Journal
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
Volume 290, Issue 4, Pages C1031-C1040Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpcell.00602.2004
Keywords
transient receptor potential channel; nonselective cation channel
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The classic type of transient receptor potential channel ( TRPC) is a molecular candidate for Ca2+-permeable cation channels in mammalian cells. Because TRPC channels have calmodulin ( CaM) binding sites at their COOH termini, we investigated the effect of CaM on mTRPC5. TRPC5 was initially activated by muscarinic stimulation with 50 mu M carbachol and then decayed rapidly even in the presence of carbachol. Intracellular CaM ( 150 mu g/ml) increased the amplitude of mTRPC5 current activated by muscarinic stimulation. CaM antagonists ( W-7 and calmidazolium) inhibited mTRPC5 currents when they were applied during the activation of mTRPC5. Pretreatment of W-7 and calmidazolium also inhibited the activation of mTRPC5 current. Inhibitors of myosin light chain kinase ( MLCK) inhibited the activation of mTRPC5 currents, whereas inhibitors of CaM-dependent protein kinase II did not. Small interfering RNA against cardiac type MLCK also inhibited the activation of mTRPC5 currents. However, inhibitors of CaM or MLCK did not show any effect on GTP gamma S-induced currents. Application of both Rho kinase inhibitor and MLCK inhibitor inhibited GTP gamma S-induced currents. We conclude that CaM and MLCK modulates the activation process of mTRPC5.
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