Jagged/Notch signalling is required for a subset of TGFβ1 responses in human kidney epithelial cells.

[1]  C. Pollock,et al.  Notch mediated epithelial to mesenchymal transformation is associated with increased expression of the Snail transcription factor. , 2010, The international journal of biochemistry & cell biology.

[2]  Robert H. Jenkins,et al.  Loss of MicroRNA-192 promotes fibrogenesis in diabetic nephropathy. , 2010, Journal of the American Society of Nephrology : JASN.

[3]  Y. Kong,et al.  Inactivation of Notch signaling in the renal collecting duct causes nephrogenic diabetes insipidus in mice. , 2009, The Journal of clinical investigation.

[4]  R. Goldschmeding,et al.  Allelic Depletion of grem1 Attenuates Diabetic Kidney Disease , 2009, Diabetes.

[5]  Raphael Kopan,et al.  The Canonical Notch Signaling Pathway: Unfolding the Activation Mechanism , 2009, Cell.

[6]  Zhiwei Wang,et al.  Acquisition of epithelial-mesenchymal transition phenotype of gemcitabine-resistant pancreatic cancer cells is linked with activation of the notch signaling pathway. , 2009, Cancer research.

[7]  M. Mattson,et al.  Notch: from neural development to neurological disorders , 2008, Journal of neurochemistry.

[8]  E. Bradley,et al.  TGF-beta coordinately activates TAK1/MEK/AKT/NFkB and SMAD pathways to promote osteoclast survival. , 2008, Experimental cell research.

[9]  F. Brosius New insights into the mechanisms of fibrosis and sclerosis in diabetic nephropathy , 2008, Reviews in Endocrine and Metabolic Disorders.

[10]  C. Lobe,et al.  Ectopic notch activation in developing podocytes causes glomerulosclerosis. , 2008, Journal of the American Society of Nephrology : JASN.

[11]  H. Kuwana,et al.  Expression and function of the Delta-1/Notch-2/Hes-1 pathway during experimental acute kidney injury. , 2008, Kidney international.

[12]  D. Brazil,et al.  Protein kinase B/Akt activity is involved in renal TGF-β1-driven epithelial-mesenchymal transition in vitro and in vivo , 2008, American journal of physiology. Renal physiology.

[13]  K. Suszták,et al.  The Notch pathway in podocytes plays a role in the development of glomerular disease , 2008, Nature Medicine.

[14]  M. Kretzler,et al.  Notch inhibition reverses kidney failure. , 2008, Nature medicine.

[15]  S. Ishikawa,et al.  p63 - Key molecule in the early phase of epithelial abnormality in idiopathic pulmonary fibrosis. , 2007, Experimental and molecular pathology.

[16]  Govind Bhagat,et al.  Mutational loss of PTEN induces resistance to NOTCH1 inhibition in T-cell leukemia , 2007, Nature Medicine.

[17]  A. McMahon,et al.  Notch2, but not Notch1, is required for proximal fate acquisition in the mammalian nephron , 2007, Development.

[18]  M. Jinnin,et al.  Characterization of SIS3, a Novel Specific Inhibitor of Smad3, and Its Effect on Transforming Growth Factor-β1-Induced Extracellular Matrix Expression , 2006, Molecular Pharmacology.

[19]  M. Kretzler,et al.  Expression of gremlin, a bone morphogenetic protein antagonist, in human diabetic nephropathy. , 2005, American journal of kidney diseases : the official journal of the National Kidney Foundation.

[20]  T. Piscione,et al.  Expression of Hairy/Enhancer of Split genes, Hes1 and Hes5, during murine nephron morphogenesis. , 2004, Gene expression patterns : GEP.

[21]  P. Cahill,et al.  Notch 1 and 3 receptors modulate vascular smooth muscle cell growth, apoptosis and migration via a CBF‐1/RBP‐Jk dependent pathway , 2004, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[22]  K. Luo,et al.  Akt interacts directly with Smad3 to regulate the sensitivity to TGF-β-induced apoptosis , 2004, Nature Cell Biology.

[23]  Stephen W. Michnick,et al.  PKB/Akt modulates TGF-β signalling through a direct interaction with Smad3 , 2004, Nature Cell Biology.

[24]  J. Zavadil,et al.  Integration of TGF‐β/Smad and Jagged1/Notch signalling in epithelial‐to‐mesenchymal transition , 2004 .

[25]  R. Kalluri,et al.  Epithelial-mesenchymal transition and its implications for fibrosis. , 2003, The Journal of clinical investigation.

[26]  Raphael Kopan,et al.  γ-Secretase activity is dispensable for mesenchyme-to-epithelium transition but required for podocyte and proximal tubule formation in developing mouse kidney , 2003, Development.

[27]  Hui Zheng,et al.  Presenilins are required for the formation of comma- and S-shaped bodies during nephrogenesis , 2003, Development.

[28]  E. Neilson,et al.  Evidence that fibroblasts derive from epithelium during tissue fibrosis. , 2002, The Journal of clinical investigation.

[29]  C. Arteaga,et al.  p38 mitogen-activated protein kinase is required for TGFbeta-mediated fibroblastic transdifferentiation and cell migration. , 2002, Journal of cell science.

[30]  R. Kalluri,et al.  Role of basic fibroblast growth factor-2 in epithelial-mesenchymal transformation. , 2002, Kidney international.

[31]  S. Hubscher,et al.  Altered Notch ligand expression in human liver disease: further evidence for a role of the Notch signaling pathway in hepatic neovascularization and biliary ductular defects. , 2002, The American journal of pathology.

[32]  Junwei Yang,et al.  Dissection of key events in tubular epithelial to myofibroblast transition and its implications in renal interstitial fibrosis. , 2001, The American journal of pathology.

[33]  J. Zavadil,et al.  Genetic programs of epithelial cell plasticity directed by transforming growth factor-β , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[34]  G. Weinmaster,et al.  Epstein-Barr Virus BamHI-A Rightward Transcript-Encoded RPMS Protein Interacts with the CBF1-Associated Corepressor CIR To Negatively Regulate the Activity of EBNA2 and NotchIC , 2001, Journal of Virology.

[35]  Raphael Kopan,et al.  Notch signaling: from the outside in. , 2000, Developmental biology.

[36]  H. Moses,et al.  Phosphatidylinositol 3-Kinase Function Is Required for Transforming Growth Factor β-mediated Epithelial to Mesenchymal Transition and Cell Migration* , 2000, The Journal of Biological Chemistry.

[37]  K. Miyazono TGF-β signaling by Smad proteins , 2000 .

[38]  R. Atkins,et al.  Tubular epithelial-myofibroblast transdifferentiation in progressive tubulointerstitial fibrosis in 5/6 nephrectomized rats. , 1998, Kidney international.

[39]  F. Strutz,et al.  Transdifferentiation: a new angle on renal fibrosis. , 1996, Experimental nephrology.

[40]  F. Strutz,et al.  Identification and characterization of a fibroblast marker: FSP1 , 1995, The Journal of cell biology.

[41]  E Ruoslahti,et al.  Expression of transforming growth factor beta is elevated in human and experimental diabetic nephropathy. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[42]  E. Ruoslahti,et al.  Transforming growth factor-beta in disease: the dark side of tissue repair. , 1992, The Journal of clinical investigation.

[43]  A. McMahon,et al.  Fate tracing reveals the pericyte and not epithelial origin of myofibroblasts in kidney fibrosis. , 2010, The American journal of pathology.

[44]  M. Iwano EMT and TGF-beta in renal fibrosis. , 2010, Frontiers in bioscience.

[45]  D. Higgins,et al.  Co-regulation of Gremlin and Notch signalling in diabetic nephropathy. , 2008, Biochimica et biophysica acta.

[46]  S. Klahr,et al.  Transforming growth factor-beta induces renal epithelial jagged-1 expression in fibrotic disease. , 2002, Journal of the American Society of Nephrology : JASN.

[47]  H. Moses,et al.  Transforming growth factor-beta1 mediates epithelial to mesenchymal transdifferentiation through a RhoA-dependent mechanism. , 2001, Molecular biology of the cell.