鞘氨醇抑制肌浆（内质）网Ca（2+）-ATP酶（SERCA）的活性。
Sphingosine inhibits the sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) activity.
作者信息
Benaim Gustavo, Pimentel Adriana A, Felibertt Pimali, Mayora Adriana, Colman Laura, Sojo Felipe, Rojas Héctor, De Sanctis Juan B
机构信息
Instituto de Estudios Avanzados (IDEA), Caracas, Venezuela; Instituto de Biología Experimental, Facultad de Ciencias, Universidad Central de Venezuela (UCV), Caracas, Venezuela.
Facultad de Farmacia, Universidad Central de Venezuela (UCV), Caracas, Venezuela.
出版信息
Biochem Biophys Res Commun. 2016 Apr 29;473(2):572-7. doi: 10.1016/j.bbrc.2016.03.123. Epub 2016 Mar 28.
The increase in the intracellular Ca(2+) concentration ([Ca(2+)]i) is the key variable for many different processes, ranging from regulation of cell proliferation to apoptosis. In this work we demonstrated that the sphingolipid sphingosine (Sph) increases the [Ca(2+)]i by inhibiting the sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA), in a similar manner to thapsigargin (Tg), a specific inhibitor of this Ca(2+) pump. The results showed that addition of sphingosine produced a release of Ca(2+) from the endoplasmic reticulum followed by a Ca(2+) entrance from the outside mileu. The results presented in this work support that this sphingolipid could control the activity of the SERCA, and hence sphingosine may participate in the regulation of [Ca(2+)]I in mammalian cells.
细胞内钙离子浓度（[Ca(2+)]i）的升高是许多不同过程的关键变量，范围从细胞增殖调节到细胞凋亡。在这项工作中，我们证明鞘脂神经鞘氨醇（Sph）通过抑制肌浆网Ca(2+)-ATP酶（SERCA）来增加[Ca(2+)]i，其方式与该Ca(2+)泵的特异性抑制剂毒胡萝卜素（Tg）类似。结果表明，添加神经鞘氨醇会导致内质网释放Ca(2+)，随后Ca(2+)从细胞外环境进入。这项工作中呈现的结果支持这种鞘脂可以控制SERCA的活性，因此神经鞘氨醇可能参与哺乳动物细胞中[Ca(2+)]i的调节。
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