Acute Suppression of Inwardly Rectifying Kir2.1 Channels by Direct Tyrosine Kinase Phosphorylation

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Structured PICO

Population

Mammalian tsA-201 cells, rat basophilic leukocytes, and Xenopus oocytes expressing wild-type or mutant (Y242F) Kir2.1 channels

Intervention

Exposure to perorthovanadate (100 microM), genistein (100 microM), nerve growth factor (0.5 microgram/ml), epidermal growth factor, or insulin

Comparator

Untreated cells or cells expressing mutant Kir2.1Y242F channels

Outcome

Currents through Kir2.1 channelssurrogate

Kir2.1 channels are direct substrates for tyrosine kinases, leading to acute suppression of their currents by neurotrophic growth factors.

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Supports Kir2.1 as tyrosine kinase substrate; hypothesis-generating for growth factor effects on cardiac excitability.

Wischmeyer et al. (1998) studied this question.

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