Fig. 6: TGFβ priming promotes IRF8 ubiquitination and degradation in response to TNF. | Nature Communications

Fig. 6: TGFβ priming promotes IRF8 ubiquitination and degradation in response to TNF.

From: TGFβ reprograms TNF stimulation of macrophages towards a non-canonical pathway driving inflammatory osteoclastogenesis

Fig. 6

a, b Immunoblot analysis (a) and qPCR analysis (n = 5/group) (b) of IRF8 expression using human CD14(+) monocytes treated with or without TGFβ priming for 3 days, followed by TNF stimulation at the indicated times. p38 was used as a loading control (a). c Immunoblot analysis of the expression of IRF8 using human CD14(+) monocytes treated with or without TGFβ priming for 3 days, followed by TNF stimulation together with DMSO or MG132 (25 µM) for the indicated times. p38 was used as a loading control. d Immunoblot analysis of the expression of IRF8 using human CD14(+) monocytes treated with or without TGFβ priming for 3 days, then CHX (50 µM) for 30 min, followed by TNF stimulation together with DMSO or MG132 (25 µM) for the indicated times. p38 was used as a loading control. e Ubiquitination of IRF8 in the human CD14(+) monocytes treated with or without TGFβ priming for 3 days, followed by TNF stimulation together with DMSO or MG132 (25 µM) for the indicated times. Cell lysates were immunoprecipitated with anti-IRF8 antibody followed by immunoblotting with anti-Ub antibody. IP, immunoprecipitation; IB, immunoblotting. b Data are mean ± SD. Source data are provided as a Source Data file.

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