Key result
An alpha(1S) subunit with a scrambled sequence in residues 681-690 restored calcium currents and skeletal-type EC coupling indistinguishably from wild-type alpha(1S) in dysgenic myotubes.
Why the study?
Does scrambling residues 681-690 of the DHPR alpha(1S) II-III loop affect excitation-contraction coupling in dysgenic myotubes?
Population
Dysgenic myotubes (which lack endogenous alpha(1S) dihydropyridine receptor subunit)
Comparison
Expression of an intact alpha subunit with… vs Wild-type alpha(1S)
Design
Preclinical
Authors
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Residues 681-690 are dispensable for DHPR function in myotubes; leaves open the minimal II-III loop determinants of skeletal EC coupling.
Does scrambling residues 681-690 of the DHPR alpha(1S) II-III loop affect excitation-contraction coupling in dysgenic myotubes?
Residues 681-690 of the DHPR alpha(1S) II-III loop are not essential for normal functioning of the DHPR, including skeletal-type EC coupling and retrograde signaling in muscle cells.
Proenza et al. (2000) studied Dysgenic myotubes lacking endogenous alpha(1S). alpha(1S) subunit with scrambled sequence in residues 681-690 (alpha(1S)-scr) vs. Wild-type alpha(1S) was evaluated on Restoration of calcium currents, skeletal-type EC coupling, and release of intracellular Ca(2+). An alpha(1S) subunit with a scrambled sequence in residues 681-690 restored calcium currents and skeletal-type EC coupling indistinguishably from wild-type alpha(1S) in dysgenic myotubes.
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