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J. Biol. Chem., Vol. 282, Issue 32, 23655-23662, August 10, 2007

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Suppression of TRPC3 Leads to Disappearance of Store-operated Channels and Formation of a New Type of Store-independent Channels in A431 Cells^*

Elena Kaznacheyeva, Lyuba Glushankova, Vladislav Bugaj, Olga Zimina, Anton Skopin, Vadim Alexeenko, Leonidas Tsiokas, Ilya Bezprozvanny^¶, and Galina N. Mozhayeva¹

From the Institute of Cytology RAS, 4 Tikhoretsky Ave., 194064 St. Petersburg, Russia, the Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, and the ^¶Department of Physiology, University of Texas Southwestern Medical Center, Dallas, Texas 75235

In most non-excitable cells, calcium (Ca²⁺) release from the inositol 1,4,5-trisphosphate (InsP₃)-sensitive intracellular Ca²⁺ stores is coupled to Ca²⁺ influx through the plasma membrane Ca²⁺ channels whose molecular composition is poorly understood. Several members of mammalian TRP-related protein family have been implicated to both receptor- and store-operated Ca²⁺ influx. Here we investigated the role of the native transient receptor potential 3 (TRPC3) homologue in mediating the store- and receptor-operated calcium entry in A431 cells. We show that suppression of TRPC3 protein levels by small interfering RNA (siRNA) leads to a significant reduction in store-operated calcium influx without affecting the receptor-operated calcium influx. With single-channel analysis, we further demonstrate that reduction of TRPC3 levels results in suppression of specific subtype of store-operated calcium channels and activation of store-independent channels. Our data suggest that TRPC3 is required for the formation of functional store-operated channels in A431 cells.

Received for publication, August 31, 2006 , and in revised form, June 14, 2007.

^* This work was supported by the Molecular and Cellular Biology RAS program (to G. N. M.), the Russian Basic Research Foundation 04-04-49057 (to E. K.), 04-04-49053 (to G. N. M.), and SS-4904.2006.4 (to G. N. M.), the Russian Science Support Foundation (to E. K.), National Institutes of Health Grant NS38082 (to I. B.), National Institutes of Health Grant DK59599, and OCAST (to L. T.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: Inst. of Cytology RAS, Tikhoretsky Ave 4, 194064 St. Petersburg, Russia. Tel.: 7-812-297-1497; Fax: 7-812-297-0341; E-mail: gnmozh{at}mail.cytspb.rssi.ru.

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