Okadaic acid inhibits glucocorticoid-induced apoptosis in T cell hybridomas at its late stage.
Okadaic acid inhibits glucocorticoid-induced apoptosis in T cell hybridomas at its late stage.
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DOI：
10.1006/bbrc.1993.2566
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发表时间：
1993-12
影响因子：
3.1
通讯作者：
Y. Ohoka;Yuji Nakai;M. Mukai;Makoto Iwata
中科院分区：
文献类型：
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作者：
Y. Ohoka;Yuji Nakai;M. Mukai;Makoto Iwata
糖皮质激素诱导小鼠T细胞杂交瘤细胞凋亡。冈田酸和calyculin A是蛋白磷酸酶1和2A的有效抑制剂，但对冈田酸的结构类似物1-诺洛卡酮没有抑制作用。即使在培养开始9 h后加入冈田酸，其抑制效果也很显著。在糖皮质激素反应元件的控制下，用含有荧光素酶基因的质粒转染的T细胞杂交瘤，冈田酸既不能阻止糖皮质激素受体从细胞质向细胞核的易位，也不能诱导荧光素酶的活性。这些结果表明，蛋白去磷酸化是糖皮质激素诱导的T细胞杂交瘤细胞凋亡的重要步骤，且该步骤处于细胞凋亡过程的后期。
Glucocorticoids induce apoptosis in murine T cell hybridomas. It was inhibited by okadaic acid and calyculin A, potent inhibitors of protein phosphatase 1 and 2A, but not by 1-norokadaone, a structural analog of okadaic acid without phosphatase inhibitory activity. The inhibitory effect of okadaic acid was significant even when it was added 9 h after the start of the culture. Okadaic acid did not prevent either the translocation of glucocorticoid receptor from the cytoplasm to the nucleus or the induction of luciferase activity in the T cell hybridoma transfected with a plasmid containing the luciferase gene under the control of glucocorticoid response elements. These results indicate that protein dephosphorylation is an essential step for glucocorticoid-induced apoptosis in T cell hybridomas, and that the step is at the late stage of the apoptotic process.