Electrophysiologic consequences of KATP gain of function in the heart: Conduction abnormalities in Cantu syndrome.
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K(ATP) channel gain-of-function leads to increased myocardial L-type Ca(2+) current and contractility in Cantu syndrome.Adenosine Triphosphate-Sensitive Potassium Currents in Heart Disease and Cardioprotection.MiR-20 regulates myocardiac ischemia by targeting KATP subunit Kir6.1.Potassium channels in the heart: structure, function and regulation.Cantu syndrome-associated SUR2 (ABCC9) mutations in distinct structural domains result in KATP channel gain-of-function by differential mechanisms.Ectopic overexpression of Kir6.1 in the mouse heart impacts on the life expectancy
P2860
Electrophysiologic consequences of KATP gain of function in the heart: Conduction abnormalities in Cantu syndrome.
description
2015 nî lūn-bûn
@nan
2015年の論文
@ja
2015年論文
@yue
2015年論文
@zh-hant
2015年論文
@zh-hk
2015年論文
@zh-mo
2015年論文
@zh-tw
2015年论文
@wuu
2015年论文
@zh
2015年论文
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name
Electrophysiologic consequence ...... normalities in Cantu syndrome.
@en
Electrophysiologic consequence ...... normalities in Cantu syndrome.
@nl
type
label
Electrophysiologic consequence ...... normalities in Cantu syndrome.
@en
Electrophysiologic consequence ...... normalities in Cantu syndrome.
@nl
prefLabel
Electrophysiologic consequence ...... normalities in Cantu syndrome.
@en
Electrophysiologic consequence ...... normalities in Cantu syndrome.
@nl
P2093
P2860
P1433
P1476
Electrophysiologic consequence ...... normalities in Cantu syndrome.
@en
P2093
Colin G Nichols
Dorothy K Grange
Gautam K Singh
Haixia Zhang
P2860
P304
P356
10.1016/J.HRTHM.2015.06.042
P577
2015-06-30T00:00:00Z