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In summary, these data show that BH3 mimetics are substrates of ABCC1 and that overexpression of ABCC1 limits the sensitivity of AML cells to BCL-2 inhibitors by reducing their intracellular concentration
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Mechanistically, this compound can inhibit the NF-κB pathway and NLRP3 inflammasome activation, reducing inflammatory responses, restoring gut barrier function by enhancing goblet cells and tight junction proteins (ZO-1 and occludin) and modulating intestinal microbiota diversity [566]
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