   3.4.21.38 | up |
transforming growth factor-beta1, TGF-beta1, a multifunctional cytokine, induces FXII expression, which is specifically repressed by the JNK inhibitor, and by JNK and Smad3 antisense oligonucleotides, but not by MEK, p38, or phosphoinositide 3-kinase blockers, overview. Treatment of human lung fibroblasts with TGF-beta1 results in a time-dependent increase in FXII production, activation of p44/42, p38, JNK, and Akt, and phosphorylation and translocation into the nucleus of Smad3. The FXII promoter contains the -299/+1 region, that is sufficient for TGF-beta1 to induce FXII expression, but the activation of FXII expression also requires Smad binding to TGF-beta1 at the a potential Smad binding element at position -272/-269 (SBE-(-272/-269)) of the TGF-beta1 promoter. JNK/Smad3 pathway plays a critical role in TGF-beta1-induced FXII expression in human lung fibroblasts |
709089 |
