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The Role of Kir2.1 in the Genesis of Native Cardiac Inward‐Rectifier K + Currents during Pre‐ and Postnatal Development
Author(s) -
NAKAMURA TOMOE Y.,
LEE KAREN,
ARTMAN MICHAEL,
RUDY BERNARDO,
COETZEE WILLIAM A.
Publication year - 1999
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1999.tb11308.x
Subject(s) - knockout mouse , biology , gene , inward rectifier potassium ion channel , microbiology and biotechnology , myocyte , potassium channel , fetus , chemistry , biophysics , genetics , ion channel , pregnancy , receptor
Our results demonstrate that (a) the Kir2.1 gene encodes a native K+ channel protein with a 21-pS conductance; (b) this channel has an important role in the genesis of adult ventricular 1K1; and (c) the contribution of Kir2.1 channel proteins to 1K1 changes during development. The lack of contribution of Kir2.1 to fetal 1K1 channels is interesting from the point of view of possible future generation of knockout mice lacking Kir2.1, since cardiac abnormalities would not be expected to result in fetal lethality. These observations provide further support for a generalized hypothesis that different genes may code for 1K1 channel proteins at various developmental stages. However, the effects of these AS-oligos must first be examined on native 1K1 channels in cardiac myocytes before definite conclusions can be reached.