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TGF-beta and epithelial-to-mesenchymal transitions.
Remarkable phenotype plasticity of epithelial cells underlies morphogenesis, epithelial repair and tumor invasiveness. Detailed understanding of the contextual cues and molecular mediators thatExpand
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Glucose-induced reactive oxygen species cause apoptosis of podocytes and podocyte depletion at the onset of diabetic nephropathy.
Diabetic nephropathy is the most common cause of end-stage renal disease in the U.S. Recent studies demonstrate that loss of podocytes is an early feature of diabetic nephropathy that predicts itsExpand
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Integration of TGF-beta/Smad and Jagged1/Notch signalling in epithelial-to-mesenchymal transition.
Epithelial-to-mesenchymal transitions (EMTs) underlie cell plasticity required in embryonic development and frequently observed in advanced carcinogenesis. Transforming growth factor-beta (TGF-beta)Expand
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TGF-beta signaling in renal disease.
Since discovery over a decade ago of a role for the cytokine TGF-beta as key mediator of glomerular and tubulointerstitial pathobiology in chronic kidney diseases, studies of TGF-beta signaling inExpand
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TGF-β and epithelial-to-mesenchymal transitions
Remarkable phenotype plasticity of epithelial cells underlies morphogenesis, epithelial repair and tumor invasiveness. Detailed understanding of the contextual cues and molecular mediators thatExpand
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Functional Characterization of Transforming Growth Factor β Signaling in Smad2- and Smad3-deficient Fibroblasts*
A prominent pathway of transforming growth factor (TGF)-β signaling involves receptor-dependent phosphorylation of Smad2 and Smad3, which then translocate to the nucleus to activate transcription ofExpand
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Caveolin-1 Regulates Transforming Growth Factor (TGF)-β/SMAD Signaling through an Interaction with the TGF-β Type I Receptor*
Transforming growth factor-β (TGF-β) signaling proceeds from the cell membrane to the nucleus through the cooperation of the type I and II serine/threonine kinase receptors and their downstream SMADExpand
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Caveolin-1 regulates transforming growth factor (TGF)-beta/SMAD signaling through an interaction with the TGF-beta type I receptor.
Transforming growth factor-beta (TGF-beta) signaling proceeds from the cell membrane to the nucleus through the cooperation of the type I and II serine/threonine kinase receptors and their downstreamExpand
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The Electronic Medical Records and Genomics (eMERGE) Network: past, present, and future
The Electronic Medical Records and Genomics Network is a National Human Genome Research Institute–funded consortium engaged in the development of methods and best practices for using the electronicExpand
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Apoptosis in podocytes induced by TGF-beta and Smad7.
Primary and secondary forms of focal segmental glomerulosclerosis (FSGS) are characterized by depletion of podocytes and constitute a central manifestation of chronic progressive glomerular diseases.Expand
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