Lysine deacetylase inhibition prevents diabetes by chromatin-independent immunoregulation and β-cell protection | Proceedings of the National Academy of Sciences thumbnail
Lysine deacetylase inhibition prevents diabetes by chromatin-independent immunoregulation and β-cell protection | Proceedings of the National Academy of Sciences
www.pnas.org
(KDACi) protect β-cells from inflammatory destruction in vitro and are promising immunomodulators reverted diabetes in a mouse model of type 1 diabetes and counteracted inflammatory target cell damage. doses that are safe and effective in human inflammatory diseases. mechanism of action was compatib
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  • (KDACi) protect β-cells from inflammatory destruction in vitro and are promising immunomodulators
  • reverted diabetes in a mouse model of type 1 diabetes and counteracted inflammatory target cell damage.
  • doses that are safe and effective in human inflammatory diseases.
  • mechanism of action was compatible with transcription factor—rather than global chromatin—hyperacetylation, causing inhibition of transcription factor binding and reduction of proinflammatory gene expression in leukocytes and β-cells.
  • nsulin-producing β-cells, givinostat did not upregulate expression of the anti-inflammatory genes Socs1-3 or sirtuin-1 but reduced levels of IL-1β + IFN-γ–induced proinflammatory Il1a, Il1b, Tnfα, Fas, Cxcl2, and reduced cytokine-induced ERK phosphorylation

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