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Niels Decher

Researcher at University of Marburg

Publications -  113
Citations -  5891

Niels Decher is an academic researcher from University of Marburg. The author has contributed to research in topics: Potassium channel & Medicine. The author has an hindex of 35, co-authored 94 publications receiving 5156 citations. Previous affiliations of Niels Decher include University of Utah & Aventis Pharma.

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Ca(V)1.2 calcium channel dysfunction causes a multisystem disorder including arrhythmia and autism.

TL;DR: Functional expression reveals that G406R produces maintained inward Ca(2+) currents by causing nearly complete loss of voltage-dependent channel inactivation, which likely induces intracellular Ca( 2+) overload in multiple cell types.
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Severe arrhythmia disorder caused by cardiac L-type calcium channel mutations

TL;DR: In this article, the authors identified de novo missense mutations in exon 8 of the spliced form of CaV1.2 in both individuals, which resulted in extreme prolongation of the QT interval on electrocardiogram.
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DCPIB is a novel selective blocker of ICl,swell and prevents swelling‐induced shortening of guinea‐pig atrial action potential duration

TL;DR: It is concluded that swelling‐induced AP shortening in isolated atrial cells is mainly caused by activation of ICl,swell, and DCPIB is a valuable pharmacological tool to study the role of I Cl, Swell in cardiac excitability under pathophysiological conditions leading to cell swelling.
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The pore structure and gating mechanism of K2P channels: K2P channel gating

TL;DR: In this paper, quaternary ammonium (QA) ions bind with high affinity deep within the pore of TREK-1 and have free access to their binding site before channel activation by intracellular pH or pressure.
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The acid-sensitive potassium channel TASK-1 in rat cardiac muscle.

TL;DR: It is suggested that in rat cardiomyocytes I(TASK) makes a substantial contribution to the outward current flowing in the plateau range of potentials and that this current component can be inhibited via alpha1A-adrenergic receptors.