June 11, 1996Proceedings of the National Academy of SciencesOpen Access

Receptor stimulation causes slow inhibition of IRK1 inwardly rectifying K+ channels by direct protein kinase A-mediated phosphorylation.

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Structured PICO

Population

Mammalian COS-7 cells heterologously expressing cloned rat IRK1 (Kir 2.1) channels and serotonin type 1A receptors

Intervention

Serotonin receptor agonists, internal perfusion with GTP[gamma-S], elevation of internal cAMP, or addition of catalytic subunits of protein kinase A (PKA)

Comparator

Mutant IRK1(S425N) channels lacking a C-terminal PKA phosphorylation site

Outcome

Inhibition of IRK1 channel activity measured by whole-cell patch-clampsurrogate

Serotonin may negatively control IRK1 channel activity in the nervous system through direct PKA-mediated phosphorylation.

Discussion

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Implication

May mediate serotonergic IRK1 control in neurons; hypothesis-generating for excitability disorders, needs in vivo confirmation.

Cite This Study

Wischmeyer et al. (1996) studied this question.

synapsesocial.com/papers/6a8a592f2a1069eaeccbf264 https://doi.org/10.1073/pnas.93.12.5819

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Receptor stimulation causes slow inhibition of IRK1 inwardly rectifying K+ channels by direct protein kinase A-mediated phosphorylation.

Structured PICO

Discussion

Implication

Cite This Study

Receptor stimulation causes slow inhibition of IRK1 inwardly rectifying K+ channels by direct protein kinase A-mediated phosphorylation.

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Also Consider