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. 2011 Aug 19;301(5):L667–L674. doi: 10.1152/ajplung.00423.2010

Fig. 6.

Fig. 6.

Schematic representation of the interactions between Rho/Rho-kinase signaling and bone morphogenetic protein (BMP)/transforming growth factor (TGF)-β signaling. In SM22-tet-BMPR2R899X mice, the levels of GTP-RhoA and MYPT1 phosphorylation were elevated, thus indicating that Rho/Rho-kinase signaling was activated. Two possible pathways, namely the Smad-dependent and Smad-independent pathways, in which BMP/TGF-β signaling activated Rho/Rho-kinase signaling are known. We confirmed that the Smad-dependent pathway was not altered. We therefore speculate that Rho/Rho-kinase signaling was activated via the Smad-independent pathway. Rho-GEF, Rho guanine nucleotide exchange factor; PP1c, catalytic subunit; M20, a 20-kDa subunit of unknown function; P, inorganic phosphate.