D H Ellison

Summary

Affiliation: Oregon Health and Science University
Country: USA

Publications

  1. pmc The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertension
    Ewout J Hoorn
    Division of Nephrology and Hypertension, Oregon Health and Science University, Portland, Oregon, USA
    Nat Med 17:1304-9. 2011
  2. pmc Ubiquitylation and the pathogenesis of hypertension
    David H Ellison
    Division of Nephrology and Hypertension, CH12R, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, Oregon 97239, USA
    J Clin Invest 123:546-8. 2013
  3. pmc Renal nerves, WNK4, glucocorticoids, and salt transport
    David H Ellison
    Division of Nephrology and Hypertension, Oregon Health and Science University, Portland, OR 97239, USA
    Cell Metab 13:619-20. 2011
  4. pmc Through a glass darkly: salt transport by the distal tubule
    David H Ellison
    Division of Nephrology and Hypertension, Oregon Health and Science University, Portland, Oregon 97239, USA
    Kidney Int 79:5-8. 2011
  5. pmc The voltage-gated K+ channel subunit Kv1.1 links kidney and brain
    David H Ellison
    Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, Oregon 97239, USA
    J Clin Invest 119:763-6. 2009
  6. pmc Renal magnification by EGF
    David H Ellison
    Division of Nephrology and Hypertension, Oregon Health and Science University, 3314 SW US Veterans Hospital Road, Portland, OR 97239, USA
    Nephrol Dial Transplant 23:1497-9. 2008
  7. ncbi request reprint Clinical practice. The syndrome of inappropriate antidiuresis
    David H Ellison
    Division of Nephrology and Hypertension and the Department of Physiology and Pharmacology, Oregon Health and Science University and Veterans Affairs Medical Center, Portland, OR 97239, USA
    N Engl J Med 356:2064-72. 2007
  8. ncbi request reprint Divalent cation transport by the distal nephron: insights from Bartter's and Gitelman's syndromes
    D H Ellison
    Division of Nephrology and Hypertension, University of Colorado School of Medicine and Veterans Affairs Medical Center, Denver, Colorado 80220, USA
    Am J Physiol Renal Physiol 279:F616-25. 2000
  9. ncbi request reprint Disorders of sodium and water
    David H Ellison
    Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, VA Medical Center, Portland, OR 97239, USA
    Am J Kidney Dis 46:356-61. 2005
  10. ncbi request reprint Diuretic therapy and resistance in congestive heart failure
    D H Ellison
    Division of Nephrology and Hypertension, Oregon Health and Science University, Portland, OR 97201, USA
    Cardiology 96:132-43. 2001

Research Grants

  1. REGULATION OF THIAZIDE SENSITIVE NACL TRANSPORT
    David Ellison; Fiscal Year: 1999
  2. REGULATION OF THIAZIDE SENSITIVE NACL TRANSPORT
    David Ellison; Fiscal Year: 2000
  3. REGULATION OF THIAZIDE SENSITIVE NACL TRANSPORT
    David Ellison; Fiscal Year: 2001
  4. REGULATION OF THIAZIDE SENSITIVE NACL TRANSPORT
    David Ellison; Fiscal Year: 2002
  5. Regulation of thiazide-sensitive NaCl transport
    David Ellison; Fiscal Year: 2004
  6. Regulation of thiazide-sensitive NaCl transport
    David Ellison; Fiscal Year: 2007
  7. Regulation of thiazide-sensitive NaCl transport
    David Ellison; Fiscal Year: 2006
  8. Regulation of thiazide-sensitive NaCl transport
    David Ellison; Fiscal Year: 2005
  9. REGULATION OF THIAZIDE SENSITIVE NACL TRANSPORT
    David Ellison; Fiscal Year: 2003
  10. REGULATION OF THIAZIDE SENSITIVE NACL TRANSPORT
    David Ellison; Fiscal Year: 2000

Collaborators

Detail Information

Publications28

  1. pmc The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertension
    Ewout J Hoorn
    Division of Nephrology and Hypertension, Oregon Health and Science University, Portland, Oregon, USA
    Nat Med 17:1304-9. 2011
    ....
  2. pmc Ubiquitylation and the pathogenesis of hypertension
    David H Ellison
    Division of Nephrology and Hypertension, CH12R, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, Oregon 97239, USA
    J Clin Invest 123:546-8. 2013
    ..Together, the results suggest that defective ubiquitylation of ENaC by Nedd4-2 may not fully explain Liddle syndrome and that Nedd4-2 modulates NCC more strongly...
  3. pmc Renal nerves, WNK4, glucocorticoids, and salt transport
    David H Ellison
    Division of Nephrology and Hypertension, Oregon Health and Science University, Portland, OR 97239, USA
    Cell Metab 13:619-20. 2011
    ..2011) shows that dietary salt excess, coupled with β-adrenergic stimulation, increases arterial pressure via glucocorticoid receptors and WNK4, suggesting interactions between these systems in the pathogenesis of hypertension...
  4. pmc Through a glass darkly: salt transport by the distal tubule
    David H Ellison
    Division of Nephrology and Hypertension, Oregon Health and Science University, Portland, Oregon 97239, USA
    Kidney Int 79:5-8. 2011
    ..This Commentary provides additional perspective on that work...
  5. pmc The voltage-gated K+ channel subunit Kv1.1 links kidney and brain
    David H Ellison
    Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, Oregon 97239, USA
    J Clin Invest 119:763-6. 2009
    ..Mechanisms by which the apical voltage is generated and howKv1.1 fits within this context are discussed herein...
  6. pmc Renal magnification by EGF
    David H Ellison
    Division of Nephrology and Hypertension, Oregon Health and Science University, 3314 SW US Veterans Hospital Road, Portland, OR 97239, USA
    Nephrol Dial Transplant 23:1497-9. 2008
  7. ncbi request reprint Clinical practice. The syndrome of inappropriate antidiuresis
    David H Ellison
    Division of Nephrology and Hypertension and the Department of Physiology and Pharmacology, Oregon Health and Science University and Veterans Affairs Medical Center, Portland, OR 97239, USA
    N Engl J Med 356:2064-72. 2007
  8. ncbi request reprint Divalent cation transport by the distal nephron: insights from Bartter's and Gitelman's syndromes
    D H Ellison
    Division of Nephrology and Hypertension, University of Colorado School of Medicine and Veterans Affairs Medical Center, Denver, Colorado 80220, USA
    Am J Physiol Renal Physiol 279:F616-25. 2000
    ..These mechanisms are based on recent insights from another inherited disease of ion transport, inherited magnesium wasting, and from a review of the chronic effects of diuretic drugs in animals and people...
  9. ncbi request reprint Disorders of sodium and water
    David H Ellison
    Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, VA Medical Center, Portland, OR 97239, USA
    Am J Kidney Dis 46:356-61. 2005
  10. ncbi request reprint Diuretic therapy and resistance in congestive heart failure
    D H Ellison
    Division of Nephrology and Hypertension, Oregon Health and Science University, Portland, OR 97201, USA
    Cardiology 96:132-43. 2001
    ..The goal of reducing the extracellular fluid volume with the least stimulation of the RAA axis and minimal changes in nephron architecture can be achieved in many patients...
  11. pmc Aldosterone mediates activation of the thiazide-sensitive Na-Cl cotransporter through an SGK1 and WNK4 signaling pathway
    David J Rozansky
    Department of Pediatrics, Oregon Health and Science University, Portland, Oregon, USA
    J Clin Invest 119:2601-12. 2009
    ..These data thus delineate what we believe to be a novel mechanism for aldosterone activation of NCC through SGK1 signaling of WNK4 kinase...
  12. ncbi request reprint Loop diuretic infusion increases thiazide-sensitive Na(+)/Cl(-)-cotransporter abundance: role of aldosterone
    J G Abdallah
    Division of Nephrology and Hypertension, University of Colorado School of Medicine and Veterans Administration Medical Center, Denver, Colorado, USA
    J Am Soc Nephrol 12:1335-41. 2001
    ..A portion of the furosemide effect can be prevented by blockade of mineralocorticoid receptors...
  13. ncbi request reprint The WNK kinase network regulating sodium, potassium, and blood pressure
    Ewout J Hoorn
    Division of Nephrology and Hypertension, Oregon Health and Sciences University, 3181 SW Sam Jackson Park Road, Portland, OR 97239 3098, USA
    J Am Soc Nephrol 22:605-14. 2011
    ..Although many questions remain unanswered, the WNKs hold promise for unraveling the link between salt and hypertension, potentially leading to more effective interventions to prevent cardiorenal damage...
  14. pmc WNK kinases regulate thiazide-sensitive Na-Cl cotransport
    Chao Ling Yang
    Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, Oregon 97239, USA
    J Clin Invest 111:1039-45. 2003
    ..Together, these results identify WNK kinases as a previously unrecognized sodium regulatory pathway of the distal nephron. This pathway likely contributes to normal and pathological blood pressure homeostasis...
  15. pmc The WNKs: atypical protein kinases with pleiotropic actions
    James A McCormick
    Division of Nephrology and Hypertension, Oregon Health and Science University and Veterans Affairs Medical Center, Portland, Oregon 97239, USA
    Physiol Rev 91:177-219. 2011
    ..Next, consequences of these effects on integrated physiological function are outlined. Finally, we discuss the known and putative pathophysiological relevance of the WNKs...
  16. pmc The thiazide-sensitive Na-Cl cotransporter is regulated by a WNK kinase signaling complex
    Chao Ling Yang
    Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, Oregon 97239, USA
    J Clin Invest 117:3403-11. 2007
    ..The results provide a mechanistic explanation for the divergent effects of WT and FHHt-mutant WNK4 on NCC activity, and for the dominant nature of FHHt in humans and genetically modified mice...
  17. ncbi request reprint WNK1 and WNK4 modulate CFTR activity
    Chao Ling Yang
    Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, OR 97239, USA
    Biochem Biophys Res Commun 353:535-40. 2007
    ..Taken together, these results suggest that WNK1 and WNK4 may modulate CFTR activity; they further suggest that WNK kinases may be potential therapeutic targets for cystic fibrosis...
  18. ncbi request reprint Dominant-negative regulation of WNK1 by its kidney-specific kinase-defective isoform
    Arohan R Subramanya
    Division of Nephrology and Hypertension, Oregon Health and Science University, PP262, 3314 SW US Veterans Hospital Road, Portland, OR 97239, USA
    Am J Physiol Renal Physiol 290:F619-24. 2006
    ..These observations suggest that KS-WNK1 plays an essential role in the renal molecular switch regulating Na+ and K+ balance; they provide insight into the kidney-specific phenotype of FHHt...
  19. pmc Mechanisms of WNK1 and WNK4 interaction in the regulation of thiazide-sensitive NaCl cotransport
    Chao Ling Yang
    Division of Nephrology and Hypertension, Oregon Health and Science University, Portland, 97239, USA
    J Clin Invest 115:1379-87. 2005
    ..These findings provide insight into the complex interrelationships between WNK1 and WNK4 and provide a molecular basis for FHHt...
  20. ncbi request reprint WNK kinases regulate sodium chloride and potassium transport by the aldosterone-sensitive distal nephron
    A R Subramanya
    Department of Medicine, Division of Nephrology and Hypertension, Oregon Health and Science University, Portland, Oregon 97239, USA
    Kidney Int 70:630-4. 2006
    ....
  21. ncbi request reprint Interaction with grp58 increases activity of the thiazide-sensitive Na-Cl cotransporter
    Bruce Wyse
    Division of Nephrology, Hypertension, and Clinical Pharmacology, Oregon Health Sciences University, Portland, Oregon 97201, USA
    Am J Physiol Renal Physiol 282:F424-30. 2002
    ..Western blot analysis did not show any effect of grp58 expression on processing of the NCC. These data indicate a novel, functionally important interaction between grp58 and the NCC in rat kidney cortex...
  22. pmc WNK kinases and renal sodium transport in health and disease: an integrated view
    James A McCormick
    Division of Nephrology and Hypertension and Heart Research Center, Department of Medicine, Oregon Health and Science University, Portland, OR 97239, USA
    Hypertension 51:588-96. 2008
  23. ncbi request reprint Comparison of WNK4 and WNK1 kinase and inhibiting activities
    Zhaohong Wang
    Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, OR 97239, USA
    Biochem Biophys Res Commun 317:939-44. 2004
    ..Together, these results suggest that WNK4 must be activated by currently unknown factors to exhibit kinase activity and that WNK4 contains an inhibitory domain that can inhibit the kinase activity of WNK1...
  24. ncbi request reprint The thiazide-sensitive na-cl cotransporter and human disease: reemergence of an old player
    David H Ellison
    J Am Soc Nephrol 14:538-40. 2003
  25. ncbi request reprint Pathophysiology of functional mutations of the thiazide-sensitive Na-Cl cotransporter in Gitelman disease
    Ernesto Sabath
    Molecular Physiology Unit, Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran, Instituto de Investigaciones Biomedicas, Universidad Nacional Autonoma de Mexico, Tlalpan 14000, Mexico City, Mexico
    Am J Physiol Renal Physiol 287:F195-203. 2004
    ..The small increase in Cl(-) and thiazide affinity in G610S and G627V suggests that the beginning of the COOH-terminal domain could be implicated in defining kinetic properties...
  26. pmc WNK1 kinase isoform switch regulates renal potassium excretion
    James B Wade
    Department of Physiology, University of Maryland School of Medicine, 655 West Baltimore Street, Baltimore, MD 21201, USA
    Proc Natl Acad Sci U S A 103:8558-63. 2006
    ..1 activity involves a WNK1 isoform switch and KS-WNK1-mediated release from L-WNK1 inhibition. Thus, these observations provide evidence for the physiological regulation of Na(+) and K(+) balance by a kinase isoform switch mechanism...
  27. ncbi request reprint Wnk4 controls blood pressure and potassium homeostasis via regulation of mass and activity of the distal convoluted tubule
    Maria D Lalioti
    Department of Genetics, Howard Hughes Medical, Institute, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    Nat Genet 38:1124-32. 2006
    ..These findings establish that Wnk4 is a molecular switch that regulates the balance between NaCl reabsorption and K+ secretion by altering the mass and function of the DCT through its effect on NCC...
  28. ncbi request reprint Renal expression of sodium transporters and aquaporin-2 in hypothyroid rats
    Roland Schmitt
    Institut fur Anatomie, Charite, Humboldt Universitat, 10115 Berlin, Germany
    Am J Physiol Renal Physiol 284:F1097-104. 2003
    ....

Research Grants13

  1. REGULATION OF THIAZIDE SENSITIVE NACL TRANSPORT
    David Ellison; Fiscal Year: 1999
    ..The underlying hypothesis of these experiments is that some Gitelman's mutations impair protein-protein interactions that are crucial for maintenance of transport activity. ..
  2. REGULATION OF THIAZIDE SENSITIVE NACL TRANSPORT
    David Ellison; Fiscal Year: 2000
    ..The underlying hypothesis of these experiments is that some Gitelman's mutations impair protein-protein interactions that are crucial for maintenance of transport activity. ..
  3. REGULATION OF THIAZIDE SENSITIVE NACL TRANSPORT
    David Ellison; Fiscal Year: 2001
    ..The underlying hypothesis of these experiments is that some Gitelman's mutations impair protein-protein interactions that are crucial for maintenance of transport activity. ..
  4. REGULATION OF THIAZIDE SENSITIVE NACL TRANSPORT
    David Ellison; Fiscal Year: 2002
    ..The underlying hypothesis of these experiments is that some Gitelman's mutations impair protein-protein interactions that are crucial for maintenance of transport activity. ..
  5. Regulation of thiazide-sensitive NaCl transport
    David Ellison; Fiscal Year: 2004
    ..Although Mendelian forms of hypertension are rare, they help to elucidate mechanisms of blood pressure regulation that almost certainly contribute to the more common essential variety. ..
  6. Regulation of thiazide-sensitive NaCl transport
    David Ellison; Fiscal Year: 2007
    ..Although Mendelian forms of hypertension are rare, they help to elucidate mechanisms of blood pressure regulation that almost certainly contribute to the more common essential variety. ..
  7. Regulation of thiazide-sensitive NaCl transport
    David Ellison; Fiscal Year: 2006
    ..Although Mendelian forms of hypertension are rare, they help to elucidate mechanisms of blood pressure regulation that almost certainly contribute to the more common essential variety. ..
  8. Regulation of thiazide-sensitive NaCl transport
    David Ellison; Fiscal Year: 2005
    ..Although Mendelian forms of hypertension are rare, they help to elucidate mechanisms of blood pressure regulation that almost certainly contribute to the more common essential variety. ..
  9. REGULATION OF THIAZIDE SENSITIVE NACL TRANSPORT
    David Ellison; Fiscal Year: 2003
    ..The underlying hypothesis of these experiments is that some Gitelman's mutations impair protein-protein interactions that are crucial for maintenance of transport activity. ..
  10. REGULATION OF THIAZIDE SENSITIVE NACL TRANSPORT
    David Ellison; Fiscal Year: 2000
    ..The underlying hypothesis of these experiments is that some Gitelman's mutations impair protein-protein interactions that are crucial for maintenance of transport activity. ..
  11. Regulation of thiazide-sensitive NaCl transport
    David H Ellison; Fiscal Year: 2010
    ..A large portion of hypertension is related to genetics. This proposal will help unravel genetic contributions to human blood pressure variation, with the goal of finding better treatments, or better preventive maneuvers. ..