Skip to main content
Fig. 8 | Journal of Neuroinflammation

Fig. 8

From: Downregulating expression of OPTN elevates neuroinflammation via AIM2 inflammasome- and RIPK1-activating mechanisms in APP/PS1 transgenic mice

Fig. 8

OPTN degrades RIPK1 through the ubiquitin proteasome pathway. A BV2 cells overexpressing OPTN were treated with bafilomycin A1 (200 nM) or MG132 (10 μM) for 6 h. The expression of RIPK1 and OPTN was detected by western blotting using β-actin as an internal control. B ImageJ software was used to semiquantitatively analyze the western blot results. C Flag-RIPk1 was ectopically expressed in OPTN-silenced BV2 cells, which were then immunoprecipitated using an anti-Flag antibody derived from mice. The precipitated protein was further detected using a ubiquitin antibody derived from rabbits. Flag antibody was used to detect RIPK1, and OPTN was used to detect the OPTN protein levels in the total protein. In the right panel, ImageJ software was used to semiquantitatively analyze ubiquitin levels. D OPTN was ectopically overexpressed in Flag-RIPk1-overexpressing BV2 cells, which were then immunoprecipitated using an anti-Flag antibody derived from mice. The precipitated protein was detected using rabbit-derived ubiquitin antibody. Flag antibodies were used to detect the protein levels of RIPK1, and OPTN was used to detect OPTN levels in whole-cell lysates. In the right panel, ImageJ software was used to semiquantitatively analyze ubiquitin levels. The data present means ± S.M. of independent experiment. OPTN silenced or overexpressed BV2 cells compared with control group, *P < 0.05, **P < 0.01

Back to article page