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1 Signal Transduction, NIEHS, NIH, DHHS, RTP, NC, USA
* To whom correspondence should be addressed. E-mail: bird{at}niehs.nih.gov.
Previous studies on the activation mechanism of Canonical Transient Receptor Potential (TRPC) channels have often produced conflicting conclusions. All seven have been shown to be activated by phospholipase C-coupled receptors but TRPC1, 2, 3, 4, 5 and 7 have also been proposed to function as store-operated channels.1 In the case of TRPC3, the expression environment as well as the expression level appears to determine the mode of regulation. Reports on a close structural relative of TRPC3, TRPC7, have presented evidence that this channel is activated by receptor activation, in one report, or by store depletion in another. Based on previous findings for TRPC3, we reasoned that subtle differences in structure or expression conditions might account for the apparent distinct gating mechanisms of TRPC7. In order to re-examine the mode of activation of TRPC7, we stably and transiently transfected human embryonic kidney HEK293 cells with cDNAs encoding for human TRPC7. We examined the ability of a phospholipase C-linkedC-activating agonist and an intracellular Ca2+ store-depleting agent to activate these channels. Our findings demonstrate that when transiently expressed in HEK293 cells, TRPC7 forms channels that are activated by phospholipase C-stimulating agonists, but not by Ca2+ store depletion. However, when stably expressed in HEK293 cells, TRPC7 can be activated by either calcium store depletion or phospholipase C activation. To our knowledge, this is the first demonstration of a channel protein that can be activated by both receptor and store-operated modes in the same cell. In addition, the results reconcile the apparently conflicting findings of other laboratories on TRPC7 regulation.
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