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- W1593270900 abstract "Muscular dysgenesis (mdg) is a lethal autosomal, recessive mutation of mice. Skeletal muscle from dysgenic mice is paralyzed due to the failure of excitation-contraction (E-C) coupling. Considerable evidence indicates that this failure results from the absence of a specific gene product, the α1 subunit of the skeletal muscle receptor for dihydropyridine calcium channel modifiers. This dihydropyridine receptor is hypothesized to function in E-C coupling of normal skeletal muscle as the voltage sensor that triggers calcium release from the sarcoplasmic reticulum and thereby causes contraction. The skeletal muscle dihydropyridine receptor is also postulated to function as the ion channel responsible for a slowly activating, dihydropyridine-sensitive calcium current (Islow). Dysgenic skeletal muscle lacks Islow but expresses, at low levels, a distinctly different dihydropyridine-sensitive calcium current (Idys). The channel protein underlying Idys is incapable of serving as a voltage sensor for E-C coupling. Studies using dysgenic skeletal muscle have provided significant insight into the role of dihydropyridine receptors in E-C coupling.— Adams, B. A.; Beam, K. G. Muscular dysgenesis: a model system for studying excitation-contraction coupling. FASEB J. 4: 2809-2816; 1990." @default.
- W1593270900 created "2016-06-24" @default.
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- W1593270900 date "1990-07-01" @default.
- W1593270900 modified "2023-09-28" @default.
- W1593270900 title "Muscular dysgenesis in mice: a model system for studying excitation‐contraction coupling" @default.
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- W1593270900 doi "https://doi.org/10.1096/fasebj.4.10.2165014" @default.
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