as “the entire sequence of reactions—excitation, inward acting link, and activation of contraction”—in skeletal muscle. It is evidence of Sandow’s foresight that 70 years later, a large community of researchers still ...
Review | Excitation–Contraction Coupling
Daniela Rossi, Maria Rosaria Catallo, Enrico Pierantozzi, Vincenzo Sorrentino
This review provides an up-to-date overview of current knowledge on myopathies caused by mutations in proteins participating in excitation–contraction coupling and store-operated Ca2+ entry mechanisms in skeletal muscle.

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