Elevated levels of inhibitory Smad7 are detected in several pathologic skin conditions; however the functional consequences of this expression have been unclear. A recent study shows that Smad7 overexpression in transgenic mouse epidermis at levels comparable to those seen in pathologic states is insufficient to block TGFbeta or BMP signaling, but instead produces striking phenotypes due to degradation of beta-catenin through a novel mechanism involving Smad7 and Smurf2.
