Background: Protein glycation is a nonenzymatic covalent reaction between proteins and carbonyl groups resulting in protein denaturation. Results: DJ-1 is the first protein deglycase that repairs proteins from glycation by glyoxals, which constitutes most glycation damage. Conclusion: DJ-1 is a novel protein repair enzyme that protects proteins against glycation. Significance: DJ-1 deglycase activity changes our view on glycation/deglycation and DJ-1-associated Parkinsonism.

Dendritic cell (DC) maturation and migration are events critical for the initiation of immune responses. After encountering pathogens, DCs upregulate the expression of costimulatory molecules and subsequently migrate to secondary lymphoid organs. Calcium (Ca2+) entry governs the functions of many hematopoietic cell types, but the role of Ca2+ entry in DC biology remains unclear. Here we report that the Ca2+-activated nonselective cation channel TRPM4 was expressed in and controlled the Ca2+ homeostasis of mouse DCs. The absence of TRPM4, which elicited Ca2+ overload, did not influence DC maturation but did considerably impair chemokine-dependent DC migration. Our results establish TRPM4-regulated Ca2+ homeostasis as crucial for DC mobility but not maturation and emphasize that DC maturation and migration are independently regulated.