Inhibition of the K + channel Kv1.4 by acidosis: protonation of an extracellular histidine slows the recovery from N‐type inactivation

Author:

Claydon T. W.1,Boyett M. R.1,Sivaprasadarao A.1,Ishii K.2,Owen J. M.1,O'Beirne H. A.1,Leach R.3,Komukai K.1,Orchard C. H.1

Affiliation:

1. Schools of Biomedical Sciences, University of Leeds, Leeds LS2 9JT, UK

2. Department of Pharmacology, Yamagata University School of Medicine, 2‐2‐2 Iida‐nishi, Yamagata 990‐9585, Japan

3. Biochemistry and Molecular Biology, University of Leeds, Leeds LS2 9JT, UK

Publisher

Wiley

Subject

Physiology

Reference25 articles.

1. Functional Knockout of the Transient Outward Current, Long-QT Syndrome, and Cardiac Remodeling in Mice Expressing a Dominant-Negative Kv4 α Subunit

2. Distinct Transient Outward Potassium Current (Ito) Phenotypes and Distribution of Fast-inactivating Potassium Channel Alpha Subunits in Ferret Left Ventricular Myocytes

3. Comparison of the effects of acidosis on cloned transient outward K+ channels fKv1.4 and rKv4.2 from ferret and rat ventricle;Claydon T. W.;The Journal of Physiology,1999

4. Cloning and characterization of an Ito‐like potassium channel from ferret ventricle;Comer M. B.;American Journal of Physiology,1994

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