Advanced Glycation End Products research

This study shows that HMGB1's B-box domain forms self-associates that enhance interactions with heparin through charge redistribution and conformational changes.

This study shows that reducing Glo1 in mice causes age- and sex-dependent metabolic issues like obesity and altered lipid metabolism without significant changes in AGEs.

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 examines how diabetes-induced AGEs and RAGE contribute to immune dysfunction and worsen tuberculosis severity in comorbid patients.

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

The paper examines how plasma glucose and albumin glycation rates relate to age and fitness in Alpine swifts, finding age-related changes and links to reproductive success and survival.

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 phosphorylation of threonine 107 in Glo1 by CamKIIδ increases its catalytic efficiency and reduces proteasomal degradation, enhancing MG detoxification.

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

The paper identifies a nuclear RAGE isoform in kidney tissue that binds to its own gene promoter, suggesting self-regulation of RAGE expression, which is altered in obesity and kidney disease.