ArticleThe Journal of biological chemistry2008
A short motif in Kir6.1 consisting of four phosphorylation repeats underlies the vascular KATP channel inhibition by protein kinase C.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
- [Exogenous nitric oxide suppresses KSheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2026Article
- KAmerican journal of physiology. Cell physiology · 2022Review
- Kir6.1 and SUR2B in Cantú syndrome.American journal of physiology. Cell physiology · 2022Review
- ATP-Sensitive Potassium Channels in Migraine: Translational Findings and Therapeutic Potential.Cells · 2022Review
- Sexual dimorphism in vascular ATP-sensitive KThe Journal of physiology · 2021Article
- The Pharmacology of ATP-Sensitive KHandbook of experimental pharmacology · 2021Article
- The Ion Channel and GPCR Toolkit of Brain Capillary Pericytes.Frontiers in cellular neuroscience · 2020Review
- Pharmacological polysulfide suppresses glucose-stimulated insulin secretion in an ATP-sensitive potassium channel-dependent manner.Scientific reports · 2019Article
- 2-Deoxy-D-Glucose Exhibits Anti-seizure Effects by Mediating the Netrin-G1-KATP Signaling Pathway in Epilepsy.Neurochemical research · 2019Article
- Acute exposure of methylglyoxal leads to activation of KATP channels expressed in HEK293 cells.Acta pharmacologica Sinica · 2014Article
- The role of ATP-sensitive potassium channels in cellular function and protection in the cardiovascular system.British journal of pharmacology · 2014Review
- Potassium channels and uterine vascular adaptation to pregnancy and chronic hypoxia.Current vascular pharmacology · 2013Review
- Differential sensitivities of the vascular K(ATP) channel to various PPAR activators.Biochemical pharmacology · 2013Article
- Prolonged exposure to methylglyoxal causes disruption of vascular KATP channel by mRNA instability.American journal of physiology. Cell physiology · 2012Article
- Mechanisms of VIP-induced inhibition of the lymphatic vessel pump.The Journal of physiology · 2012Article
- K(ATP) channel action in vascular tone regulation: from genetics to diseases.Sheng li xue bao : [Acta physiologica Sinica] · 2012Review
- Regulation of the ATP-sensitive potassium channel subunit, Kir6.2, by a Ca2+-dependent protein kinase C.The Journal of biological chemistry · 2012Article
- Rosiglitazone inhibits vascular KATP channels and coronary vasodilation produced by isoprenaline.British journal of pharmacology · 2011Article
- Article
- Molecular basis and structural insight of vascular K(ATP) channel gating by S-glutathionylation.The Journal of biological chemistry · 2011Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Vascular ATP-sensitive K(+) channels are inhibited by multiple vasoconstricting hormones via the protein kinase C (PKC) pathway. However, the molecular substrates for PKC phosphorylation remain unknown. To identify the PKC sites, Kir6.1/SUR2B and Kir6.2/SUR2B were expressed in HEK293 cells. Following channel activation by pinacidil, the catalytic fragment of PKC inhibited the Kir6.1/SUR2B currents but not the Kir6.2/SUR2B currents. Phorbol 12-myristate 13-acetate (a PKC activator) had similar effects. Using Kir6.1-Kir6.2 chimeras, two critical protein domains for the PKC-dependent channel inhibition were identified. The proximal N terminus of Kir6.1 was necessary for channel inhibition. Because there was no PKC phosphorylation site in the N-terminal region, our results suggest its potential involvement in channel gating. The distal C terminus of Kir6.1 was crucial where there are several consensus PKC sites. Mutation of Ser-354, Ser-379, Ser-385, Ser-391, or Ser-397 to nonphosphorylatable alanine reduced PKC inhibition moderately but significantly. Combined mutations of these residues had greater effects. The channel inhibition was almost completely abolished when 5 of them were jointly mutated. In vitro phosphorylation assay showed that 4 of the serine residues were necessary for the PKC-dependent (32)P incorporation into the distal C-terminal peptides. Thus, a motif containing four phosphorylation repeats is identified in the Kir6.1 subunit underlying the PKC-dependent inhibition of the Kir6.1/SUR2B channel. The presence of the phosphorylation motif in Kir6.1, but not in its close relative Kir6.2, suggests that the vascular K(ATP) channel may have undergone evolutionary optimization, allowing it to be regulated by a variety of vasoconstricting hormones and neurotransmitters.
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