Michelle Winn

Summary

Affiliation: Duke University Medical Center
Country: USA

Publications

  1. pmc Inverted formin 2 mutations with variable expression in patients with sporadic and hereditary focal and segmental glomerulosclerosis
    Rasheed A Gbadegesin
    Department of Pediatrics, Duke University Medical Center, Durham, North Carolina 27710, USA
    Kidney Int 81:94-9. 2012
  2. doi request reprint 2007 Young Investigator Award: TRP'ing into a new era for glomerular disease
    Michelle P Winn
    Department of Medicine and Center for Human Genetics, Duke University Medical Center, Duke Box 2903, Durham, NC 27705, USA
    J Am Soc Nephrol 19:1071-5. 2008
  3. ncbi request reprint Unexpected role of TRPC6 channel in familial nephrotic syndrome: does it have clinical implications?
    Michelle P Winn
    Department of Medicine, Duke University Medical Center, Box 2903, Durham, NC 27710, USA
    J Am Soc Nephrol 17:378-87. 2006
  4. ncbi request reprint A mutation in the TRPC6 cation channel causes familial focal segmental glomerulosclerosis
    Michelle P Winn
    Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Science 308:1801-4. 2005
  5. pmc Pathogenesis and therapy of focal segmental glomerulosclerosis: an update
    Rasheed Gbadegesin
    Department of Pediatrics, Duke University Medical Center, Durham, NC 27710, USA
    Pediatr Nephrol 26:1001-15. 2011
  6. ncbi request reprint Association of genetic polymorphisms with risk of renal injury after coronary bypass graft surgery
    Mark Stafford-Smith
    Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710, USA
    Am J Kidney Dis 45:519-30. 2005
  7. ncbi request reprint Approach to the evaluation of heritable diseases and update on familial focal segmental glomerulosclerosis
    Michelle P Winn
    Duke Medical Center, Division of Nephrology, Durham, North Carolina 27710, USA
    Nephrol Dial Transplant 18:vi14-20. 2003
  8. pmc Modulation of the BP response to diet by genes in the renin-angiotensin system and the adrenergic nervous system
    Laura P Svetkey
    Duke University Medical Center, Durham, North Carolina, USA
    Am J Hypertens 24:209-17. 2011
  9. pmc A new locus for familial FSGS on chromosome 2p
    Rasheed Gbadegesin
    Department of Pediatrics, Duke University Medical Center, Durham, NC 27710, USA
    J Am Soc Nephrol 21:1390-7. 2010
  10. pmc Exclusion of homozygous PLCE1 (NPHS3) mutations in 69 families with idiopathic and hereditary FSGS
    Rasheed Gbadegesin
    Department of Pediatrics, Duke University Medical Center, Durham, NC, 27710, USA
    Pediatr Nephrol 24:281-5. 2009

Collaborators

Detail Information

Publications17

  1. pmc Inverted formin 2 mutations with variable expression in patients with sporadic and hereditary focal and segmental glomerulosclerosis
    Rasheed A Gbadegesin
    Department of Pediatrics, Duke University Medical Center, Durham, North Carolina 27710, USA
    Kidney Int 81:94-9. 2012
    ..Hence, screening for these mutations may represent a rapid, non-invasive and cost-effective method for the diagnosis of autosomal dominant FSGS...
  2. doi request reprint 2007 Young Investigator Award: TRP'ing into a new era for glomerular disease
    Michelle P Winn
    Department of Medicine and Center for Human Genetics, Duke University Medical Center, Duke Box 2903, Durham, NC 27705, USA
    J Am Soc Nephrol 19:1071-5. 2008
    ..This creates the intriguing possibility that blocking TRPC6 channels within the podocyte may translate into long-lasting clinical benefits in patients with FSGS...
  3. ncbi request reprint Unexpected role of TRPC6 channel in familial nephrotic syndrome: does it have clinical implications?
    Michelle P Winn
    Department of Medicine, Duke University Medical Center, Box 2903, Durham, NC 27710, USA
    J Am Soc Nephrol 17:378-87. 2006
  4. ncbi request reprint A mutation in the TRPC6 cation channel causes familial focal segmental glomerulosclerosis
    Michelle P Winn
    Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Science 308:1801-4. 2005
    ..Previous work has emphasized the importance of cytoskeletal and structural proteins in proteinuric kidney diseases. Our findings suggest an alternative mechanism for the pathogenesis of glomerular disease...
  5. pmc Pathogenesis and therapy of focal segmental glomerulosclerosis: an update
    Rasheed Gbadegesin
    Department of Pediatrics, Duke University Medical Center, Durham, NC 27710, USA
    Pediatr Nephrol 26:1001-15. 2011
    ..This review focuses on recent advances in the molecular pathogenesis of FSGS and currently available therapeutic agents as well as potential novel therapies...
  6. ncbi request reprint Association of genetic polymorphisms with risk of renal injury after coronary bypass graft surgery
    Mark Stafford-Smith
    Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710, USA
    Am J Kidney Dis 45:519-30. 2005
    ..Therefore, we tested the hypothesis that selected gene variants are associated with acute renal injury, reflected by a serum creatinine level increase after cardiac surgery...
  7. ncbi request reprint Approach to the evaluation of heritable diseases and update on familial focal segmental glomerulosclerosis
    Michelle P Winn
    Duke Medical Center, Division of Nephrology, Durham, North Carolina 27710, USA
    Nephrol Dial Transplant 18:vi14-20. 2003
    ..The existence of hereditary forms of FSGS permits the use of molecular genetics techniques to study the pathogenesis of this disorder...
  8. pmc Modulation of the BP response to diet by genes in the renin-angiotensin system and the adrenergic nervous system
    Laura P Svetkey
    Duke University Medical Center, Durham, North Carolina, USA
    Am J Hypertens 24:209-17. 2011
    ..The purpose of this study was to identify genes that modulate BP response to dietary interventions...
  9. pmc A new locus for familial FSGS on chromosome 2p
    Rasheed Gbadegesin
    Department of Pediatrics, Duke University Medical Center, Durham, NC 27710, USA
    J Am Soc Nephrol 21:1390-7. 2010
    ..These data support a new gene locus for familial FSGS on chromosome 2p15. Identification of the mutated gene at this locus may provide further insight into the disease mechanisms of FSGS...
  10. pmc Exclusion of homozygous PLCE1 (NPHS3) mutations in 69 families with idiopathic and hereditary FSGS
    Rasheed Gbadegesin
    Department of Pediatrics, Duke University Medical Center, Durham, NC, 27710, USA
    Pediatr Nephrol 24:281-5. 2009
    ..Kindreds appropriate for genome-wide screening are currently being subjected to analysis with the aim of identifying other genetic causes of FSGS...
  11. ncbi request reprint Parkin mutations and susceptibility alleles in late-onset Parkinson's disease
    Sofia A Oliveira
    Department of Medicine and Center for Human Genetics, Institute for Genome Sciences and Policy, Duke University Medical Center, Durham, NC 27710, USA
    Ann Neurol 53:624-9. 2003
    ..These findings suggest that mutations in Parkin contribute to the common form of PD and that heterozygous mutations, especially those lying in exon 7, act as susceptibility alleles for late-onset form of Parkinson disease...
  12. pmc Therapeutic targets in focal and segmental glomerulosclerosis
    Peter J Lavin
    Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
    Curr Opin Nephrol Hypertens 17:386-92. 2008
    ....
  13. ncbi request reprint TRPC6 and FSGS: the latest TRP channelopathy
    Nirvan Mukerji
    Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
    Biochim Biophys Acta 1772:859-68. 2007
    ..This creates the exciting possibility that blocking TRPC6 channels within the podocyte may translate into long-lasting clinical benefits in patients with FSGS...
  14. ncbi request reprint Focal and segmental glomerulosclerosis: varying biologic mechanisms underlie a final histopathologic end point
    Nikki Daskalakis
    Department of Medicine, and the Center for Human Genetics, Duke University Medical Center, Durham, NC 27710, USA
    Semin Nephrol 26:89-94. 2006
    ..Mutations in cytoskeletal proteins that affect podocyte structure have been the target until recently. Here we review the current understanding of this glomerular disease and areas for future concentration...
  15. pmc TRPC6 enhances angiotensin II-induced albuminuria
    Jason Eckel
    Center for Human Genetics, Duke University Medical Center, Durham, NC 27710, USA
    J Am Soc Nephrol 22:526-35. 2011
    ..Our findings suggest that TRPC6 promotes albuminuria, perhaps by promoting angiotensin II-dependent increases in Ca(2+), suggesting that TRPC6 blockade may be therapeutically beneficial in proteinuric kidney disease...
  16. ncbi request reprint Linkage of a gene causing familial membranoproliferative glomerulonephritis type III to chromosome 1
    John J Neary
    Departments of Nephrology, Beaumont Hospital, Dublin, Ireland
    J Am Soc Nephrol 13:2052-7. 2002
    ..The data provide evidence for a gene for familial MPGN on chromosome 1q...
  17. ncbi request reprint Not all in the family: mutations of podocin in sporadic steroid-resistant nephrotic syndrome
    Michelle P Winn
    J Am Soc Nephrol 13:577-9. 2002

Research Grants10

  1. AUTOSOMAL DOMINANT FOCAL SEGMENTAL GLOMERULOSCLEROSIS
    Michelle Winn; Fiscal Year: 2004
    ..Information derived from this research will also allow a better understanding of the pathogenesis of nonhereditary forms of FSGS and may provide insights regarding management of the more common idiopathic forms of this disorder. ..
  2. GENETICS OF FAMILIAL FOCAL SEGMENTAL GLOMERULOSCLEROSIS
    Michelle Winn; Fiscal Year: 2005
    ..New mutations found in the genes known to cause FSGS will enhance our understanding of the genetics and biology of thi., disorder, takin 9 advantage of our entire resource of families. ..
  3. Characterization of TRPC6 As A Cause for Focal and Segmental Glomerulosclerosis
    Michelle P Winn; Fiscal Year: 2010
    ..Our original hypothesis suggests that the absence of TRPC6 may confer resistance to kidney injury and proteinuria. We will test this in models of induced renal disease. ..