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You are here:Home-Inhibitors & Agonists-TGF-beta/Smad-TGF beta-Smad

Request The Product List ofTGF beta-Smad TGF beta-Smad

Transforming growth factor-beta (TGF-beta) is a multifunctional cytokine that regulates proliferation, migration, differentiation, and survival of many different cell types. Deletion or mutation of different members of the TGF-β family have been shown to cause vascular remodeling defect and absence of mural cell formation, leading to embryonic lethality or severe vascular disorders. TGF-β induces smooth muscle differentiation via Notch or SMAD2 and SMAD3 signaling in ES cells or in a neural crest stem cell line. TGF-β binds to TGF-βRI and to induce phosphorylation of SMAD2/3, thereby inhibiting proliferation, tube formation, and migration of endothelial cells (ECs).

TGF-β is a pluripotent cytokine with dual tumour-suppressive and tumour-promoting effects. TGF-β induces the epithelial-to-mesenchymal transition (EMT) leading to increased cell plasticity at the onset of cancer cell invasion and metastasis.

Cat. No. Product Name CAS No. Information
GY03111

Disitertide

272105-42-7

Disitertide (P144) is a TGF-β1 antagonist peptide; induces apoptosis in GBM cell lines and reduces SMAD2 phosphorylation with downregulation of SKI and an upregulation of SMAD7 at both transcriptional and translational levels; active in vivo.

GY01324

SIS3

521984-48-5

SIS3 (Specific Inhibitor of Smad3) is a potent, selective inhibitor of Smad3 function and TGF-β signaling, attenuates the TGF-β1-induced phosphorylation of Smad3 (IC50=3 uM) and interaction of Smad3 with Smad4; decreases the levels of the DNA-Smad3 binding by approximately 50% at 3 uM; shows no effect on phosphorylated levels of Smad2, Smad4 and Smad7, as well as the phosphorylation of other signaling pathways, such as MAPK/p38; attenuates the effects of TGF-beta1 by reducing the transcriptional activity, also inhibits the myofibroblast differentiation of fibroblasts by TGF-beta1, completely diminishes the constitutive phosphorylation of Smad3 as well as the up-regulated type I collagen expression in scleroderma fibroblasts.

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