PYR-41 and Thalidomide Impair Dendritic Cell Cross-Presentation by Inhibiting Myddosome Formation and Attenuating the Endosomal Recruitments of p97 and Sec61 via NF-κB Inactivation
Treatment with PYR-41 or thalidomide inhibits LPS-induced NF-κB activation. Murine bone marrow-derived DC (cultured for 4 d) conferred thalidomide (30 μM), PYR-41 (5 μM), or DMSO treatment prior to LPS (50 ng/ml) stimulation. (a–c) The effects of LPS, PYR-41, and thalidomide on NF-κB activation were determined by Western blot by revealing IκBα degradation and p65 phosphorylation. GAPDH was used as internal control. (d) The effects of LPS, PYR-41, and thalidomide on NF-κB activation were determined by confocal microscope by revealing the nuclei relocation of phosphorylated p65. Nuclei were counterstained with DAPI (blue). Original magnification, ×600. Data were presented as the mean ± SEM, , and one-way ANOVA with Newman–Keuls post test. One representative from 3 independent experiments was shown.
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