HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 290/4/C1031    most recent 00602.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Kim, M. T. Articles by Kim, K. W. Search for Related Content PubMed PubMed Citation Articles by Kim, M. T. Articles by Kim, K. W.

MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

Involvement of calmodulin and myosin light chain kinase in activation of mTRPC5 expressed in HEK cells

¹Department of Physiology and Biophysics, Seoul National University College of Medicine, Seoul; and ²Department of Physiology, College of Medicine, Kwandong University, Kangneung, Korea

Submitted 8 December 2004 ; accepted in final form 16 November 2005

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 µM carbachol and then decayed rapidly even in the presence of carbachol. Intracellular CaM (150 µg/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 GTPS-induced currents. Application of both Rho kinase inhibitor and MLCK inhibitor inhibited GTPS-induced currents. We conclude that CaM and MLCK modulates the activation process of mTRPC5.

transient receptor potential channel; nonselective cation channel

This article has been cited by other articles:

				N. T. Blair, J. S. Kaczmarek, and D. E. Clapham Intracellular calcium strongly potentiates agonist-activated TRPC5 channels J. Gen. Physiol., May 1, 2009; 133(5): 525 - 546. [Abstract] [Full Text] [PDF]

				A. P. Albert, S. N. Saleh, C. M. Peppiatt-Wildman, and W. A. Large Multiple activation mechanisms of store-operated TRPC channels in smooth muscle cells J. Physiol., August 15, 2007; 583(1): 25 - 36. [Abstract] [Full Text] [PDF]