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. Author manuscript; available in PMC: 2019 Jan 18.
Published in final edited form as: Cell Chem Biol. 2017 Nov 9;25(1):67–77.e3. doi: 10.1016/j.chembiol.2017.09.009

Figure 5. Exon 14-deleted c-Met has increased stability and resistance to HGF-mediated degradation that can be combated by foretinib-based PROTAC 7.

Figure 5

A – Quantitation of WT c-Met or exon 14-deleted c-Met degradation upon treatment with HGF, PROTAC 7 or DMSO control in the presence of cycloheximide (CHX). B – Table of calculated half-lives. C – Representative CHX time course of WT c-Met degradation and signalling in MDA-MB-231 cells treated with HGF. D – Representative CHX time course of exon 14 deleted c-Met degradation and signalling in Hs746T cells treated with HGF. E - Representative CHX time course of exon 14-deleted c-Met degradation in Hs746T cells treated with PROTAC 7. F and G – Both MDA-MB-231 and Hs746T cells were treated with either DMSO or PROTAC for 18 hours before the addition of HGF and lysis at the indicated time points following stimulation. H – Immunoprecipitation of c-Met from PROTAC 7 (1μM) or DMSO treated Hs746T cells followed by immunoblotting for Ubiquitin. I – Tandem Ubiquitin Binding Entity 1 (TUBE1) pulldown from PROTAC 7 (1μM) or DMSO treated Hs746T cells followed by immunoblotting for c-Met See also Figure S6.