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. 2021 Oct 12;9:764727. doi: 10.3389/fcell.2021.764727

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Copyright © 2021 Stuelten and Zhang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Canonical and alternative TGF-β signaling cascades. TGF-β can be activated by (1) traction force mediated release from the latent complex after binding to integrin αvβ6 or by (2) proteolysis after binding of the latent complex to integrin αvβ8. (3) TGF-β binds to specific receptors, TGFβR2 and TGFβR1 (ALK5), to initiate canonical Smad2/3 signaling. Alternatively, TGF-β can bind to (4) TGFβR2/ALK1/endoglin complexes or (5) TGFβR2/ALK5—TGFβR2/ALK1/2 complexes to activate Smad1/5/8 signaling. Alternatively to the Smad2/3 signaling cascade TGFβR2/ALK5 complexes can also activate MAPK-, Rho/ROCK- and cdc42/Rac/Pac signaling cascaded. pSmad3 itself can bind to (7) PCBP1 to support alternative mRNA splicing. (8) The binding of Smad2/3/Smad4 complexes to YAP/TAZ also alters gene expression profiles.