Trafficking-deficient long QT syndrome mutation KCNQ1-T587M confers severe clinical phenotype by impairment of KCNH2 membrane localization: Evidence for clinically significant IKr-IKs α-subunit interaction-Reference-Cited by-同舟云学术

Trafficking-deficient long QT syndrome mutation KCNQ1-T587M confers severe clinical phenotype by impairment of KCNH2 membrane localization: Evidence for clinically significant IKr-IKs α-subunit interaction

Published:2009-12 Issue:12 Volume:6 Page:1792-1801
ISSN:1547-5271
Container-title:Heart Rhythm
language:en
Short-container-title:Heart Rhythm

Author:

Biliczki Peter,Girmatsion Zenawit,Brandes Ralf P.,Harenkamp Sabine,Pitard Bruno,Charpentier Flavien,Hébert Terence E.,Hohnloser Stefan H.,Baró Isabelle,Nattel Stanley,Ehrlich Joachim R.

Publisher

Elsevier BV

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine

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4. A common genetic variant in the NOS1 regulator NOS1AP modulates cardiac repolarization;Arking;Nat Genet,2006

5. Cellular properties of C-terminal KCNH2 long QT syndrome mutations: description and divergence from clinical phenotypes;Biliczki;Heart Rhythm,2008

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