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TGF-beta and epithelial-to-mesenchymal transitions.
TLDR
The distinct physiological contexts of EMT and the underlying molecular signaling networks controlled by TGF-beta are reviewed. Expand
Glucose-induced reactive oxygen species cause apoptosis of podocytes and podocyte depletion at the onset of diabetic nephropathy.
TLDR
It is demonstrated for the first time that glucose-induced ROS production initiates podocyte apoptosis and podocyte depletion in vitro and in vivo and suggested that podocytes apoptosis/depletion represents a novel early pathomechanism(s) leading to diabetic nephropathy in murine type 1 and type 2 diabetic models. Expand
Integration of TGF-beta/Smad and Jagged1/Notch signalling in epithelial-to-mesenchymal transition.
TLDR
It is reported that expression of the hairy/enhancer-of-split-related transcriptional repressor Hey1, and the Notch-ligand Jagged1 (Jag1), was induced by TGF-beta at the onset of EMT in epithelial cells from mammary gland, kidney tubules, and epidermis. Expand
TGF-β and epithelial-to-mesenchymal transitions
TLDR
The distinct physiological contexts of EMT and the underlying molecular signaling networks controlled by TGF-β are reviewed. Expand
Integration of TGF‐β/Smad and Jagged1/Notch signalling in epithelial‐to‐mesenchymal transition
TLDR
It is reported that expression of the hairy/enhancer‐of‐split‐related transcriptional repressor Hey1, and the Notch‐ligand Jagged1 (Jag1), was induced by TGF‐β at the onset of EMT in epithelial cells from mammary gland, kidney tubules, and epidermis. Expand
Functional Characterization of Transforming Growth Factor β Signaling in Smad2- and Smad3-deficient Fibroblasts*
TLDR
Analysis of the effects of TGF-β1 on fibroblasts derived from mouse embryos deficient in Smad2 (S2KO) or Smad3 (S3KO) indicates specific roles for Smad 2 and Smad 3 in TGF -β1 signaling. Expand
TGF-beta signaling in renal disease.
TLDR
Evidence is described in support of nonlinear models and functional roles of TGF-beta signaling in mediating apoptosis and epithelial-to-mesenchymal transdifferentiation in chronic progressive renal disease. Expand
Caveolin-1 Regulates Transforming Growth Factor (TGF)-β/SMAD Signaling through an Interaction with the TGF-β Type I Receptor*
TLDR
This work localizes the Type I TGF-β receptor interaction to the scaffolding domain of Cav-1 and shows that it occurs in a physiologically relevant time frame, acting to rapidly dampen signaling initiated by the TGF -β receptor complex. Expand
Caveolin-1 regulates transforming growth factor (TGF)-beta/SMAD signaling through an interaction with the TGF-beta type I receptor.
TLDR
This work localizes the Type I TGF-beta receptor interaction to the scaffolding domain of Cav-1 and shows that it occurs in a physiologically relevant time frame, acting to rapidly dampen signaling initiated by the TGF -beta receptor complex. Expand
A Novel Role for the Adaptor Molecule CD2-associated Protein in Transforming Growth Factor-β-induced Apoptosis*
TLDR
In vitro and in vivo findings suggest that TGF-β-induced podocyte apoptosis is an early pathomechanism in mice developing focal-segmental glomerulosclerosis associated with functional impairment of CD2AP. Expand
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