Smad7: licensed to kill beta-catenin.
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.
Millar
Sarah E
SE
Department of Dermatology, University of Pennsylvania, M8D Stellar-Chance Laboratories, 422 Curie Boulevard, Philadelphia, 19104, USA.
D000818:Animals; D019485:Bone Morphogenetic Proteins / Q000378:metabolism; D002454:Cell Differentiation; D018859:Hair Follicle / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D008954:Models, Biological; D015398:Signal Transduction; D051906:Smad7 Protein / Q000378:metabolism / Q000502:physiology*; D013234:Stem Cells / Q000502:physiology*; D016212:Transforming Growth Factor beta / Q000378:metabolism; D044767:Ubiquitin-Protein Ligases / Q000378:metabolism; D051176:beta Catenin / Q000378:metabolism*
D019485:Bone Morphogenetic Proteins; D051906:Smad7 Protein; D016212:Transforming Growth Factor beta; D051176:beta Catenin; C471641:SMURF2 protein, human; D044767:Ubiquitin-Protein Ligases