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. 2019 Oct 16;294(48):18057–18068. doi: 10.1074/jbc.RA119.008925

Figure 6.

Figure 6.

TSG101 interacts with and augments the function of Parkin in endotoxin-treated hearts. A, coimmunoprecipitation (IP) using anti-TSG101 and immunoblotting (IB) for PINK1, Parkin, and TSG101 in hearts of WT and TG mice subjected to PBS or LPS treatment for 6 h. n = 4 for all groups. B, coimmunoprecipitation using anti-Parkin and immunoblotting for PINK1, Parkin, and TSG101 in hearts of WT and TG mice subjected to PBS or LPS treatment for 6 h. n = 4 for all groups. C, immunofluorescence staining for mitochondria (MitoTracker), TSG101, and Parkin in NRCMs treated with either PBS or LPS (1 μg/ml) for 3 h. n = 6 plates for each group. D, full-length human TSG101 (domains: UEV, proline-rich region (PRR), coiled coil (CC), and steadiness box (SB)) and the indicated myc-tagged TSG101 truncated mutations. E, representative immunoblots showing the expression of mCherry-Parkin and TSG101 mutants in HEK293T cells. n = 4 independent experiments. F, coimmunoprecipitation using anti-mCherry and immunoblotting for anti-myc in HEK293T cells cotransfected with mCherry-Parkin and myc-tagged TSG101 mutants. n = 4 independent experiments. G, coimmunoprecipitation using anti-myc and immunoblotting for anti-mCherry in HEK293T cells cotransfected with mCherry-Parkin and myc-tagged TSG101 mutants. n = 4 independent experiments.