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. 2015 Nov 1;26(21):3867–3878. doi: 10.1091/mbc.E15-06-0442

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© 2015 Hughes, Oudin, et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 8: — Model for Mena-dependent regulation of RTK signaling. In average primary tumor cells, activation of EGFR leads to rapid recruitment of a SHIP2-Mena-PTP1B complex, which leads to receptor dephosphorylation by PTP1B and sensitivity to TKIs. However, in the invasive tumor cell population, where levels of Mena^INV are high, SHIP2-dependent recruitment of PTP1B to EGFR is abolished, eliminating PTP1B-mediated dephosphorylation of EGFR, causing sensitivity to EGF, as well as resistance to TKIs.