Constance E Runyan

Summary

Affiliation: Northwestern University
Country: USA

Publications

  1. pmc Role of SARA (SMAD anchor for receptor activation) in maintenance of epithelial cell phenotype
    Constance E Runyan
    Department of Pediatrics, Northwestern University, Chicago, Illinois 60611, USA
    J Biol Chem 284:25181-9. 2009
  2. pmc Phosphatidylinositol 3-kinase and Rab5 GTPase inversely regulate the Smad anchor for receptor activation (SARA) protein independently of transforming growth factor-β1
    Constance E Runyan
    Department of Pediatrics, Northwestern University, Chicago, Illinois 60611, USA
    J Biol Chem 287:35815-24. 2012
  3. ncbi request reprint The role of internalization in transforming growth factor beta1-induced Smad2 association with Smad anchor for receptor activation (SARA) and Smad2-dependent signaling in human mesangial cells
    Constance E Runyan
    Department of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA
    J Biol Chem 280:8300-8. 2005
  4. ncbi request reprint TGF-beta receptor-binding proteins: complex interactions
    Constance E Runyan
    Department of Pediatrics, Feinberg School of Medicine, Chicago, IL, USA
    Cell Signal 18:2077-88. 2006
  5. ncbi request reprint The phosphatidylinositol 3-kinase/Akt pathway enhances Smad3-stimulated mesangial cell collagen I expression in response to transforming growth factor-beta1
    Constance E Runyan
    Department of Pediatrics, Northwestern University, Chicago, Illinois 60611, USA
    J Biol Chem 279:2632-9. 2004
  6. ncbi request reprint Cytoskeletal rearrangement and signal transduction in TGF-beta1-stimulated mesangial cell collagen accumulation
    Susan C Hubchak
    Department of Pediatrics, Northwestern University Medical School, Chicago, Illinois, USA
    J Am Soc Nephrol 14:1969-80. 2003
  7. ncbi request reprint Smad3 and PKCdelta mediate TGF-beta1-induced collagen I expression in human mesangial cells
    Constance E Runyan
    Northwestern Univ, Dept of Pediatrics, Chicago, IL 60611 3008, USA
    Am J Physiol Renal Physiol 285:F413-22. 2003
  8. pmc Interdependence of HIF-1α and TGF-β/Smad3 signaling in normoxic and hypoxic renal epithelial cell collagen expression
    Rajit K Basu
    Divisions of Critical Care, Northwestern University Feinberg School of Medicine, Chicago, IL, USA
    Am J Physiol Renal Physiol 300:F898-905. 2011
  9. ncbi request reprint TGF-beta signal transduction in chronic kidney disease
    H William Schnaper
    Division of Kidney Diseases, Department of Pediatrics, Northwestern University Feinberg School of Medicine, 303 E Chicago Ave Chicago, IL 60611 3008, USA
    Front Biosci (Landmark Ed) 14:2448-65. 2009
  10. doi request reprint A conceptual framework for the molecular pathogenesis of progressive kidney disease
    H William Schnaper
    Division of Kidney Diseases, Department of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA
    Pediatr Nephrol 25:2223-30. 2010

Detail Information

Publications11

  1. pmc Role of SARA (SMAD anchor for receptor activation) in maintenance of epithelial cell phenotype
    Constance E Runyan
    Department of Pediatrics, Northwestern University, Chicago, Illinois 60611, USA
    J Biol Chem 284:25181-9. 2009
    ..In part, this is achieved by enhancing the association of Smad2 with Smurf2, leading to Smad2 degradation...
  2. pmc Phosphatidylinositol 3-kinase and Rab5 GTPase inversely regulate the Smad anchor for receptor activation (SARA) protein independently of transforming growth factor-β1
    Constance E Runyan
    Department of Pediatrics, Northwestern University, Chicago, Illinois 60611, USA
    J Biol Chem 287:35815-24. 2012
    ..Together, these data suggest that although TGF-β1 can induce epithelial-to-mesenchymal transition through reduction in SARA expression, SARA is also basally regulated by its interaction with PI3K...
  3. ncbi request reprint The role of internalization in transforming growth factor beta1-induced Smad2 association with Smad anchor for receptor activation (SARA) and Smad2-dependent signaling in human mesangial cells
    Constance E Runyan
    Department of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA
    J Biol Chem 280:8300-8. 2005
    ....
  4. ncbi request reprint TGF-beta receptor-binding proteins: complex interactions
    Constance E Runyan
    Department of Pediatrics, Feinberg School of Medicine, Chicago, IL, USA
    Cell Signal 18:2077-88. 2006
    ..The present article reviews our current understanding of the roles and mechanisms of action of this relatively understudied group of molecules...
  5. ncbi request reprint The phosphatidylinositol 3-kinase/Akt pathway enhances Smad3-stimulated mesangial cell collagen I expression in response to transforming growth factor-beta1
    Constance E Runyan
    Department of Pediatrics, Northwestern University, Chicago, Illinois 60611, USA
    J Biol Chem 279:2632-9. 2004
    ..This cross-talk between the Smad and PI3K pathways likely contributes to TGF-beta1 induction of glomerular scarring...
  6. ncbi request reprint Cytoskeletal rearrangement and signal transduction in TGF-beta1-stimulated mesangial cell collagen accumulation
    Susan C Hubchak
    Department of Pediatrics, Northwestern University Medical School, Chicago, Illinois, USA
    J Am Soc Nephrol 14:1969-80. 2003
    ..Thus, TGF-beta1-mediated collagen I accumulation is associated with cytoskeletal rearrangement and Rho-GTPase signaling...
  7. ncbi request reprint Smad3 and PKCdelta mediate TGF-beta1-induced collagen I expression in human mesangial cells
    Constance E Runyan
    Northwestern Univ, Dept of Pediatrics, Chicago, IL 60611 3008, USA
    Am J Physiol Renal Physiol 285:F413-22. 2003
    ..Thus cross talk among multiple signaling pathways likely contributes to the pathogenesis of glomerular matrix accumulation...
  8. pmc Interdependence of HIF-1α and TGF-β/Smad3 signaling in normoxic and hypoxic renal epithelial cell collagen expression
    Rajit K Basu
    Divisions of Critical Care, Northwestern University Feinberg School of Medicine, Chicago, IL, USA
    Am J Physiol Renal Physiol 300:F898-905. 2011
    ..Taken together, our data demonstrate cooperation in signaling between Smad3 and HIF-1α and suggest a new paradigm in which HIF-1α is necessary for normoxic, TGF-β1-stimulated renal cell fibrogenesis...
  9. ncbi request reprint TGF-beta signal transduction in chronic kidney disease
    H William Schnaper
    Division of Kidney Diseases, Department of Pediatrics, Northwestern University Feinberg School of Medicine, 303 E Chicago Ave Chicago, IL 60611 3008, USA
    Front Biosci (Landmark Ed) 14:2448-65. 2009
    ..Studies of these mechanisms in kidney cells and in whole-animal experimental models, reviewed here, are beginning to provide insight into the role of TGF-beta in the pathogenesis of renal dysfunction and its potential treatment...
  10. doi request reprint A conceptual framework for the molecular pathogenesis of progressive kidney disease
    H William Schnaper
    Division of Kidney Diseases, Department of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA
    Pediatr Nephrol 25:2223-30. 2010
    ..Application of this schema could have significant relevance to both research inquiry and clinical practice...
  11. ncbi request reprint Cell phenotype-specific down-regulation of Smad3 involves decreased gene activation as well as protein degradation
    Anne Christine Poncelet
    Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98109, USA
    J Biol Chem 282:15534-40. 2007
    ..Smad3 down-regulation could represent a feedback loop controlling TGF-beta signaling in a cell phenotype-specific manner...