کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1937395 | 1050715 | 2007 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Kcnq1 contributes to an adrenergic-sensitive steady-state K+ current in mouse heart
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
It has been suggested that Kcne1 subunits are required for adrenergic regulation of Kcnq1 potassium channels. However, in adult mouse hearts, which do not express Kcne1, loss of Kcnq1 causes a Long QT phenotype during adrenergic challenge, raising the possibility that native Kcnq1 currents exist and are adrenergically regulated even in absence of Kcne1. Here, we used immunoblotting and immunohistochemical staining to show that Kcnq1 protein is present in adult mouse hearts. Voltage-clamp experiments demonstrated that Kcnq1 contributes to a steady-state outward current (ISS) in wild-type (Kcnq1+/+) ventricular myocytes during isoproterenol stimulation, resulting in a significant 7.1% increase in ISS density (0.43 ± 0.16 pA/pF, p < 0.05, n = 15), an effect that was absent in Kcnq1-deficient (Kcnq1â/â) myocytes (â0.14 ± 0.13 pA/pF, n = 17). These results demonstrate for the first time that Kcnq1 protein is expressed in adult mouse hearts where it contributes to a β-adrenergic-induced component of ISS that does not require co-assembly with Kcne1.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 360, Issue 1, 17 August 2007, Pages 212-218
Journal: Biochemical and Biophysical Research Communications - Volume 360, Issue 1, 17 August 2007, Pages 212-218
نویسندگان
Bjorn C. Knollmann, Syevda Sirenko, Qi Rong, Alexander N. Katchman, Mathew Casimiro, Karl Pfeifer, Steven N. Ebert,