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Example sentences for: dhpr
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The mechanism by which the DHPR signals the RyR1 is poorly understood [ 12 13 ] . Domains in the cytoplasmic linker between repeats II and III have been clearly implicated [ 14 15 16 17 18 19 ] , and some regions such as Thr671-Lue690 were suggested to trigger RyR1 opening by binding to RyR1 [ 15 ] . However, extensive deletions within the II-III linker that eliminate the RyR1 binding region, and other suggested signaling regions in the II-III loop [ 16 ] , do not entirely eliminate EC coupling [ 20 21 ] . Hence additional domains of α 1S and/or other DHPR subunits appear to be engaged by the voltage sensor and contribute to an EC coupling signal.
Hence, a premature stop codon in the II-III loop upstream of M701 may not necessarily cause a loss of DHPR function because in these cases, function would be recovered by complementation between protein fragments expressed by the same cDNA.
The dihydropyridine receptor (DHPR) of skeletal muscle consists of α 1S , α 2 , β 1a and γ 1 subunits [ 1 ] . The α 1 subunit is a large four-repeat transmembrane protein of ~220 KDa that contains the basic functional elements of the L-type Ca 2+channel, including the Ca 2+selective pore and S4 "voltage-sensing" transmembrane segments in each of the four internal repeats [ 2 ] . β subunits are ~65 kDa cytosolic proteins essential for membrane trafficking, modulation of channel kinetics, and for excitation-contraction (EC) coupling [ 3 4 ] . The α 2 subunit is a highly glycosylated ~175 kDa protein formed by two disulfide-linked peptides [ 5 ] , whereas the γ 1 subunit is a ~32 kDa skeletal muscle-specific protein of four presumptive transmembrane domains with almost unknown function [ 6 7 ] .
The impact of the γ 1 null mutation on myotube EC coupling was inferred from intramembrane charge movements, the bulk of which have been shown to originate from the DHPR voltage sensor [ 27, 28].
To measure DHPR charge movements and to separate these charge movements from those produced by other voltage-gated channels, a) ionic currents were blocked; b) the linear component of the cell capacity was subtracted using a P/4 procedure and by analog compensation; and c) we used a pulse protocol that eliminated the immobilization-sensitive charge movements from voltage-gated Na +channels and presumably also from T-type Ca 2+channels.
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