Protein O-GlcNAcylation: A critical regulator of the cellular response to stress.
Protein O-GlcNAcylation: A critical regulator of the cellular response to stress.
复制标题
蛋白O-Glcnacylation：细胞对应激反应的关键调节剂。
DOI：
10.2174/157436210790226492
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发表时间：
2010-01
影响因子：
--
通讯作者：
Marchase RB
中科院分区：
文献类型：
--
作者：
Chatham JC;Marchase RB
通过单糖-N-乙酰基-葡糖胺（O-GlcNAc）的O-连接的核和细胞质蛋白的丝氨酸和苏氨酸残基的翻译后修饰是高度动态和普遍存在的蛋白质修饰，其在调节许多生物过程中起关键作用。我们对O-GlcNAc对细胞功能作用的机制的理解大多是在慢性疾病过程的背景下。然而，越来越多的证据表明，O-GlcNAc水平在应激反应中增加，并且这种反应的急性增强是细胞保护性的，至少在短期内是如此。相反，O-GlcNAc水平的降低似乎与响应于急性应激的细胞存活降低相关。在这里，我们总结了我们目前对蛋白质O-GlcNAc化对细胞应激反应和介导细胞保护机制的理解，主要集中在心血管系统作为一个例子。我们考虑了O-GlcNAc化和心肌细胞钙稳态之间的潜在联系，并探讨了O-GlcNAc信号和氧化还原信号之间的相似之处。我们还讨论了明显的矛盾之间的报道增加O-GlcNAcylation与其最近报道的作用，在介导细胞存活机制的不利影响。
The post-translational modification of serine and threonine residues of nuclear and cytoplasmic proteins by the O-linked attachment of the monosaccharide ß-N-acetyl-glucosamine (O-GlcNAc) is a highly dynamic and ubiquitous protein modification that plays a critical role in regulating numerous biological processes. Much of our understanding of the mechanisms underlying the role of O-GlcNAc on cellular function has been in the context of chronic disease processes. However, there is increasing evidence that O-GlcNAc levels are increased in response to stress and that acute augmentation of this response is cytoprotective, at least in the short term. Conversely, a reduction in O-GlcNAc levels appears to be associated with decreased cell survival in response to an acute stress. Here we summarize our current understanding of protein O-GlcNAcylation on the cellular response to stress and in mediating cellular protective mechanisms focusing primarily on the cardiovascular system as an example. We consider the potential link between O-GlcNAcylation and cardiomyocyte calcium homeostasis and explore the parallels between O-GlcNAc signaling and redox signaling. We also discuss the apparent paradox between the reported adverse effects of increased O-GlcNAcylation with its recently reported role in mediating cell survival mechanisms.