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Channel activators regulate ATP‐sensitive potassium channel (KIR6.1) expression in chick cardiomyocytes
Author(s) -
Lu Changwan,
Halvorsen Stanley W
Publication year - 1997
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(97)00760-6
Subject(s) - pinacidil , glibenclamide , atp sensitive potassium channel , potassium channel , kir6.2 , microbiology and biotechnology , chemistry , myocyte , potassium channel opener , signal transduction , protein subunit , biophysics , biology , biochemistry , endocrinology , gene , diabetes mellitus
ATP‐sensitive potassium channels (K ATP ) are widely expressed and yet little is known about the mechanisms regulating their expression. Here we report that expression of chick heart Kir6.1 is regulated by channel activators. Activation of K ATP with either ATP depletion or pinacidil, up‐regulated Kir6.1 mRNA 1.8‐ to 2.4‐fold in cultured ventricular myocytes as measured by competitive PCR. Pinacidil treatment also increased Kir6.1 protein as detected using an antibody to Kir6.1. Glibenclamide, a K ATP inhibitor, completely blocked the pinacidil‐induced increase in Kir6.1 levels. It appears that Kir6.1 is up‐regulated by an unknown signal transduction pathway initiated by K ATP opening.