A cGAS-mediated mechanism in naked mole-rats potentiates DNA repair and delays aging.
www.science.org/doi/10.1126/...
JCI - Altered immune and metabolic molecular pathways drive islet cell dysfunction in human type 1 diabetes www.jci.org/articles/vie...
Frustration in the protein-protein interface plays a central role in the cooperativity of PROTAC ternary complexes.
www.nature.com/articles/s41...
Glycemia shifts pancreatic islet rhythmicity by influencing interactions between δ cells and α cells: Cell Systems www.cell.com/cell-systems...
Human pancreatic α-cell heterogeneity and trajectory inference analyses reveal SMOC1 as a β-cell dedifferentiation gene.
www.nature.com/articles/s41...
A metabolic atlas of mouse aging: Cell Metabolism www.cell.com/cell-metabol...
Cell-specific DNA methylation in human alpha and beta cells regulates gene expression in type 2 diabetes.
www.nature.com/articles/s42...
Taming Autoimmunity: Alpha-1 Antitrypsin Overexpressing Mesenchymal Stem/Stromal Cells Promote Regulatory T Cell Crosstalk to Reverse Diabetes: Molecular Therapy www.cell.com/molecular-th...
www.biorxiv.org
Geming Lu
Mapping of genome-wide DNA methylation patterns in human islet alpha and beta cells highlights age- and type 2 diabetes-dependent adaptations, and CRISPR-based epigenetic editing strategies validate k...
Efficient DNA repair might make possible the longevity of naked mole-rats. However, whether they have distinctive mechanisms to optimize functions of DNA repair suppressors is unclear. We find that na...
PROTACs induce degradation by bridging a target protein and E3 ubiquitin ligase. Here, authors show that protein interface frustration correlates with cooperativity, offering a structural metric to prioritize PROTAC candidates prior to synthesis.
Mapping of genome-wide DNA methylation patterns in human islet alpha and beta cells highlights age- and type 2 diabetes-dependent adaptations, and CRISPR-based epigenetic editing strategies validate k...
β-cell dysfunction and dedifferentiation towards an α-cell-like phenotype are hallmarks of type 2 diabetes. Her,e the authors detect five α-cell subpopulations, find differences between healthy and diabetic donors, and identify SMOC1 as an inducer of human β-cell dysfunction and dedifferentiation.
www.nature.com
Pilley et al. describe how metabolite levels change in 12 organs from male and female
mice across five ages, spanning adolescence to old age. They reveal that organs show
distinct age- and sex-specifi...
Glycemic fluctuations trigger a fast-slow oscillation switch in islet Ca2+ activity
in vivo. We show that this rhythmicity depends on α-δ cell interactions, is impaired
in diabetes, and is restored by...
AAT-overexpressing MSCs reverse new-onset diabetes in NOD mice by enhancing Treg expansion,
suppressing pathogenic CD4+ and CD8+ T cells, and improving immune communication in
pancreatic tissues. This...
