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. Author manuscript; available in PMC: 2013 Mar 1.
Published in final edited form as: J Cell Mol Med. 2012 Mar;16(3):445–455. doi: 10.1111/j.1582-4934.2011.01419.x

Figure 2.

Figure 2

αV integrins recognize a RGD motif present in the LAP of TGF-β. This binding induces either adhesion-mediated cell forces and/or brings latent TGF-β into the proximity of MMPs which consequently lead to the liberation/activation of the TGF-β homodimer from its latent complex. Upon activation, the TGF-β homodimer will bind to the Type II TGF-β receptor initiating TGF-β-Smad signaling which upregulates the expression of αV integrins in addition to that of other EMT markers. These newly formed integrins can liberate more TGF-β from its latent complex, sustaining and reinforcing TGF-β induced EMT progression. This cooperative feed forward loop between αV integrins and TGF-β can lead to the unregulated TGF-β signaling responsible for a number of TGF-β-associated disorders.