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Nature 杂志导读,第489卷,2012年9月13日:304–308

发布者:鑫达医学翻译 发布时间:2012-09-14阅读:

doi:10.1038/nature11468
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题目:蛋白酶体亚基PSMD11调控着人类胚胎干细胞内蛋白组的稳定

Summary:胚胎干细胞可以连续复制而不会衰老,因此可以进行无限期的体外培养。稳定的基因组是干细胞存活所必需,稳定的蛋白组可能在干细胞保持均一化和发挥正常功能起着同样重要的作用。在干细胞非对称分裂的过程中,如果亲代细胞把损伤的蛋白传给子代细胞可能会破坏子代细胞的正常代谢功能,从而影响继续增殖。因此,充分认识干细胞蛋白组的运作显得尤为重要。David Vilchez等研究发现,人类胚胎干细胞(hESCs)表现出很高的蛋白酶体活性:细胞内19S 蛋白酶体亚基 PSMD11 (果蝇中为RPN-6)高水平表达并且相应的提高了26S/30S 蛋白酶体的表达。而且异位表达PSMD11就足以提高蛋白酶体表达并增加其活性。而且发现转录因子FOXO4可以通过调控PSMD11的表达来影响蛋白酶体的表达,而 FOXO4又受一种胰岛素/类胰岛素生长因子(IGF-I)调控。研究还发现如果蛋白酶体的活性受到了抑制,就会影响多能型分子标记进和不同胚层分子特定分子标记的表达。David Vilchez等研究揭开了一种新的调控人类胚胎干细胞中蛋白组稳定的机制,它在干细胞长期存活和抗胁迫环境中发挥重要作用。

点评:作者认为胚胎干细胞为了保持长寿和快速分裂,需要很高的蛋白酶体活性来及时清除受损伤的蛋白从而保持基因组和蛋白组的完整与稳定。通过分析蛋白酶体活性及其调控因子揭开了一条干细胞保持蛋白组稳定的机制。
 
Increased proteasome activity in human embryonic stem cells is regulated by PSMD11

David Vilchez,  Leah Boyer, Ianessa Morantte, Margaret Lutz, Carsten Merkwirth, Derek Joyce, Brian Spencer, Lesley Page, Eliezer Masliah, W. Travis Berggren, Fred H. Gage & Andrew Dillin
Embryonic stem cells can replicate continuously in the absence of senescence and, therefore, are immortal in culture1, 2. Although genome stability is essential for the survival of stem cells, proteome stability may have an equally important role in stem-cell identity and function. Furthermore, with the asymmetric divisions invoked by stem cells, the passage of damaged proteins to daughter cells could potentially destroy the resulting lineage of cells. Therefore, a firm understanding of how stem cells maintain their proteome is of central importance. Here we show that human embryonic stem cells (hESCs) exhibit high proteasome activity that is correlated with increased levels of the 19S proteasome subunit PSMD11 (known as RPN-6 in Caenorhabditis elegans)3, 4, 5 and a corresponding increased assembly of the 26S/30S proteasome. Ectopic expression of PSMD11 is sufficient to increase proteasome assembly and activity. FOXO4, an insulin/insulin-like growth factor-I (IGF-I) responsive transcription factor associated with long lifespan in invertebrates6, 7, regulates proteasome activity by modulating the expression of PSMD11 in hESCs. Proteasome inhibition in hESCs affects the expression of pluripotency markers and the levels of specific markers of the distinct germ layers. Our results suggest a new regulation of proteostasis in hESCs that links longevity and stress resistance in invertebrates to hESC function and identity.
 


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