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Increased tolerance to stress in cardiac expressed gain-of-function of adenosine triphosphate-sensitive potassium channel subunit Kir6.1.

Identifieur interne : 000F70 ( Main/Exploration ); précédent : 000F69; suivant : 000F71

Increased tolerance to stress in cardiac expressed gain-of-function of adenosine triphosphate-sensitive potassium channel subunit Kir6.1.

Auteurs : Matthew C. Henn [États-Unis] ; M Burhan Janjua [États-Unis] ; Haixia Zhang [États-Unis] ; Evelyn M. Kanter [États-Unis] ; Carol M. Makepeace [États-Unis] ; Richard B. Schuessler [États-Unis] ; Colin G. Nichols [États-Unis] ; Jennifer S. Lawton [États-Unis]

Source :

RBID : pubmed:27884343

Descripteurs français

English descriptors

Abstract

The adenosine triphosphate-sensitive potassium (KATP) channel opener diazoxide (DZX) prevents myocyte volume derangement and reduced contractility secondary to stress. KATP channels are composed of pore-forming (Kir6.1 or Kir6.2) and regulatory (sulfonylurea receptor, SUR1 or SUR2) subunits. Gain of function (GOF) of Kir6.1 subunits has been implicated in cardiac pathology in Cantu syndrome in humans (cardiomegaly, lymphedema, and pericardial effusions). We hypothesized that GOF of Kir6.1 subunits would result in altered myocyte response to stress.

DOI: 10.1016/j.jss.2016.08.043
PubMed: 27884343


Affiliations:


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Le document en format XML

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<term>Animals</term>
<term>Cardiomegaly (genetics)</term>
<term>Cardiomegaly (physiopathology)</term>
<term>Cell Size (drug effects)</term>
<term>Diazoxide (pharmacology)</term>
<term>Genetic Markers</term>
<term>Hypertrichosis (genetics)</term>
<term>Hypertrichosis (physiopathology)</term>
<term>KATP Channels (genetics)</term>
<term>KATP Channels (physiology)</term>
<term>Mice</term>
<term>Mice, Transgenic</term>
<term>Mutation</term>
<term>Myocytes, Cardiac (drug effects)</term>
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<term>Animaux</term>
<term>Canaux KATP (génétique)</term>
<term>Canaux KATP (physiologie)</term>
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<term>Cardiomégalie (physiopathologie)</term>
<term>Diazoxide (pharmacologie)</term>
<term>Hypertrichose (génétique)</term>
<term>Hypertrichose (physiopathologie)</term>
<term>Marqueurs génétiques</term>
<term>Mutation</term>
<term>Myocytes cardiaques ()</term>
<term>Myocytes cardiaques (physiologie)</term>
<term>Ostéochondrodysplasies (génétique)</term>
<term>Ostéochondrodysplasies (physiopathologie)</term>
<term>Souris</term>
<term>Souris transgéniques</term>
<term>Stress physiologique ()</term>
<term>Stress physiologique (physiologie)</term>
<term>Taille de la cellule ()</term>
<term>Vasodilatateurs (pharmacologie)</term>
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<term>KATP Channels</term>
</keywords>
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<term>Cardiomegaly</term>
<term>Hypertrichosis</term>
<term>Osteochondrodysplasias</term>
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<term>Canaux KATP</term>
<term>Cardiomégalie</term>
<term>Hypertrichose</term>
<term>Ostéochondrodysplasies</term>
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<term>Stress physiologique</term>
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<front>
<div type="abstract" xml:lang="en">The adenosine triphosphate-sensitive potassium (KATP) channel opener diazoxide (DZX) prevents myocyte volume derangement and reduced contractility secondary to stress. KATP channels are composed of pore-forming (Kir6.1 or Kir6.2) and regulatory (sulfonylurea receptor, SUR1 or SUR2) subunits. Gain of function (GOF) of Kir6.1 subunits has been implicated in cardiac pathology in Cantu syndrome in humans (cardiomegaly, lymphedema, and pericardial effusions). We hypothesized that GOF of Kir6.1 subunits would result in altered myocyte response to stress.</div>
</front>
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<name sortKey="Henn, Matthew C" sort="Henn, Matthew C" uniqKey="Henn M" first="Matthew C" last="Henn">Matthew C. Henn</name>
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