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J. Biol. Chem., Vol. 282, Issue 37, 27327-27333, September 14, 2007

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Luminal Chloride-dependent Activation of Endosome Calcium Channels

PATCH CLAMP STUDY OF ENLARGED ENDOSOMES^*

From the Department of Cell Biology and Physiology, Washington University, St. Louis, Missouri 63110

Although Ca²⁺ release from early endosomes (EE) is important for the fusion of primary endosomes, the presence of an ion channel responsible for releasing calcium from the EE has not been shown. A recent proteomics study has identified the TRPV2 channel protein in EE, suggesting that transient receptor potential-like Ca²⁺ channels may be in endosomes. The submicron size of endosomes has made it difficult to study their ion channels in the past. We have overcome this problem by generating enlarged EE with the help of a hydrolysis-deficient SKD1/VPS4B mutant in HEK293 cells. Here we report the first patch clamp recording of a novel endosome calcium channel (ECC) in these enlarged EE. The ECC shows a similar pharmacology to that of the TRPV2 channel. In addition, the ECC has a unique chloride-dependent regulation; it is inhibited by the endosome luminal chloride with a K₅₀ of 82 mM.

Received for publication, March 26, 2007 , and in revised form, May 18, 2007.

^* This work was supported in part by a grant from the National Institutes of Health (to P. S.) and by the American Cancer Society (to M. S.). 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: Dept. of Cell Biology and Physiology, Washington University, 660 S. Euclid Ave., St. Louis, MO 63110; Tel.: 314-362-8702; Fax: 314-362-7463; E-mail: msaito{at}cellbiology.wustl.edu.

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