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昆虫类固醇激素在类固醇诱导的程序性细胞死亡中的非基因组作用。

Nongenomic action of an insect steroid hormone in steroid-induced programmed cell death.

作者信息

Iga Masatoshi, Iwami Masafumi, Sakurai Sho

机构信息

Division of Life Sciences, Graduate School of Natural Science and Technology, Kanazawa University, Kakumamachi, Kanazawa 920-1192, Japan.

出版信息

Mol Cell Endocrinol. 2007 Jan 15;263(1-2):18-28. doi: 10.1016/j.mce.2006.08.005. Epub 2006 Oct 11.

Abstract

Programmed cell death (PCD) of the silkworm silk glands is triggered by the insect steroid hormone, 20-hydroxyecdysone (20E), and proceeds sequentially through cell shrinkage, nuclear condensation, DNA fragmentation, nuclear fragmentation and apoptotic body formation. A protein synthesis inhibitor, cycloheximide (CHX, 2 mM) induced a cell death that exhibited only nuclear and DNA fragmentation. A concentration of 0.2 mM CHX was ineffective at inducing the cell death when added alone, but in the presence of 20E, a cell death similar to that induced by 2 mM CHX was resulted with accompanying nuclear condensation. Since 2 and 0.2 mM CHX inhibited protein synthesis equally, the DNA and nuclear fragmentation appear to be mediated by a nongenomic action of 20E. In addition, we show a possible involvement of Ca2+-PKC-caspase-3 like protease pathway in the nongenomic action. The data suggest that 20E-induced PCD is accomplished through the integration of genomic and nongenomic actions.

摘要

家蚕丝腺的程序性细胞死亡(PCD)由昆虫类固醇激素20-羟基蜕皮酮(20E)触发,并依次经历细胞收缩、核浓缩、DNA片段化、核碎片化和凋亡小体形成。蛋白质合成抑制剂环己酰亚胺(CHX,2 mM)诱导的细胞死亡仅表现为核和DNA片段化。单独添加时,0.2 mM的CHX浓度在诱导细胞死亡方面无效,但在20E存在的情况下,会导致与2 mM CHX诱导的细胞死亡相似的情况,并伴有核浓缩。由于2 mM和0.2 mM的CHX对蛋白质合成的抑制作用相同,DNA和核片段化似乎是由20E的非基因组作用介导的。此外,我们展示了Ca2+-PKC-半胱天冬酶-3样蛋白酶途径可能参与非基因组作用。数据表明,20E诱导的PCD是通过基因组和非基因组作用的整合来完成的。

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