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Tyrosine phosphorylation modulates store‐operated calcium entry in cultured rat epididymal basal cells

Tyrosine phosphorylation modulates store‐operated calcium entry in cultured rat epididymal basal... Store‐operated calcium entry (SOCE) is essential for many cellular processes. In this study, we investigated modulation of SOCE by tyrosine phosphorylation in rat epididymal basal cells. The intracellular Ca2+([Ca2+]i) measurement showed that SOCE occurred in rat epididymal basal cells by pretreating the cells with thapsigargin (Tg), the inhibitor of sarco‐endoplasmic reticulum Ca2+‐ATPase. To identify the role of Ca2+ channels in this response, we examined the effects of transient receptor potential canonical channel blockers 2‐aminoethoxydiphenyl borate (2‐APB), 1‐[β‐[3‐(4‐methoxyphenyl)pro‐poxy]‐4‐methoxyphenethyl]‐1H‐imidazole hydrochloride(SKF96365), Gd3+, and non‐selective cation channel blocker Ni2+ respectively on SOCE and found that these blockers could inhibit the Ca2+ influx to different extent. Furthermore, we studied the regulation of SOCE by tyrosine kinase pathway. The inhibitor of tyrosine kinase genistein remarkably suppressed the SOCE response, whereas sodium orthovanadate, the inhibitor of tyrosine phosphatase, greatly enhanced it. The results suggest that tyrosine kinase pathway plays a significant role in the initiation of SOCE and positively modulates SOCE in epididymal basal cells. J. Cell. Physiol. 226: 1069–1073, 2011. © 2010 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Cellular Physiology Wiley

Tyrosine phosphorylation modulates store‐operated calcium entry in cultured rat epididymal basal cells

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References (38)

Publisher
Wiley
Copyright
Copyright © 2011 Wiley Subscription Services
ISSN
0021-9541
eISSN
1097-4652
DOI
10.1002/jcp.22429
pmid
20857412
Publisher site
See Article on Publisher Site

Abstract

Store‐operated calcium entry (SOCE) is essential for many cellular processes. In this study, we investigated modulation of SOCE by tyrosine phosphorylation in rat epididymal basal cells. The intracellular Ca2+([Ca2+]i) measurement showed that SOCE occurred in rat epididymal basal cells by pretreating the cells with thapsigargin (Tg), the inhibitor of sarco‐endoplasmic reticulum Ca2+‐ATPase. To identify the role of Ca2+ channels in this response, we examined the effects of transient receptor potential canonical channel blockers 2‐aminoethoxydiphenyl borate (2‐APB), 1‐[β‐[3‐(4‐methoxyphenyl)pro‐poxy]‐4‐methoxyphenethyl]‐1H‐imidazole hydrochloride(SKF96365), Gd3+, and non‐selective cation channel blocker Ni2+ respectively on SOCE and found that these blockers could inhibit the Ca2+ influx to different extent. Furthermore, we studied the regulation of SOCE by tyrosine kinase pathway. The inhibitor of tyrosine kinase genistein remarkably suppressed the SOCE response, whereas sodium orthovanadate, the inhibitor of tyrosine phosphatase, greatly enhanced it. The results suggest that tyrosine kinase pathway plays a significant role in the initiation of SOCE and positively modulates SOCE in epididymal basal cells. J. Cell. Physiol. 226: 1069–1073, 2011. © 2010 Wiley‐Liss, Inc.

Journal

Journal of Cellular PhysiologyWiley

Published: Jan 1, 2011

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