R93W mutation in Orai1 causes impaired calcium influx in platelets

Wolfgang Bergmeier, Oh Hora Masatsugu, Christie Ann McCarl, R. Claire Roden, Paul F. Bray, Stefan Feske

研究成果: ジャーナルへの寄稿学術誌査読

112 被引用数 (Scopus)

抄録

The intracellular Ca2+concentration of many nonexcitable cells is regulated by calcium store release and store-operated calcium entry (SOCE). In platelets, STIM1 was recently identified as the main calcium sensor expressed in the endoplasmic reticulum. To evaluate the role of the SOC channel moiety, Orai1, in platelet SOCE, we generated mice expressing a mutated, inactive form of Orai1 in blood cells only (Orai1R93W). Platelets expressing Orai1R93W were characterized by markedly reduced SOCE and impaired agonistinduced increases in [Ca2+]i. Orai1R93W platelets showed reduced integrin activation and impaired degranulation when stimulated with low agonist concentrations under static conditions. This defect, however, did not significantly affect the ability of Orai1R93W platelets to aggregate or to adhere to collagen under arterial flow conditions ex vivo. In contrast, these adherent Orai1R93W platelets were defective in surface phosphatidylserine exposure, suggesting that Orai1 is crucial for the platelets' procoagulant response rather than for other Ca 2+-dependent cellular responses.

本文言語英語
ページ(範囲)675-678
ページ数4
ジャーナルBlood
113
3
DOI
出版ステータス出版済み - 1月 15 2009
外部発表はい

!!!All Science Journal Classification (ASJC) codes

  • 生化学
  • 免疫学
  • 血液学
  • 細胞生物学

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