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Participation of Intracellular Ca~(2+) /Calmodulin and Protein Kinase (s) in the Pathway of Apoptosis Induced by a Drosophila Cell Death Gene, reaper

机译:果蝇细胞死亡基因,收割者诱导细胞内Ca〜(2 +)/钙调蛋白和蛋白激酶参与细胞凋亡途径

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摘要

To elucidate the apoptotic signaling pathway, we have generated a cell culture model:S2 cells stably transfected with a Drosophila cell death gene, reaper(rpr).Following rpr overexpression, caspase activation-mediated apoptotic cell death was induced in the cells. Apoptosis triggered by rpr required intracellular Ca~(2+) ions and calmodulin .Furthermore, protein kinase inhibitors H-7(a PKC PKA, PKG, MLCK, and CKI inhibitor), calphostin C(a PKC inhibitor) , or H-89(a PKA and PKG inhibitor ) completely blocked apoptosis induced by rpr, suggesting that some kind of serine/threonine protein kinase(s) act upstream of caspase in apoptotic pathway induced by rpr in S2 cells
机译:为了阐明细胞凋亡的信号通路,我们建立了一个细胞培养模型:用果蝇细胞死亡基因reaper(rpr)稳定转染S2细胞。 rpr触发的细胞凋亡需要细胞内Ca〜(2+)离子和钙调蛋白。此外,蛋白激酶抑制剂H-7(PKC PKA,PKG,MLCK和CKI抑制剂),钙磷蛋白C(PKC抑制剂)或H-89 (一种PKA和PKG抑制剂)完全阻断了rpr诱导的细胞凋亡,表明某种丝氨酸/苏氨酸蛋白激酶在rpr诱导的S2细胞凋亡途径中的半胱天冬酶上游起作用

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