Advanced Glycation End Products research

Engineered HMGB1 construct with tandem Box B domains promotes tissue regeneration without potential for deleterious inflammation or thrombosis

Ancestral protein reconstruction reveals the mechanism of substrate specificity in FN3K-mediated deglycation.

This study uses ancestral protein reconstruction to uncover the molecular mechanism of substrate specificity in FN3K and KT3K enzymes, revealing an allosteric network that modulates substrate recognition.

Discovery of Glycation-Derived Crosslinks at Arginine

This study discovers a new type of glycation crosslink, MIDAL, formed by methylglyoxal in Arg-Arg sites, and presents a platform for studying crosslinking AGEs.

Dicarbonyl stress debilitates mesothelial defense against metastasizing ovarian cancer

This study shows dicarbonyl stress weakens mesothelial barriers, enabling ovarian cancer metastasis, and identifies GLO-1 as a potential therapeutic target.

Methylglyoxal-induced glycation stress promotes aortic stiffening: Putative mechanistic roles of oxidative stress and cellular senescence

This study shows that methylglyoxal-induced glycation stress causes aortic stiffening through oxidative stress and cellular senescence, and a glycation-lowering compound mitigates these effects.

Glycation enhances protein association with lipid bilayer membranes

This study shows glycation increases the binding of bovine serum albumin to negatively charged lipid bilayers, altering protein-membrane interactions and potentially affecting biomarker behavior and disease mechanisms.

Histone serves as an eat-me signal to induce RAGE-mediated phagocytosis

The paper identifies histones as RAGE-mediated eat-me signals that enhance phagocytosis of apoptotic cells and show physiological relevance in wound healing.

A Chemical Mechanistic Path Leads the Way to Cellular Argpyrimidine

This study identifies a chemical mechanism for argpyrimidine formation from methylglyoxal, showing phosphorylated residues promote APY formation and linking glycation to phosphorylation.

Glycation-lowering compounds inhibit ghrelin signaling to reduce food intake, lower insulin resistance, and extend lifespan.

Gly-Low compounds reduce glycation, lower food intake, improve insulin sensitivity, and extend lifespan in mice by inhibiting ghrelin signaling and enhancing mTOR pathways.

Predictable modulation of a spontaneous post-translational modification in living cells

This paper introduces dialAGE, a method to control site-specific glycation in proteins, showing it works in vitro and in living cells.

Variation in albumin glycation rates in birds suggests resistance to relative hyperglycaemia rather than conformity to the pace of life syndrome hypothesis

This study examines glycation rates and glucose levels across 88 bird species to assess their relationship with life history traits, finding resistance to glycation in high glucose species and unexpected patterns in lifespan and diet.

The sex-specific effects of RAGE signaling and Type 2 Diabetes on mouse cortical bone mechanics, structure, and material properties

This study examines how RAGE signaling and Type 2 Diabetes affect cortical bone mechanics, structure, and material properties in mice, showing sex-specific improvements with RAGE ablation.

The molecular basis of Human FN3K mediated phosphorylation of glycated substrate

This study determines crystal structures of HsFN3K to elucidate its substrate recognition and kinase activity, providing insights for small molecule design targeting FN3K.

AGEing of Collagen: The Effects of Glycation on Collagen's Stability, Mechanics and Assembly

This study examines how glycation affects collagen stability, mechanics, and self-assembly, showing reduced triple helical stability, increased stiffness, and impaired fibril formation.

Increased levels of circulating methylglyoxal have no consequence for cerebral microvascular integrity and cognitive function in young healthy mice

This study shows increased circulating methylglyoxal in healthy mice does not cause cerebral microvascular dysfunction or cognitive impairment.

Study on the influence of G82S RAGE polymorphism on RAGE-Amyloid interaction in AD pathology

This study investigates how the G82S RAGE polymorphism affects RAGE-Amyloid interaction in AD by using molecular dynamics and in vitro binding experiments, finding that the mutant has higher binding affinity for Aβ42.

Globally elevating the AGE clearance receptor, OST48, does not protect against the development of diabetic kidney disease, despite improving insulin secretion.

This study shows that increasing OST48 expression in diabetic mice improves insulin secretion but does not prevent diabetic kidney disease despite enhancing AGE clearance.