| Literature DB >> 25416785 |
Gilbert Richarme1, Mouadh Mihoub2, Julien Dairou3, Linh Chi Bui3, Thibaut Leger4, Aazdine Lamouri5.
Abstract
Glycation is an inevitable nonenzymatic covalent reaction between proteins and endogenous reducing sugars or dicarbonyls (methylglyoxal, glyoxal) that results in protein inactivation. DJ-1 was reported to be a multifunctional oxidative stress response protein with poorly defined function. Here, we show that human DJ-1 is a protein deglycase that repairs methylglyoxal- and glyoxal-glycated amino acids and proteins by acting on early glycation intermediates and releases repaired proteins and lactate or glycolate, respectively. DJ-1 deglycates cysteines, arginines, and lysines (the three major glycated amino acids) of serum albumin, glyceraldehyde-3-phosphate dehydrogenase, aldolase, and aspartate aminotransferase and thus reactivates these proteins. DJ-1 prevented protein glycation in an Escherichia coli mutant deficient in the DJ-1 homolog YajL and restored cell viability in glucose-containing media. These results suggest that DJ-1-associated Parkinsonism results from excessive protein glycation and establishes DJ-1 as a major anti-glycation and anti-aging protein.Entities:
Keywords: Carbonyl Stress; Dicarbonyl Compounds; Electrophile Stress; Glycation; Protein Aggregation; Protein Chemical Modification; Protein Conformation; Protein Denaturation
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Year: 2014 PMID: 25416785 PMCID: PMC4340429 DOI: 10.1074/jbc.M114.597815
Source DB: PubMed Journal: J Biol Chem ISSN: 0021-9258 Impact factor: 5.157