L Quarles

Summary

Publications

  1. pmc Conditional mesenchymal disruption of pkd1 results in osteopenia and polycystic kidney disease
    Ni Qiu
    Department of Medicine, University of Tennessee Health Science Center, Memphis, United States of America
    PLoS ONE 7:e46038. 2012
  2. pmc A comparative transcriptome analysis identifying FGF23 regulated genes in the kidney of a mouse CKD model
    Bing Dai
    University of Tennessee Health Science Center, Medicine Nephrology, Memphis, Tennessee, United States of America
    PLoS ONE 7:e44161. 2012
  3. pmc Assessment of 24,25(OH)2D levels does not support FGF23-mediated catabolism of vitamin D metabolites
    Bing Dai
    Division of Nephrology, Department of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA
    Kidney Int 82:1061-70. 2012
  4. pmc Calcium regulates FGF-23 expression in bone
    Valentin David
    MD, Coleman College of Medicine Building, Suite B226, University of Tennessee Health Science Center, 956 Court Avenue, Memphis Tennessee 38163
    Endocrinology 154:4469-82. 2013
  5. pmc Reducing cardiovascular mortality in chronic kidney disease: something borrowed, something new
    L Darryl Quarles
    University of Tennessee Health Science Center, 956 Court Ave, Suite B226, Memphis, Tennessee, USA
    J Clin Invest 123:542-3. 2013
  6. ncbi A systems biology preview of the relationships between mineral and metabolic complications in chronic kidney disease
    L Darryl Quarles
    Department of Medicine and Division of Nephrology, University of Tennessee Health Science Center, Memphis, TN 38163, USA
    Semin Nephrol 33:130-42. 2013
  7. pmc Role of FGF23 in vitamin D and phosphate metabolism: implications in chronic kidney disease
    L Darryl Quarles
    Department of Medicine and Division of Nephrology, University of Tennessee Health Science Center, Memphis, TN 38163, USA
    Exp Cell Res 318:1040-8. 2012
  8. ncbi Skeletal secretion of FGF-23 regulates phosphate and vitamin D metabolism
    L Darryl Quarles
    Division of Nephrology, Department of Medicine, University of Tennessee Health Science Center, 19 South Manassas Street, Memphis, TN 38163, USA
    Nat Rev Endocrinol 8:276-86. 2012
  9. pmc Conditional deletion of Pkd1 in osteocytes disrupts skeletal mechanosensing in mice
    Zhousheng Xiao
    Department of Medicine, The University of Tennessee Health Science Center, Memphis, TN 38165, USA
    FASEB J 25:2418-32. 2011
  10. pmc Compound deletion of Fgfr3 and Fgfr4 partially rescues the Hyp mouse phenotype
    Hua Li
    University of Tennessee Health Science Center, 956 Court Ave, Memphis, TN 38163, USA
    Am J Physiol Endocrinol Metab 300:E508-17. 2011

Collaborators

Detail Information

Publications11

  1. pmc Conditional mesenchymal disruption of pkd1 results in osteopenia and polycystic kidney disease
    Ni Qiu
    Department of Medicine, University of Tennessee Health Science Center, Memphis, United States of America
    PLoS ONE 7:e46038. 2012
    ..The non-lethality of Col1a1(3.6)-Cre;Pkd1(flox/flox) mice establishes a new model to study abnormalities in bone development and cyst formation in pancreas and kidney caused by Pkd1 gene inactivation...
  2. pmc A comparative transcriptome analysis identifying FGF23 regulated genes in the kidney of a mouse CKD model
    Bing Dai
    University of Tennessee Health Science Center, Medicine Nephrology, Memphis, Tennessee, United States of America
    PLoS ONE 7:e44161. 2012
    ..These gene products provide a possible mechanistic links between elevated FGF23 and pathways responsible for renal failure progression and cardiovascular diseases...
  3. pmc Assessment of 24,25(OH)2D levels does not support FGF23-mediated catabolism of vitamin D metabolites
    Bing Dai
    Division of Nephrology, Department of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA
    Kidney Int 82:1061-70. 2012
    ..Thus, we failed to find support for FGF23-mediated catabolism of vitamin D metabolites in chronic kidney disease assessed by 24,25(OH)(2)D levels...
  4. pmc Calcium regulates FGF-23 expression in bone
    Valentin David
    MD, Coleman College of Medicine Building, Suite B226, University of Tennessee Health Science Center, 956 Court Avenue, Memphis Tennessee 38163
    Endocrinology 154:4469-82. 2013
    ..The effects of chronic low calcium to prevent 1,25(OH)2D and PTH stimulation of FGF-23 in these mutant mouse models suggest that suppression of FGF-23 plays an important physiological adaptive response to hypocalcemia. ..
  5. pmc Reducing cardiovascular mortality in chronic kidney disease: something borrowed, something new
    L Darryl Quarles
    University of Tennessee Health Science Center, 956 Court Ave, Suite B226, Memphis, Tennessee, USA
    J Clin Invest 123:542-3. 2013
    ..Medications included chlorthalidone, amlodipine, carvedilol, cholecalciferol, erythropoietin, and a phosphate binder. What additional therapy should be initiated to reduce vascular calcifications and cardiovascular mortality?..
  6. ncbi A systems biology preview of the relationships between mineral and metabolic complications in chronic kidney disease
    L Darryl Quarles
    Department of Medicine and Division of Nephrology, University of Tennessee Health Science Center, Memphis, TN 38163, USA
    Semin Nephrol 33:130-42. 2013
    ..The complex interconnections between the various endocrine networks in chronic kidney disease may account for the difficulty in treating the uremic state...
  7. pmc Role of FGF23 in vitamin D and phosphate metabolism: implications in chronic kidney disease
    L Darryl Quarles
    Department of Medicine and Division of Nephrology, University of Tennessee Health Science Center, Memphis, TN 38163, USA
    Exp Cell Res 318:1040-8. 2012
    ..Finally, increments in FGF23 are associated with increased cardiovascular mortality in CKD. Whether these effects represent direct effects of FGF23 or represent a marker of other abnormalities in CKD remains to be determined...
  8. ncbi Skeletal secretion of FGF-23 regulates phosphate and vitamin D metabolism
    L Darryl Quarles
    Division of Nephrology, Department of Medicine, University of Tennessee Health Science Center, 19 South Manassas Street, Memphis, TN 38163, USA
    Nat Rev Endocrinol 8:276-86. 2012
    ....
  9. pmc Conditional deletion of Pkd1 in osteocytes disrupts skeletal mechanosensing in mice
    Zhousheng Xiao
    Department of Medicine, The University of Tennessee Health Science Center, Memphis, TN 38165, USA
    FASEB J 25:2418-32. 2011
    ..These data indicate that polycystin-1 is essential for the anabolic response to skeletal loading in osteoblasts/osteocytes...
  10. pmc Compound deletion of Fgfr3 and Fgfr4 partially rescues the Hyp mouse phenotype
    Hua Li
    University of Tennessee Health Science Center, 956 Court Ave, Memphis, TN 38163, USA
    Am J Physiol Endocrinol Metab 300:E508-17. 2011
    ..These studies suggest that FGFR1, FGFR3, and FGFR4 act in concert to mediate FGF23 effects on the kidney and that loss of FGFR function leads to feedback stimulation of Fgf23 expression in bone...

Research Grants40

  1. DIFFERENTIAL FUNCTION AND REGULATION OF RUNX2 ISOFORMS
    L Quarles; Fiscal Year: 2003
    ..These studies will define the unique functions of the N-terminal domains, and determine if translational regulation contributes to the tissue-specific expression of Runx2-I and Runx2-II isoforms. ..
  2. PEX FUNCTION IN OSTEOBLASTS
    L Quarles; Fiscal Year: 2000
    ..The study of Pex may yield an entirely new view of mineral metabolism. ..
  3. GENETICS OF FAMILIAL FOCAL SEGMENTAL GLOMERULOSCLEROSIS
    L Quarles; Fiscal Year: 2000
    ..Knowledge derived from FFSGS will also allow a better understanding of pathogenesis of non-hereditary forms FSGS and may provide insights regarding management of the more common sporadic forms of this disorder. ..
  4. DIFFERENTIAL FUNCTION AND REGULATION OF RUNX2 ISOFORMS
    L Quarles; Fiscal Year: 2006
    ..These studies will define the unique functions of the N-terminal domains, and determine if translational regulation contributes to the tissue-specific expression of Runx2-I and Runx2-II isoforms. ..
  5. GENETICS OF FAMILIAL FOCAL SEGMENTAL GLOMERULOSCLEROSIS
    L Quarles; Fiscal Year: 2001
    ..Knowledge derived from FFSGS will also allow a better understanding of pathogenesis of non-hereditary forms FSGS and may provide insights regarding management of the more common sporadic forms of this disorder. ..
  6. PHARMACOLOGICALLY INDUCED NEO-OSTEOGENESIS
    L Quarles; Fiscal Year: 2004
    ....
  7. PEX FUNCTION IN OSTEOBLASTS
    L Quarles; Fiscal Year: 2002
    ..The study of Pex may yield an entirely new view of mineral metabolism. ..
  8. DIFFERENTIAL FUNCTION AND REGULATION OF RUNX2 ISOFORMS
    L Quarles; Fiscal Year: 2003
    ..These studies will define the unique functions of the N-terminal domains, and determine if translational regulation contributes to the tissue-specific expression of Runx2-I and Runx2-II isoforms. ..
  9. DIFFERENTIAL FUNCTION AND REGULATION OF RUNX2 ISOFORMS
    L Quarles; Fiscal Year: 2004
    ..These studies will define the unique functions of the N-terminal domains, and determine if translational regulation contributes to the tissue-specific expression of Runx2-I and Runx2-II isoforms. ..
  10. PHARMACOLOGICALLY INDUCED NEO-OSTEOGENESIS
    L Quarles; Fiscal Year: 2000
    ..It is hoped that such kn owledge will permit a better understanding of physiologic and pharmacologic control of de novo bone formation by cations that may lead to new therapies for osteopenic disorders. ..
  11. DIFFERENTIAL FUNCTION AND REGULATION OF RUNX2 ISOFORMS
    L Quarles; Fiscal Year: 2005
    ..These studies will define the unique functions of the N-terminal domains, and determine if translational regulation contributes to the tissue-specific expression of Runx2-I and Runx2-II isoforms. ..
  12. Extrarenal Functions of Polycystin-1
    L Darryl Quarles; Fiscal Year: 2010
    ..In addition, a greater knowledge of polycystins and primary cilia functions in a different cellular context could translate into a broader understanding of their functions in the kidney. ..
  13. PHARMACOLOGICALLY INDUCED NEO-OSTEOGENESIS
    L Quarles; Fiscal Year: 1999
    ..It is hoped that such kn owledge will permit a better understanding of physiologic and pharmacologic control of de novo bone formation by cations that may lead to new therapies for osteopenic disorders. ..
  14. Pathogenesis of XLH/Hyp: Role of Phex MEPE and FGF23
    L Quarles; Fiscal Year: 2007
    ..abstract_text> ..
  15. PHARMACOLOGICALLY INDUCED NEO-OSTEOGENESIS
    L Quarles; Fiscal Year: 2005
    ....
  16. PHARMACOLOGICALLY INDUCED NEO-OSTEOGENESIS
    L Quarles; Fiscal Year: 1992
    ..Information obtained from these studies will likely lead to a better understanding of a novel agent(s) with osteogenic potential and may be useful in designing effective therapy for currently refractory osteopenic disorders...
  17. Pathogenesis of XLH/Hyp: Role of Phex MEPE and FGF23
    L Quarles; Fiscal Year: 2006
    ..abstract_text> ..
  18. DIFFERENTIAL FUNCTION AND REGULATION OF RUNX2 ISOFORMS
    L Quarles; Fiscal Year: 2007
    ..These studies will define the unique functions of the N-terminal domains, and determine if translational regulation contributes to the tissue-specific expression of Runx2-I and Runx2-II isoforms. ..
  19. EXTRACELLULAR CALCIUM-SENSING RECEPTORS IN OSTEOBLASTS
    L Quarles; Fiscal Year: 2009
    ..Successful completion of this project is certain to yield important new knowledge regarding the function of GPRC6A. ..
  20. EXTRACELLULAR CALCIUM-SENSING RECEPTORS IN OSTEOBLASTS
    L Darryl Quarles; Fiscal Year: 2009
    ..Successful completion of this project is certain to yield important new knowledge regarding the function of GPRC6A. ..
  21. PHARMACOLOGICALLY INDUCED NEO-OSTEOGENESIS
    L Quarles; Fiscal Year: 1993
    ..Information obtained from these studies will likely lead to a better understanding of a novel agent(s) with osteogenic potential and may be useful in designing effective therapy for currently refractory osteopenic disorders...
  22. PEX FUNCTION IN OSTEOBLASTS
    L Quarles; Fiscal Year: 1999
    ..The study of Pex may yield an entirely new view of mineral metabolism. ..
  23. PHARMACOLOGICALLY INDUCED NEO-OSTEOGENESIS
    L Quarles; Fiscal Year: 2002
    ....
  24. GENETICS OF FAMILIAL FOCAL SEGMENTAL GLOMERULOSCLEROSIS
    L Quarles; Fiscal Year: 2002
    ..Knowledge derived from FFSGS will also allow a better understanding of pathogenesis of non-hereditary forms FSGS and may provide insights regarding management of the more common sporadic forms of this disorder. ..
  25. PEX FUNCTION IN OSTEOBLASTS
    L Quarles; Fiscal Year: 2003
    ..The study of Pex may yield an entirely new view of mineral metabolism. ..
  26. PHARMACOLOGICALLY INDUCED NEO-OSTEOGENESIS
    L Quarles; Fiscal Year: 1991
    ..Information obtained from these studies will likely lead to a better understanding of a novel agent(s) with osteogenic potential and may be useful in designing effective therapy for currently refractory osteopenic disorders...
  27. GENETICS OF FAMILIAL FOCAL SEGMENTAL GLOMERULOSCLEROSIS
    L Quarles; Fiscal Year: 1999
    ..Knowledge derived from FFSGS will also allow a better understanding of pathogenesis of non-hereditary forms FSGS and may provide insights regarding management of the more common sporadic forms of this disorder. ..
  28. PHARMACOLOGICALLY INDUCED NEO-OSTEOGENESIS
    L Quarles; Fiscal Year: 2001
    ....
  29. PEX FUNCTION IN OSTEOBLASTS
    L Quarles; Fiscal Year: 2001
    ..The study of Pex may yield an entirely new view of mineral metabolism. ..
  30. PHARMACOLOGICALLY INDUCED NEO-OSTEOGENESIS
    L Quarles; Fiscal Year: 2003
    ....
  31. Pathogenesis of XLH/Hyp: Role of Phex MEPE and FGF23
    L Quarles; Fiscal Year: 2004
    ..abstract_text> ..
  32. Pathogenesis of XLH/Hyp: Role of Phex MEPE and FGF23
    L Quarles; Fiscal Year: 2005
    ..abstract_text> ..
  33. EXTRACELLULAR CALCIUM-SENSING RECEPTORS IN OSTEOBLASTS
    L Quarles; Fiscal Year: 2007
    ..Successful completion of this project is certain to yield important new knowledge regarding the function of GPRC6A. ..
  34. PHARMACOLOGICALLY INDUCED NEO-OSTEOGENESIS
    L Quarles; Fiscal Year: 2004
    ....