Neurodegenerative diseases such as Alzheimer's and Parkinson's remain highly prevalent and incurable disorders. A major challenge in fully understanding and combating the progression of these diseases is the complexity of the network of processes that lead to progressive neuronal dysfunction and death. An ideal therapeutic avenue is conceivably one that could address many if not all of these multiple misregulated mechanisms. Over the years, chemical intervention for the up-regulation of the endogenous posttranslational modification (PTM) O-GlcNAc has been proposed as a potential strategy to slow down the progression of neurodegeneration. Through the development and application of tools that allow dissection of the mechanistic roles of this PTM, there is now a growing body of evidence that O-GlcNAc influences a variety of important neurodegeneration-pertinent mechanisms, with an overall protective effect. As a PTM that is appended onto numerous proteins that participate in protein quality control and homeostasis, metabolism, bioenergetics, neuronal communication, inflammation, and programmed death, O-GlcNAc has demonstrated beneficence in animal models of neurodegenerative diseases, and its up-regulation is now being pursued in multiple clinical studies.
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Cover Image
Tyrosine (Tyr) phosphorylation has recently emerged as being important for plant receptor kinase (RK)-mediated signalling, particularly during plant immunity. In this issue Mühlenbeck and colleagues (pp. 2759–2774) discuss the current understanding of plant RK Tyr phosphorylation focusing on the critical role of a pTyr site (‘VIa-Tyr’) conserved in several plant RKs. The cover image shows transmembrane signalling mechanisms in choanozoans and plants involving protein kinases. Image courtesy of Cyril Zipfel.
Mechanistic roles for altered O-GlcNAcylation in neurodegenerative disorders Available to Purchase
Aaron T. Balana, Matthew R. Pratt; Mechanistic roles for altered O-GlcNAcylation in neurodegenerative disorders. Biochem J 30 July 2021; 478 (14): 2733–2758. doi: https://doi.org/10.1042/BCJ20200609
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