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. 2018 Mar 5;143(3):679–685. doi: 10.1002/ijc.31332

Figure 1.

Figure 1

Lung adenocarcinoma‐driven EGFR mutants are oncogenic in the absence of tyrosine phosphorylation. (a) Schematic diagram of C‐terminal tyrosine residues and CYF10 mutants. (b) Tyrosine phosphorylation was not detectable in the CYF10 mutants. Whole‐cell lysates from NIH‐3T3 cells stably expressing wild‐type EGFR, L858R, Ex19Del or Ex20Ins mutants with or without the CYF10 mutation were subjected to immunoblotting with antibodies against phospho‐specific EGFR, phospho‐tyrosine (4G10), EGFR, p‐STAT3, STAT3, p‐Src and Src. (c–f) Transforming ability of mutant EGFR was not affected by abrogation of C‐terminal phosphorylation. Anchorage‐independent growth was assayed in the NIH‐3T3 cells used for immunoblotting in panel (b). The bar graph is depicted as relative number of colonies normalized to cell lines expressing the parental EGFR mutants (n = 3, mean + SD).