Calmodulin Is Essential for Cardiac I KS Channel Gating and Assembly
نویسندگان
چکیده
منابع مشابه
Calmodulin is essential for cardiac IKS channel gating and assembly: impaired function in long-QT mutations.
The slow IKS K+ channel plays a major role in repolarizing the cardiac action potential and consists of the assembly of KCNQ1 and KCNE1 subunits. Mutations in either KCNQ1 or KCNE1 genes produce the long-QT syndrome, a life-threatening ventricular arrhythmia. Here, we show that long-QT mutations located in the KCNQ1 C terminus impair calmodulin (CaM) binding, which affects both channel gating a...
متن کاملEF hands at the N-lobe of calmodulin are required for both SK channel gating and stable SK–calmodulin interaction
Small conductance calcium-activated potassium (SK) channels respond to intracellular Ca(2+) via constitutively associated calmodulin (CaM). Previous studies have proposed a modular design for the interaction between CaM and SK channels. The C-lobe and the linker of CaM are thought to regulate the constitutive binding, whereas the N-lobe binds Ca(2+) and gates SK channels. However, we found that...
متن کاملIntracellular ATP binding is required to activate the slowly activating K+ channel I(Ks).
Gating of ion channels by ligands is fundamental to cellular function, and ATP serves as both an energy source and a signaling molecule that modulates ion channel and transporter functions. The slowly activating K(+) channel I(Ks) in cardiac myocytes is formed by KCNQ1 and KCNE1 subunits that conduct K(+) to repolarize the action potential. Here we show that intracellular ATP activates heterolo...
متن کاملCardiac-enriched LIM domain protein fhl2 is required to generate I(Ks) in a heterologous system.
OBJECTIVE Co-expression of the KvLQT1 and minK potassium channel subunits is required to recapitulate I(Ks), the slow component of the cardiac delayed rectifier current, and mutations in either gene cause the congenital Long QT syndrome. It is becoming increasingly well-recognized that multiprotein channel complexes containing proteins capable of modulating channel function assemble at the plas...
متن کاملThe cardiac sodium channel: gating function and molecular pharmacology.
Cardiac sodium (Na) channels are dynamic molecules that undergo rapid structural changes in response to the changing electrical field in the myocardium. Inherited mutations in SCN5A, the gene encoding the cardiac Na channel, provoke life-threatening cardiac arrhythmias, often by modifying these voltage-dependent conformational changes. These disorders (i.e. the long QT syndrome and Brugada synd...
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ژورنال
عنوان ژورنال: Circulation Research
سال: 2006
ISSN: 0009-7330,1524-4571
DOI: 10.1161/01.res.0000218979.40770.69