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Regulation of the cloned L‐type cardiac calcium channel by cyclic‐AMP‐dependent protein kinase
Author(s) -
Perez-Reyes Edward,
Yuan Weilong,
Wei Xiangyang,
Bers Donald M.
Publication year - 1994
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 - 10.1016/0014-5793(94)80484-2
Subject(s) - protein kinase a , chemistry , l type calcium channel , calcium , calcium channel , n type calcium channel , microbiology and biotechnology , biochemistry , kinase , biology , t type calcium channel , organic chemistry
Hormones can regulate cardiac L‐type Ca 2+ channels via cAMP‐dependent protein kinase (PKA) phosphorylation. However, regulation of the cloned L‐type Ca 2+ channel has been difficult to demonstrate conclusively. We stably transfected a human embryonic kidney (HEK‐293) cell with the cardiac α 1 andβ 2 subunits, then examined PKA modulation of the α 2+ current. Although forskolin did not increase basal Ca 2+ current, the PKA inhibitors, H‐89 and Rp‐cAMPS, could inhibit basal current. We reversed H‐89 inhibition with either forskolin or okadaic acid. We conclude that the channel was phosphorylated under basal conditions, and that inhibition of PKA allowed dephosphorylation. These studies demonstrate that reversible PKA regulation of cloned Ca 2+ channels can be studied in HEK‐293 cells.