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• W2031489794 abstract "FEBS LettersVolume 368, Issue 3 p. 405-410 Full-length articleFree Access Endogenous cardiac Ca2+ channels do not overcome the E-C coupling defect in immortalized dysgenic muscle cells: evidence for a missing link First published: July 24, 1995 https://doi.org/10.1016/0014-5793(95)00697-8Citations: 2AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Abstract The expression of subunit genes of the Ca2+ channel complex was studied in differentiating, immortalized mouse mdg cells. These cells expressedα1 andα2/δ transcripts of the skeletal muscle Ca2+ channel genes, a cardiac Ca2+ channelα1 subunit gene and several known transcript variants of skeletal, cardiac and brain β genes. The mdg mutation is retained in the 129DA3 cell line and occurs exclusively at nucleotide position 4010 in the skeletalα1 transcript in which a cytosine residue is deleted. In early stages of differentiation and fusion, Ba2+ currents were detected in dysgenic myotubes the same as the cardiac L-type Ca2+ channel. These data provide specific structural evidence [Chaudhari, N. (1992) J. Biol. Chem. 267, 25636–25639] for the major genetic defect in mouse muscular dysgenesis and show a change in the expression levels ofα1c andα1c.The upregulation of the expression ofα1c results in functional Ca2+ channel activity, however, presumably not sufficient for excitation-contraction coupling. Reference [1] Glueckson-Waelsch S., Science, 142, (1963), 1269– 1279. [2] Pai A.C., Dev. 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• W2031489794 title "Endogenous cardiac Ca2+channels do not overcome the E-C coupling defect in immortalized dysgenic muscle cells: evidence for a missing link" @default.
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