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. 2017 Apr 1;353(1):46–53. doi: 10.1016/j.yexcr.2017.03.005

Fig. 4.

Fig. 4.

CHIP degrades CD166 through the ubiquitin-proteasome pathway in HNC cells. (A) The potential direct interaction of endogenous CD166 and CHIP was determined by co-IP analysis in HN13 and HN30 cells. (B) The direct co-localization of CD166 and CHIP in HN13 and HN30 cells was detected by confocal microscopy (red for CD166, green for CHIP). Nuclei were counter stained with DAPI (blue), bar=50 µm. (C) MG132 (10 μM) blocked the reduction in CD166 expression levels in HN13 cells transfected with exogenous CHIP. (D) The effects of MG132 and CHIP on the ubiquitination of exogenous CD166 were determined using a co-IP assay in 293 T cells. (E) The effects of CHIP on the ubiquitination of endogenous CD166 were determined by co-IP in HN13 cells co-transfected with HA-Ub. (F) The effect of 17-DMAG (2 μM) and CHIP on the protein expression levels of HSP90, HSP70 and CD166 in HN13 cells.