Suppression of Kir2.3 Activity by Protein Kinase C Phosphorylation of the Channel Protein at Threonine 53

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Population

Xenopus oocytes expressing recombinant and mutant Kir2.3 channels

Comparison

Phorbol 12-myristate 13-acetate and… vs Wild-type Kir2.3 and Kir2.1 channels

Design

Preclinical

Authors

Discussion

Establishes Thr53 as the PKC site in Kir2.3; hypothesis-generating for cardiac excitability and arrhythmia mechanisms.

Population

Xenopus oocytes expressing recombinant and mutant Kir2.3 channels

Intervention

Phorbol 12-myristate 13-acetate (PMA) and site-directed mutagenesis (chimeras with Kir2.1, point mutations at S5, S36, S39, T53)

Comparator

Wild-type Kir2.3 and Kir2.1 channels

Outcome

Whole-cell Kir currents (channel sensitivity to PMA)surrogate

Threonine 53 is the specific protein kinase C phosphorylation site responsible for the suppression of Kir2.3 channel activity.

Zhu et al. (1999) studied this question.

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