ArticleThe Journal of physiology2005
Protein kinase C shifts the voltage dependence of KCNQ/M channels expressed in Xenopus oocytes.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 43 citations in OpenAlex.
- Donepezil as a new therapeutic potential in KCNQ2- and KCNQ3-related autism.Frontiers in cellular neuroscience · 2024Article
- Phosphoproteomic of the acetylcholine pathway enables discovery of the PKC-β-PIX-Rac1-PAK cascade as a stimulatory signal for aversive learning.Molecular psychiatry · 2022Article
- PKC regulation of ion channels: The involvement of PIPThe Journal of biological chemistry · 2022Review
- A PIPCommunications biology · 2020Article
- Pharmacological Manipulation of KFrontiers in physiology · 2020Review
- Phosphatidylinositol 4,5-bisphosphate (PIPThe Journal of biological chemistry · 2018Article
- Protein kinase C activity is a protective modifier of Purkinje neuron degeneration in cerebellar ataxia.Human molecular genetics · 2018Article
- Updating In Vivo and In Vitro Phosphorylation and Methylation Sites of Voltage-Gated Kv7.2 Potassium Channels.Proteomics · 2017Article
- Phosphorylation regulates the sensitivity of voltage-gated Kv7.2 channels towards phosphatidylinositol-4,5-bisphosphate.The Journal of physiology · 2017Article
- The Voltage Activation of Cortical KCNQ Channels Depends on Global PIP2 Levels.Biophysical journal · 2016Article
- Differential protein kinase C-dependent modulation of Kv7.4 and Kv7.5 subunits of vascular Kv7 channels.The Journal of biological chemistry · 2014Article
- PIP2 regulation of KCNQ channels: biophysical and molecular mechanisms for lipid modulation of voltage-dependent gating.Frontiers in physiology · 2014Review
- The neuronal serum- and glucocorticoid-regulated kinase 1.1 reduces neuronal excitability and protects against seizures through upregulation of the M-current.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- KCNQ5 channels control resting properties and release probability of a synapse.Nature neuroscience · 2011Article
- Mass spectrometry-based phosphoproteomics reveals multisite phosphorylation on mammalian brain voltage-gated sodium and potassium channels.Seminars in cell & developmental biology · 2011Review
- Article
- Analysis and functional implications of phosphorylation of neuronal voltage-gated potassium channels.Neuroscience letters · 2010Review
- Protein Phosphatase 2a and glycogen synthase kinase 3 signaling modulate prepulse inhibition of the acoustic startle response by altering cortical M-Type potassium channel activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Cholesterol inhibits M-type K+ channels via protein kinase C-dependent phosphorylation in sympathetic neurons.The Journal of biological chemistry · 2010Article
- Functional study of the effect of phosphatase inhibitors on KCNQ4 channels expressed in Xenopus oocytes.Acta pharmacologica Sinica · 2009Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well established that stimulation of G(q)-coupled receptors such as the M1 muscarinic acetylcholine receptor inhibits KCNQ/M currents. While it is generally accepted that this muscarinic inhibition is mainly caused by the breakdown of PIP(2), the role of the subsequent activation of protein kinase C (PKC) is not well understood. By reconstituting M currents in Xenopus oocytes, we observed that stimulation of coexpressed M1 receptors with 10 microm oxotremorine M (oxo-M) induces a positive shift (4-30 mV, depending on which KCNQ channels are expressed) in the conductance-voltage relationship (G-V) of KCNQ channels. When we applied phorbol 12-myristate 13-acetate (PMA), a potent PKC activator, we observed a large positive shift (17.8 +/- 1.6 mV) in the G-V curve for KCNQ2, while chelerythrine, a PKC inhibitor, attenuated the shift caused by the stimulation of M1 receptors. By contrast, reducing PIP(2) had little effect on the G-V curve for KCNQ2 channels; although pretreating cells with 10 mum wortmannin for 30 min reduced KCNQ2 current amplitude by 80%, the G-V curve was shifted only slightly (5 mV). Apparently, the shift induced by muscarinic stimulation in Xenopus oocytes was mainly caused by PKC activation. When KCNQ2/3 channels were expressed in HEK 293T cells, the G-V curve seemed already to be shifted in a positive direction, even before activation of PKC, and PMA failed to shift the curve any further. That alkaline phosphatase in the patch pipette shifted the G-V curve in a negative direction suggests KCNQ2/3 channels are constitutively phosphorylated in HEK 293T cells.
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