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. Author manuscript; available in PMC: 2019 May 2.
Published in final edited form as: Oncogene. 2018 Nov 2;38(11):1936–1950. doi: 10.1038/s41388-018-0537-0

Fig. 7.

Fig. 7.

EGFR is another RTK substrate of MET phosphorylated in the Golgi. (a) MHCC97-H cells were serum starved and treated −/+MET inhibitor for 18 hours (100nM capmatinib) and assayed for RTK phosphorylation using phospho-RTK array. (b) MHCC97-H cells were treated with EGFR inhibitor (10μM gefitinib), or MET inhibitor (100nM capmatinib), for 12 hours in serum-free media then fixed and stained for phospho-EGFR. Scale bars are 50μm.