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Fig. 7. Model for latent TGF-ß activation in ECR3E-Myc and ECR3E-1-2-Myc skin. (A) In the presence of wild-type LTBP and/or ECR3E-1-2-Myc, the latent TGF-ß SLC is bound to LTBP and sequestered into the matrix. This prevents latent TGF-ß from interacting with cell-associated activators until the appropriate time. (B) In the situation in which ECR3E-Myc is overproduced, it out-competes LTBP for binding to SLC. The complex of ECR3E-Myc and SLC is not incorporated into the ECM as it is missing the N- and C-terminal matrix binding sites of LTBP. The soluble latent TGF-ß complex, therefore, interacts with cell-associated activators generating active TGF-ß, which causes increased signaling through its receptor and accumulation of nuclear pSmad2/3.
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