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Inhibition of Transforming Growth Factor (TGF)-β1–Induced Extracellular Matrix with a Novel Inhibitor of the TGF-β Type I Receptor Kinase Activity: SB-431542

Molecular Pharmacology · 2002 · Vol. 62(1) · pp. 58–64

Nicholas J. Laping✉(GlaxoSmithKline (United Kingdom))Eugene T. Grygielko(GlaxoSmithKline (United Kingdom))Anil Mathur(GlaxoSmithKline (United States))Sebastian Butter(GlaxoSmithKline (United States))Jennifer M. Bomberger(GlaxoSmithKline (United Kingdom))Christopher Tweed(GlaxoSmithKline (United States))W. Martin(GlaxoSmithKline (United Kingdom))James A. Fornwald(GlaxoSmithKline (United States))Ruth Lehr(GlaxoSmithKline (United Kingdom))John D. Harling(GlaxoSmithKline (United States))Laramie M. Gaster(GlaxoSmithKline (United States))James F. Callahan(GlaxoSmithKline (United Kingdom))Barbara A. Olson(GlaxoSmithKline (United Kingdom))

View via DOI Publisher page

TGF-β signaling in diseases Parathyroid Disorders and Treatments Connective Tissue Growth Factor ResearchSMADMAPK/ERK pathwayKinaseProtein kinase ACell biologyTransforming growth factorChemistryp38 mitogen-activated protein kinasesMAP kinase kinase kinaseSignal transduction

MeSH terms

Receptor, Transforming Growth Factor-beta Type IBenzamidesDioxolesEnzyme InhibitorsExtracellular MatrixFibronectinsHumansImidazolesPyridinesRNA, MessengerTumor Cells, CulturedTransforming Growth Factor betaProtein Serine-Threonine KinasesPlasminogen Activator Inhibitor 1Receptors, Transforming Growth Factor beta

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TGFβ/activin/nodal signaling is necessary for the maintenance of pluripotency in human embryonic stem cells