| Literature DB >> 27660393 |
Cécile Mathieu1, Romain Duval1, Angélique Cocaign1, Emile Petit1, Linh-Chi Bui1, Iman Haddad2, Joelle Vinh2, Catherine Etchebest3,4,5,6,7, Jean-Marie Dupret1,7, Fernando Rodrigues-Lima8,7.
Abstract
Brain glycogen and its metabolism are increasingly recognized as major players in brain functions. Moreover, alteration of glycogen metabolism in the brain contributes to neurodegenerative processes. In the brain, both muscle and brain glycogen phosphorylase isozymes regulate glycogen mobilization. However, given their distinct regulatory features, these two isozymes could confer distinct metabolic functions of glycogen in brain. Interestingly, recent proteomics studies have identified isozyme-specific reactive cysteine residues in brain glycogen phosphorylase (bGP). In this study, we show that the activity of human bGP is redox-regulated through the formation of a disulfide bond involving a highly reactive cysteine unique to the bGP isozyme. We found that this disulfide bond acts as a redox switch that precludes the allosteric activation of the enzyme by AMP without affecting its activation by phosphorylation. This unique regulatory feature of bGP sheds new light on the isoform-specific regulation of glycogen phosphorylase and glycogen metabolism.Entities:
Keywords: allosteric regulation; brain metabolism; carbohydrate metabolism; disulfide; glycogen; glycogen storage disease; redox regulation
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Year: 2016 PMID: 27660393 PMCID: PMC5104910 DOI: 10.1074/jbc.M116.757062
Source DB: PubMed Journal: J Biol Chem ISSN: 0021-9258 Impact factor: 5.157