Transforming growth factor β-mediated site-specific Smad linker region phosphorylation in vascular endothelial cells (original) (raw)

Transforming growth factor-β signalling: Role and consequences of Smad linker region phosphorylation

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Smad linker region phosphorylation is a signalling pathway in its own right and not only a modulator of canonical TGF-β signalling

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Smad7 and protein phosphatase 1α are critical determinants in the duration of TGF-β/ALK1 signaling in endothelial cells

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Tgf-beta induced Erk phosphorylation of smad linker region regulates smad signaling

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Smad2 Mediates Transforming Growth Factor-beta Induction of Endothelial Nitric Oxide Synthase Expression

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Small C-terminal domain phosphatases dephosphorylate the regulatory linker regions of Smad2 and Smad3 to enhance transforming growth factor-β signaling

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KLF2 Suppresses TGF- Signaling in Endothelium Through Induction of Smad7 and Inhibition of AP-1

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TGF-β induces proangiogenic and antiangiogenic factorsvia parallel but distinct Smad pathways1

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Smad2 transduces common signals from receptor serine–threonine and tyrosine kinases

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CREB binding protein is a required coactivator for Smad-dependent, transforming growth factor transcriptional responses in endothelial cells

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CREB binding protein is a required coactivator for Smad-dependent, transforming growth factor β transcriptional responses in endothelial cells

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TGF-β and HGF transmit the signals through JNK-dependent Smad2/3 phosphorylation at the linker regions

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Balancing the activation state of the endothelium via two distinct TGF-beta type I receptors

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TGF-beta receptor-mediated signalling through Smad2, Smad3 and Smad4

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Few Smad proteins and many Smad-interacting proteins yield multiple functions and action modes in TGFβ/BMP signaling in vivo

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Smad7: not only a regulator, but also a cross-talk mediator of TGF-β signalling

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TGF-β through Smad3 signaling stimulates vascular smooth muscle cell proliferation and neointimal formation

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A Negative Feedback Control of Transforming Growth Factor- Signaling by Glycogen Synthase Kinase 3-mediated Smad3 Linker Phosphorylation at Ser-204

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Data from Molecular Imaging of TGFβ-Induced Smad2/3 Phosphorylation Reveals a Role for Receptor Tyrosine Kinases in Modulating TGFβ Signaling

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Identification of novel Smad2 and Smad3 associated proteins in response to TGF-β1

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Transforming growth factor-β1-induced endothelial barrier dysfunction involves Smad2-dependent p38 activation and subsequent RhoA activation

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Mechanisms of PAR-1 mediated kinase receptor transactivation: Smad linker region phosphorylation

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Smad proteins and transforming growth factor-beta signaling

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SMAD regulation in TGF-beta signal transduction

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Smad regulation in TGF-β signal transduction

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Protein Kinase A Modulates Transforming Growth Factor- Signaling through a Direct Interaction with Smad4 Protein

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Functional Characterization of Transforming Growth Factor beta Signaling in Smad2- and Smad3-deficient Fibroblasts

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Regulation of TGF-β signaling by Smad7

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Identification of Smad7, a TGFbeta-inducible antagonist of TGF-beta signalling

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Nitric Oxide Regulates Transforming Growth Factor- Signaling in Endothelial Cells

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