Varaico: Literature-Extracted Genetic Variants

Gene:KCNA5
Variant:p.V512A
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KCNA5

NM_002234.4:p.V512A

Associated Papers

Open channel block of Kv1.5 channels by HMQ1611.

Dong C et al.

Frontiers in Pharmacology, 2022

Identification of Verapamil Binding Sites Within Human Kv1.5 Channel Using Mutagenesis and Docking Simulation.

Ding WG et al.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology, 2019

Regulation of human cardiac Kv1.5 channels by extracellular acidification.

Wang S et al.

Pflugers Archiv : European Journal of Physiology, 2016

Putative binding sites for arachidonic acid on the human cardiac Kv 1.5 channel.

Bai JY et al.

British Journal of Pharmacology, 2015

High-throughput analysis of drug binding interactions for the human cardiac channel, Kv1.5.

Karczewski J et al.

Biochemical Pharmacology, 2009

Structural basis for competition between drug binding and Kvbeta 1.3 accessory subunit-induced N-type inactivation of Kv1.5 channels.

Decher N et al.

Molecular Pharmacology, 2005

Molecular basis for Kv1.5 channel block: conservation of drug binding sites among voltage-gated K+ channels.

Decher N et al.

The Journal of Biological Chemistry, 2004

Regulation of N- and C-type inactivation of Kv1.4 by pHo and K+: evidence for transmembrane communication.

Li X et al.

American Journal of Physiology. Heart and Circulatory Physiology, 2003

Mutations throughout the S6 region of the hKv1.5 channel alter the stability of the activation gate.

Rich TC et al.

American Journal of Physiology. Cell Physiology, 2002

Distinct domains of the voltage-gated K+ channel Kv beta 1.3 beta-subunit affect voltage-dependent gating.

Uebele VN et al.

The American Journal of Physiology, 1998

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Regarding the variants extracted from papers and shown text snippets from research papers, the following holds: "Some rights reserved. This work permits non-commercial use, distribution and reproduction in any medium, provided the original author and source are credited."