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. Author manuscript; available in PMC: 2014 Feb 26.
Published in final edited form as: Nat Rev Cancer. 2013 Jul 11;13(8):559–571. doi: 10.1038/nrc3563

Figure 3. Active ABL kinases regulate epithelial cell polarity through β1-integrin.

Figure 3

A. Epithelial cells expressing control vector or constitutively active forms of the ABL kinases were grown in collagen gels and stained for the apical polarity marker gp135, the adherens junction marker E-cadherin and the nuclear DAPI stain. Active ABL2, and to a lesser extent ABL1, promote polarity inversion. All pictures were taken at 40× magnification. Scale bar: 25 μm. B. Model for the inversion of epithelial cell polarity by active ABL kinase. Activation of ABL downstream of RTKs, chemokine receptors, oxidative stress and other signals leads to disruption of β1-integrin signaling and localization by regulation of the Rap1 GTPase via ABL2-mediated phosphorylation of CRK and disruption of the CRK-C3G (RAPGEF1) complex. Active ABL2 also impairs Rac1-mediated laminin assembly in epithelial cysts111.