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

Wu Lin Zuo, Jian Yang Du, Jie Hong Huang, Sheng Li, Geng Zhang, Si Liang Chen, Yechun Ruan, Christopher H.K. Cheng, Wen Liang Zhou

Research output: Journal article publicationJournal articleAcademic researchpeer-review

7 Citations (Scopus)


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.
Original languageEnglish
Pages (from-to)1069-1073
Number of pages5
JournalJournal of Cellular Physiology
Issue number4
Publication statusPublished - 1 Apr 2011
Externally publishedYes

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

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