Activin Receptor-Like Kinase Receptors ALK5 and ALK1 Are Both Required for TGFβ-Induced Chondrogenic Differentiation of Human Bone Marrow-Derived Mesenchymal Stem Cells

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Cartilage Repair With Autologous Bone Marrow Mesenchymal Stem Cell Transplantation

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Human Fetal and Adult Bone Marrow-Derived Mesenchymal Stem Cells Use Different Signaling Pathways for the Initiation of Chondrogenesis

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Dynamics of TGF-β/Smad signaling

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Failed cartilage repair for early osteoarthritis defects: a biochemical, histological and immunohistochemical analysis of the repair tissue after treatment with marrow-stimulation techniques

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The specificities of small molecule inhibitors of the TGFß and BMP pathways

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Myostatin (GDF-8) inhibits chondrogenesis and chondrocyte proliferationin vitroby suppressing Sox-9 expression

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Modulation of transforming growth factor beta signalling pathway genes by transforming growth factor beta in human osteoarthritic chondrocytes: involvement of Sp1 in both early and late response cells to transforming growth factor beta

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Osteochondrogenic potential of marrow mesenchymal progenitor cells exposed to TGF-β1 or PDGF-BB as assayed in vivo and in vitro

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Smad Signaling Determines Chondrogenic Differentiation of Bone-Marrow-Derived Mesenchymal Stem Cells: Inhibition of Smad1/5/8P Prevents Terminal Differentiation and Calcification

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Critical roles of the TGF-β type I receptor ALK5 in perichondrial formation and function, cartilage integrity, and osteoblast differentiation during growth plate development

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Increase in ALK1/ALK5 Ratio as a Cause for Elevated MMP-13 Expression in Osteoarthritis in Humans and Mice

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ALK1 Opposes ALK5/Smad3 Signaling and Expression of Extracellular Matrix Components in Human Chondrocytes

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