IndraLab

"As a control, we monitored phosphorylation of transfected TbetaRI, and observed phosphorylation of the receptor upon treatment of cells with TGFbeta1, as expected (Figure 6C, second from the top panel)."

"The binding of TGF-beta1 to a type II TGF-beta receptor causes the recruitment and phosphorylation of TGF-beta receptor type I, which in turn recruits and phosphorylates the receptor regulated Smad2/3[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"TGFbeta1 signaling is initiated by binding to the constitutively active type II serine threonine kinase receptor which, in turn, recruits and phosphorylates the type I receptor, the so called activin receptor like kinese 5, ALK5 32."

"Interestingly, TGF-beta1 promoted TbetaRI phosphorylation in VSMCs, while AAT1 or AAT2 overexpression indeed downregulated the TGF-beta1-induced TbetaRI phosphorylation (XREF_FIG)."

"Binding of TGFbeta1 to TbetaRII, a cell surface TGFbeta1 receptor, phosphorylates TbetaRI, which subsequently phosphorylates Smad2 and Smad3 for the induction of fibrogenic response [53]."

"Sal B treatment attenuated TGF-β1-induced TβR-I and Smad2/3 phosphorylation and up-regulated Smad7 expression in HK-2 cells."

"TGF-β1 binds to the Type II receptor at the cell surface and recruits and phosphorylates the Type I receptor."

"Simplified schematic drawing of the TGF-?-Smad pathway. Binding of TGF-? to its type II receptor in concert with the type I receptor (A) leads to formation of a receptor complex and phosphorylation of the type I receptor. The type I receptor subsequently phosphorylates Smad2 or 3 (B), allowing this complex to associate with Smad4 and move into the nucleus (C). In the nucleus, the Smad complex associates with a transcription factor and this complex binds to specific enhancers in target genes (down-) regulating transcription (D). TNF is able to interfere with TGF-? signaling through the upregulation of the inhibitory Smad7 protein (E). Smad7 is capable of inhibiting the Smad2 and 3 phosphorylating process by competing with the receptor interaction but Smad7 also can dephosphorylate the complex. In addition, Smad7 itself is capable to upregulate TGF? gene expression. As described in the discussion, CSE is most likely capable to interfere with the Smad pathway although this is not yet fully elucidated. (F). Phosphorylated Smad3 is able to stimulate the transcription of the decorin gene (G)."

"The SEB staphylococcal enterotoxin B XlYl motif (using single-letter code for amino acids), TGF-p transforming growth factor p needed for the binding of CD28 and (:?,A--! to B7 lig- ands, is not[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"Abbreviations CNS ECM CS-PGs GAG 3-D DRG RPTWB O-2A TGFb EGF TGFclcentral nervous system extracellular matrix chondroitin sulphateproteoglycans glycosaminoglycan three- dimensional [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"TGF-beta1 could significantly increase the phosphorylation of TbetaRI (P < 0.05), whereas SO 2 treatment markedly attenuated serine phosphorylation of TbetaRI (P < 0.05)."