Maximus Peto’s Commentary
Here, these researchers report on deglycase activity of DJ-1, which apparently acts to deglycate glyoxal- and methylglyoxal-glycated proteins. I leave readers to decide whether this is new, interesting, and/or relevant for age-related accumulation of AGEs.
Parkinsonism-associated protein DJ-1 is a bona fide deglycase.
Biochem Biophys Res Commun.
2017 Jan 29;483(1):387-391.
Richarme G, Dairou J
PubMed publication date (edat): 12/26/2016
We discovered recently that Parkinsonism-associated DJ-1 and its bacterial homologs function as protein deglycases that repair glyoxal- and methylglyoxal-glycated proteins. Protein glycation levels are 2- to 10-fold increased in deglycase-depleted cells, and deglycase mutants display up to 500-fold loss of viability in methylglyoxal or glucose-containing media, suggesting that these deglycases play important roles in protecting cells against electrophile and carbonyl stress. Although the deglycase activity of DJ-1 is well supported by extensive biochemical work, Pfaff et al….claimed in a recent study that deglycation of the hemithioacetal formed upon cysteine glycation by methylglyoxal results from a Tris buffer artefact. Here, we show that this is not the case, and that DJ-1 and its homologs are the bona fide deglycases awaited since the Maillard discovery.