Advanced Glycation End Products research

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.

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.

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

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.

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.

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

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

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

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

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.

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.

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

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

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

This study identifies Glyoxalase-1 (GLO1) as significantly upregulated in cervical cancer tissues and shows its role in cancer metabolism, suggesting it as a potential biomarker and therapeutic target.

The paper identifies glycated amines and glycated urea in diabetic patients' plasma as potential biomarkers for diabetic nephropathy.

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.

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