Joel Weinberg

Summary

Affiliation: University of Michigan
Country: USA

Publications

  1. pmc The role of glycine in regulated cell death
    Joel M Weinberg
    Division of Nephrology, Department of Internal Medicine, Veterans Affairs Ann Arbor Healthcare System and University of Michigan, Room 1560, MSRB II, Ann Arbor, MI, 48109 0676, USA
    Cell Mol Life Sci 73:2285-308. 2016
  2. pmc Substrate modulation of fatty acid effects on energization and respiration of kidney proximal tubules during hypoxia/reoxygenation
    Anja Bienholz
    Division of Nephrology, Department of Internal Medicine, Veterans Affairs Ann Arbor Healthcare System and University of Michigan, Ann Arbor, Michigan, United States of America Division of Nephrology, Department of Internal Medicine, University Duisburg Essen, Essen, Germany
    PLoS ONE 9:e94584. 2014
  3. pmc 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
  4. doi request reprint 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
  5. pmc 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
  6. ncbi request reprint 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
  7. pmc 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
  8. pmc 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
  9. pmc 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
  10. pmc 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

Research Grants

  1. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel Weinberg; Fiscal Year: 2007

Collaborators

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

Detail Information

Publications20

  1. pmc The role of glycine in regulated cell death
    Joel M Weinberg
    Division of Nephrology, Department of Internal Medicine, Veterans Affairs Ann Arbor Healthcare System and University of Michigan, Room 1560, MSRB II, Ann Arbor, MI, 48109 0676, USA
    Cell Mol Life Sci 73:2285-308. 2016
    ....
  2. pmc Substrate modulation of fatty acid effects on energization and respiration of kidney proximal tubules during hypoxia/reoxygenation
    Anja Bienholz
    Division of Nephrology, Department of Internal Medicine, Veterans Affairs Ann Arbor Healthcare System and University of Michigan, Ann Arbor, Michigan, United States of America Division of Nephrology, Department of Internal Medicine, University Duisburg Essen, Essen, Germany
    PLoS ONE 9:e94584. 2014
    ....
  3. pmc 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
    ....
  4. doi request reprint 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...
  5. pmc 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...
  6. ncbi request reprint 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...
  7. pmc 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
    ....
  8. pmc 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
    ....
  9. pmc 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...
  10. pmc 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
    ....
  11. ncbi request reprint 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...
  12. ncbi request reprint 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 request reprint 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
    ....
  14. ncbi request reprint 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
    ....
  15. pmc 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
    ....
  16. ncbi request reprint 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...
  17. ncbi request reprint 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...
  18. ncbi request reprint 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
  19. ncbi request reprint 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...
  20. ncbi request reprint 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 Grants1

  1. CELLULAR PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE
    Joel Weinberg; Fiscal Year: 2007
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