Trafficking defect and proteasomal degradation contribute to the phenotype of a novel KCNH2 long QT syndrome mutation.

Trafficking defect and proteasomal degradation contribute to the phenotype of a novel KCNH2 long QT syndrome mutation.

The Kv11.1 (hERG) K+ channel plays a fundamental role in cardiac repolarization. Missense mutations in KCNH2, the gene encoding Kv11.1, cause long QT syndrome (LQTS) and frequently cause channel trafficking-deficiencies. This study characterized the properties of a novel KCNH2 mutation discovered in...

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Bibliographic Details
Main Authors: Anton Mihic, Vijay S Chauhan, Xiaodong Gao, Gavin Y Oudit, Robert G Tsushima
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2011-03-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3069070?pdf=render

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http://europepmc.org/articles/PMC3069070?pdf=render

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