Joel Weinberg

Summary

Affiliation: University of Michigan
Country: USA

Publications

  1. ncbi Preserving postischemic reperfusion in the kidney: a role for extracellular adenosine
    Joel M Weinberg
    Division of Nephrology, Department of Internal Medicine, Veterans Affairs Ann Arbor Healthcare System, University of Michigan, Ann Arbor, Michigan, USA
    J Clin Invest 122:493-6. 2012
  2. ncbi Mitochondrial biogenesis in kidney disease
    Joel M Weinberg
    Nephrology Division, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109 5676, USA
    J Am Soc Nephrol 22:431-6. 2011
  3. ncbi TWEAK-Fn14 as a mediator of acute kidney injury
    Joel M Weinberg
    Division of Nephrology, Department of Internal Medicine, Veterans Affairs Ann Arbor Healthcare System and University of Michigan, Ann Arbor, Michigan, USA
    Kidney Int 79:151-3. 2011
  4. ncbi Lipotoxicity
    J M Weinberg
    Division of Nephrology, Department of Internal Medicine, Veterans Affairs Ann Arbor Healthcare System and University of Michigan, Ann Arbor, Michigan, USA
    Kidney Int 70:1560-6. 2006
  5. ncbi Cytosolic-free calcium increases to greater than 100 micromolar in ATP-depleted proximal tubules
    J M Weinberg
    Division of Nephrology, Department of Internal Medicine, University of Michigan and Veteran s Affairs Medical Center, Ann Arbor, Michigan 48109, USA
    J Clin Invest 100:713-22. 1997
  6. ncbi Energetic determinants of tyrosine phosphorylation of focal adhesion proteins during hypoxia/reoxygenation of kidney proximal tubules
    J M Weinberg
    Department of Internal Medicine, Division of Nephrology, University of Michigan and the Veteran s Administration Medical Center, Ann Arbor, Michigan 48109 0676, USA
    Am J Pathol 158:2153-64. 2001
  7. ncbi Mitochondrial dysfunction during hypoxia/reoxygenation and its correction by anaerobic metabolism of citric acid cycle intermediates
    J M Weinberg
    Division of Nephrology, Department of Internal Medicine, University of Michigan and Veteran s Administration Medical Center, Ann Arbor, MI 48109, USA
    Proc Natl Acad Sci U S A 97:2826-31. 2000
  8. ncbi Anaerobic and aerobic pathways for salvage of proximal tubules from hypoxia-induced mitochondrial injury
    J M Weinberg
    Division of Nephrology, Department of Internal Medicine, University of Michigan and Veteran s Administration Medical Center, Ann Arbor, Michigan 48109, USA
    Am J Physiol Renal Physiol 279:F927-43. 2000
  9. ncbi Site-specific alteration of actin assembly visualized in living renal epithelial cells during ATP depletion
    Eric A Shelden
    Department of Cell and Developmental Biology, Division of Nephrology, University of Michigan Medical School, Ann Arbor 48109, USA
    J Am Soc Nephrol 13:2667-80. 2002
  10. ncbi Alleviation of fatty acid and hypoxia-reoxygenation-induced proximal tubule deenergization by ADP/ATP carrier inhibition and glutamate
    Thorsten Feldkamp
    Division of Nephrology, Department of Internal Medicine, Veterans Affairs Ann Arbor Healthcare System and University of Michigan, Ann Arbor, Michigan 48109 0676, USA
    Am J Physiol Renal Physiol 292:F1606-16. 2007

Research Grants

  1. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel Weinberg; Fiscal Year: 2000
  2. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel Weinberg; Fiscal Year: 2004
  3. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel Weinberg; Fiscal Year: 2007
  4. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel M Weinberg; Fiscal Year: 2010
  5. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel Weinberg; Fiscal Year: 1992
  6. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel Weinberg; Fiscal Year: 1993
  7. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel M Weinberg; Fiscal Year: 2010

Collaborators

  • T Feldkamp
  • Z Dong
  • E A Shelden
  • Pothana Saikumar
  • JOSEPH VINCENT BONVENTRE
  • Jeong Soon Park
  • Myung Ja Lee
  • Kan Zhang
  • Ratna Pasupulati
  • Nancy F Roeser
  • Meenalakshmi M Mariappan
  • Balakuntalam S Kasinath
  • Marc Foretz
  • Goutam Ghosh Choudhury
  • Denis Feliers
  • Myung-Ja Lee
  • Kavithalakshmi Sataranatarajan
  • Benoit Viollet
  • Nicolas Musi
  • Lenin Mahimainathan
  • Manjeri A Venkatachalam

Detail Information

Publications18

  1. ncbi Preserving postischemic reperfusion in the kidney: a role for extracellular adenosine
    Joel M Weinberg
    Division of Nephrology, Department of Internal Medicine, Veterans Affairs Ann Arbor Healthcare System, University of Michigan, Ann Arbor, Michigan, USA
    J Clin Invest 122:493-6. 2012
    ....
  2. ncbi Mitochondrial biogenesis in kidney disease
    Joel M Weinberg
    Nephrology Division, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109 5676, USA
    J Am Soc Nephrol 22:431-6. 2011
    ..The available data indicate that these pathways will be fruitful areas for study in the modification of renal disease...
  3. ncbi TWEAK-Fn14 as a mediator of acute kidney injury
    Joel M Weinberg
    Division of Nephrology, Department of Internal Medicine, Veterans Affairs Ann Arbor Healthcare System and University of Michigan, Ann Arbor, Michigan, USA
    Kidney Int 79:151-3. 2011
    ..Their data suggest paracrine and autocrine effects in which TWEAK produced by tubule cells feeds back on them via upregulated Fn-14 receptors expressed downstream in the proximal tubule...
  4. ncbi Lipotoxicity
    J M Weinberg
    Division of Nephrology, Department of Internal Medicine, Veterans Affairs Ann Arbor Healthcare System and University of Michigan, Ann Arbor, Michigan, USA
    Kidney Int 70:1560-6. 2006
    ..Both acute and chronic kidney disease are associated with systemic manifestations of the metabolic syndrome...
  5. ncbi Cytosolic-free calcium increases to greater than 100 micromolar in ATP-depleted proximal tubules
    J M Weinberg
    Division of Nephrology, Department of Internal Medicine, University of Michigan and Veteran s Affairs Medical Center, Ann Arbor, Michigan 48109, USA
    J Clin Invest 100:713-22. 1997
    ....
  6. ncbi Energetic determinants of tyrosine phosphorylation of focal adhesion proteins during hypoxia/reoxygenation of kidney proximal tubules
    J M Weinberg
    Department of Internal Medicine, Division of Nephrology, University of Michigan and the Veteran s Administration Medical Center, Ann Arbor, Michigan 48109 0676, USA
    Am J Pathol 158:2153-64. 2001
    ....
  7. ncbi Mitochondrial dysfunction during hypoxia/reoxygenation and its correction by anaerobic metabolism of citric acid cycle intermediates
    J M Weinberg
    Division of Nephrology, Department of Internal Medicine, University of Michigan and Veteran s Administration Medical Center, Ann Arbor, MI 48109, USA
    Proc Natl Acad Sci U S A 97:2826-31. 2000
    ....
  8. ncbi Anaerobic and aerobic pathways for salvage of proximal tubules from hypoxia-induced mitochondrial injury
    J M Weinberg
    Division of Nephrology, Department of Internal Medicine, University of Michigan and Veteran s Administration Medical Center, Ann Arbor, Michigan 48109, USA
    Am J Physiol Renal Physiol 279:F927-43. 2000
    ..These results bear on the understanding of a fundamental mode of mitochondrial dysfunction during tubule injury and on strategies to prevent and reverse it...
  9. ncbi Site-specific alteration of actin assembly visualized in living renal epithelial cells during ATP depletion
    Eric A Shelden
    Department of Cell and Developmental Biology, Division of Nephrology, University of Michigan Medical School, Ann Arbor 48109, USA
    J Am Soc Nephrol 13:2667-80. 2002
    ..The results also reveal that actin reorganization continues after ATP levels are maximally decreased and that epithelial cell-cell attachments are sites of actin assembly in ATP-depleted cells...
  10. ncbi Alleviation of fatty acid and hypoxia-reoxygenation-induced proximal tubule deenergization by ADP/ATP carrier inhibition and glutamate
    Thorsten Feldkamp
    Division of Nephrology, Department of Internal Medicine, Veterans Affairs Ann Arbor Healthcare System and University of Michigan, Ann Arbor, Michigan 48109 0676, USA
    Am J Physiol Renal Physiol 292:F1606-16. 2007
    ....
  11. ncbi F1FO-ATPase activity and ATP dependence of mitochondrial energization in proximal tubules after hypoxia/reoxygenation
    Thorsten Feldkamp
    Division of Nephrology, Department of Internal Medicine, Veterans Affairs Ann Arbor Healthcare System and University of Michigan, Ann Arbor, MI, USA
    J Am Soc Nephrol 16:1742-51. 2005
    ....
  12. ncbi Mitochondrial function
    Joel M Weinberg
    Division of Nephrology, University of Michigan Medical Center, Ann Arbor, MI, USA
    Methods Mol Med 86:351-71. 2003
  13. ncbi Cyclophilin D and the mitochondrial permeability transition in kidney proximal tubules after hypoxic and ischemic injury
    Jeong Soon Park
    Nephrology Division, Dept of Internal Medicine, Rm 1560, MSRB II, University of Michigan Medical Center, Ann Arbor, MI 48109 0676, USA
    Am J Physiol Renal Physiol 301:F134-50. 2011
    ....
  14. ncbi Accumulation of nonesterified fatty acids causes the sustained energetic deficit in kidney proximal tubules after hypoxia-reoxygenation
    Thorsten Feldkamp
    Nephrology Division, Department of Internal Medicine, Rm. 1560, MSRB II, University of Michigan Medical Center, Ann Arbor, MI 48109-0676, USA
    Am J Physiol Renal Physiol 290:F465-77. 2006
    ..We conclude that NEFA overload is the primary cause of energetic failure of reoxygenated proximal tubules and lowering NEFA substantially contributes to the benefit from supplementation with alpha-KG/MAL...
  15. ncbi Assessment of mitochondrial membrane potential in proximal tubules after hypoxia-reoxygenation
    Thorsten Feldkamp
    Nephrology Div, Dept. of Internal Medicine, Rm. 1560, MSRB II, Univ. of Michigan Medical Ctr, Ann Arbor, MI 48109-0676, USA
    Am J Physiol Renal Physiol 288:F1092-102. 2005
    ..Both types of energization measured using safranin O in tubules permeabilized after H/R were impaired, but combining substrates and ATP substantially restored DeltaPsim...
  16. ncbi Recent advances in the pathophysiology of ischemic acute renal failure
    Joseph V Bonventre
    Renal Division, Brigham and Women's Hospital, and Department of Medicine, Harvard Medical School, and the Harvard--MIT, Division of Health Sciences and Technology, Charlestown, Massachusetts, USA
    J Am Soc Nephrol 14:2199-210. 2003
  17. ncbi A role for AMP-activated protein kinase in diabetes-induced renal hypertrophy
    Myung Ja Lee
    Dept of Nephrology, University of Texas Health Science Center, San Antonio, TX 78229, USA
    Am J Physiol Renal Physiol 292:F617-27. 2007
    ..AMPK is a newly identified regulator of renal hypertrophy in diabetes...
  18. ncbi Glycine protection of PC-12 cells against injury by ATP-depletion
    Kan Zhang
    Department of Pathology, University of Texas Health Science Center, San Antonio, Texas, USA
    Neurochem Res 28:893-901. 2003
    ..In short, this study has provided the first evidence for glycine protection of cells with neuronal properties. Cytoprotection may involve the glycine receptor; however, it can be dissociated from its channel activity...

Research Grants23

  1. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel Weinberg; Fiscal Year: 2000
    ..dependent, disassembly/reassembly of focal adhesions in the glycine-protected, isolated tubules. ..
  2. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel Weinberg; Fiscal Year: 2004
    ..3) Assess expression of the lesion and test efficacy of protective metabolites during ischemia/reperfusion of the kidney in vivo. ..
  3. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel Weinberg; Fiscal Year: 2007
    ..abstract_text> ..
  4. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel M Weinberg; Fiscal Year: 2010
    ....
  5. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel Weinberg; Fiscal Year: 1992
    ..The studies in this proposal provide an established and versatile approach for achieving this...
  6. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel Weinberg; Fiscal Year: 1993
    ..Glycine cytoprotection is an extraordinarily powerful tool for this purpose with implications for injury to the kidney and other organs..
  7. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel M Weinberg; Fiscal Year: 2010
    ....