Molecular Functions of Glycoconjugates in Autophagy.
Molecular Functions of Glycoconjugates in Autophagy.
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DOI：
10.1016/j.jmb.2016.06.011
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发表时间：
2016-08-14
影响因子：
5.6
通讯作者：
Zachara NE
中科院分区：
文献类型：
--
作者：
Fahie K;Zachara NE
糖缀合物、聚糖、碳水化合物和糖：这些术语包括一类形式和功能多样的生物分子，从游离寡糖、糖蛋白和蛋白聚糖到构成影响正常生理和疾病的复杂聚糖密码的糖脂。最近的数据表明，糖缀合物影响生理学的一种机制是通过调节自噬过程。自噬是细胞分化、生物体发育以及维持细胞和组织稳态所必需的降解途径。在这篇综述中，我们将重点介绍糖缀合物对自噬的调控，重点是细胞外表面的信号传导机制和细胞内聚糖的调控作用。来自细胞外基质的聚糖信号传导会聚于自噬的“主”调节剂，包括AMPK和mTORC 1，从而影响它们的定位、活性和/或表达。在细胞内环境中，神经节苷脂是自噬体膜的成分，组成自噬机制的蛋白质的子集由糖基化调节，并且细胞溶质中的寡糖暴露触发自噬反应。讨论的例子提供了一些聚糖调节自噬的机制的见解，并揭示了未来的研究领域。
Glycoconjugates, glycans, carbohydrates, and sugars: these terms encompass a class of biomolecules that are diverse in both form and function ranging from free oligosaccharides, glycoproteins and proteoglycans, to glycolipids that make up a complex glycan-code that impacts normal physiology and disease. Recent data suggests that one mechanism by which glycoconjugates impact physiology is through the regulation of the process of autophagy. Autophagy is a degradative pathway necessary for differentiation, organism development, and the maintenance of cell and tissue homeostasis. In this review, we will highlight what is known about the regulation of autophagy by glycoconjugates focusing on signaling mechanisms from the extracellular surface and the regulatory roles of intracellular glycans. Glycan signaling from the extracellular matrix converges on “master” regulators of autophagy including AMPK and mTORC1, thus impacting their localization, activity and/or expression. Within the intracellular milieu, gangliosides are constituents of the autophagosome membrane, a subset of proteins composing the autophagic machinery are regulated by glycosylation, and oligosaccharide exposure in the cytosol triggers an autophagic response. The examples discussed provide some mechanistic insights into glycan regulation of autophagy and reveals areas for future investigation.
DOI：
10.1083/jcb.73.1.111
发表时间：
1977-04
期刊：
The Journal of cell biology
影响因子：
--
作者：
Albertini DF;Anderson E
通讯作者：
Anderson E