ArticleThe Journal of physiology2000
Evidence for myosin light chain kinase mediating noradrenaline-evoked cation current in rabbit portal vein myocytes.
Article in The Journal of physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 43 citations in OpenAlex.
- High glucose upregulates myosin light chain kinase to induce microfilament cytoskeleton rearrangement in hippocampal neurons.Molecular medicine reports · 2018Article
- Myosin light chain kinase controls voltage-dependent calcium channels in vascular smooth muscle.Pflugers Archiv : European journal of physiology · 2014Article
- Regulation of calcium channels in smooth muscle: new insights into the role of myosin light chain kinase.Channels (Austin, Tex.) · 2014Review
- Nogo-A is a negative regulator of CNS angiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Differential effects of myosin light chain kinase inhibition on contractility, force development and myosin light chain 20 phosphorylation of rat cervical and thoracic duct lymphatics.The Journal of physiology · 2011Article
- Inhibition of native TRPC6 channel activity by phosphatidylinositol 4,5-bisphosphate in mesenteric artery myocytes.The Journal of physiology · 2008Article
- Myosin light chain kinase-independent inhibition by ML-9 of murine TRPC6 channels expressed in HEK293 cells.British journal of pharmacology · 2007Article
- Ca2+-calmodulin-dependent myosin light chain kinase is essential for activation of TRPC5 channels expressed in HEK293 cells.The Journal of physiology · 2006Article
- Signal transduction pathways and gating mechanisms of native TRP-like cation channels in vascular myocytes.The Journal of physiology · 2006Review
- Multiple regulation by calcium of murine homologues of transient receptor potential proteins TRPC6 and TRPC7 expressed in HEK293 cells.The Journal of physiology · 2004Article
- Activation of TRPC6 channel proteins: evidence for an essential role of phosphorylation.The Journal of physiology · 2004Review
- Distribution and expression of non-muscle myosin light chain kinase in rabbit livers.World journal of gastroenterology · 2003Article
- Synergism between inositol phosphates and diacylglycerol on native TRPC6-like channels in rabbit portal vein myocytes.The Journal of physiology · 2003Article
- Role of sarcoplasmic reticulum in control of membrane potential and nitrergic response in opossum lower esophageal sphincter.British journal of pharmacology · 2003Article
- Myosin phosphatase and myosin phosphorylation in differentiating C2C12 cells.Journal of muscle research and cell motility · 2003Article
- Activation of store-operated channels by noradrenaline via protein kinase C in rabbit portal vein myocytes.The Journal of physiology · 2002Article
- The developing relationship between receptor-operated and store-operated calcium channels in smooth muscle.British journal of pharmacology · 2002Review
- Preliminary research on myosin light chain kinase in rabbit liver.World journal of gastroenterology · 2001Article
- Comparison of spontaneous and noradrenaline-evoked non-selective cation channels in rabbit portal vein myocytes.The Journal of physiology · 2001Article
- Agents that increase tyrosine phosphorylation activate a non-selective cation current in single rabbit portal vein smooth muscle cells.The Journal of physiology · 2001Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of myosin light chain kinase (MLCK) in the activation of the noradrenaline-evoked non-selective cation current (Icat) was examined with the whole-cell recording technique in single rabbit portal vein smooth muscle cells. Intracellular dialysis with 5 microM MLCK(11-19)amide, a substrate-specific peptide inhibitor of MLCK, markedly reduced the amplitude and rate of activation of noradrenaline-evoked Icat. A similar result was obtained when the cells were dialysed with 10 microM AV25, which also inhibits MLCK by an action at the auto-inhibitory domain of MLCK. Inhibitors of binding of ATP to MLCK, wortmannin and synthetic naphthalenesulphonyl derivatives (ML-7 and ML-9), at micromolar concentrations, also reduced the amplitude of noradrenaline-evoked Icat. ML-7 and ML-9 (both at 5 microM) reduced the amplitude of Icat induced by both guanosine 5'-O-(3-thiotriphosphate) (GTPgammaS) and 1-oleoyl-2-acetyl-sn-glycerol (OAG). MLCK(11-19)amide, AV25 and ML-9 did not inhibit the noradrenaline-evoked Ca2+-activated potassium current at a holding potential of 0 mV. In addition, MLCK(11-19)amide and AV25 did not reduce the non-selective cation current induced by ATP in rabbit ear artery cells. Intracellular dialysis with 2 microM Ca2+ and 9 microM calmodulin activated Icat, which developed over a period of about 5 min. Intracellular dialysis with the non-hydrolysable analogue of ATP, 5'-adenylylimidodiphosphate (AMP-PNP), reduced the amplitude and rate of activation of noradrenaline-evoked Icat. The results indicate that MLCK mediates noradrenaline-activated Icat in rabbit portal vein smooth muscle cells.
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