https://www.selleckchem.com/products/sc-43.html
BACKGROUND AND PURPOSE Th17 cells play critical roles in chronic inflammation, including fibrosis. Histone acetyltransferase p300, a bromodomain-containing protein, acetylates RORγt and promotes Th17 cell development. The bromodomain inhibitor JQ1, was shown to alleviate Th17-mediated pathologies, but the underlying mechanism remains unclear. We hypothesized that JQ1 suppresses the response of Th17 cells by impairing p300-mediated acetylation of RORγt. EXPERIMENTAL APPROACH The effect of JQ1 on p300-mediated acetylation of RORγt was inves
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