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Kir2.3 knock‐down decreases I K1 current in neonatal rat cardiomyocytes
Author(s) -
He Yusong,
Pan Qin,
Li Jun,
Chen Huaizhi,
Zhou Qinshu,
Hong Kui,
Brugada Ramon,
Perez Guillermo J.,
Brugada Pedro,
Chen Yi-Han
Publication year - 2008
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/j.febslet.2008.05.023
Subject(s) - inward rectifier potassium ion channel , potassium channel , knockout mouse , protein subunit , gene knockin , chemistry , protein expression , medicine , endocrinology , microbiology and biotechnology , biology , biochemistry , ion channel , gene , receptor
Inward rectifier potassium Kir2.x channels mediate cardiac inward rectifier potassium currents ( I K1 ). As a subunit of Kir2.x, the physiological role of Kir2.3 in native cardiomyocytes has not been reported. This study shows that Kir2.3 knock‐down remarkably down‐regulates Kir2.3 expression (Kir2.3 protein was reduced to 19.91 ± 3.24% on the 2nd or 3rd day) and I K1 current densities (at −120 mV, control vs. knock‐down: −5.03 ± 0.24 pA/pF, n = 5 vs. −1.16 ± 0.19 pA/pF, n = 7, P < 0.001) in neonatal rat cardiomyocytes. The data suggest that Kir2.3 plays a potentially important role in I K1 currents in neonatal rat cardiomyocytes.