منابع مشابه
KCNQ1 assembly and function is blocked by long-QT syndrome mutations that disrupt interaction with calmodulin.
Calmodulin (CaM) has been recognized as an obligate subunit for many ion channels in which its function has not been clearly established. Because channel subunits associate early during channel biosynthesis, CaM may provide a mechanism for Ca(2+)-dependent regulation of channel formation. Here we show that CaM is a constitutive component of KCNQ1 K+ channels, the most commonly mutated long-QT s...
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ژورنال
عنوان ژورنال: Nature Reviews Immunology
سال: 2002
ISSN: 1474-1733,1474-1741
DOI: 10.1038/nri902