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Genomes and Genes | M B BurgSummaryAffiliation: National Institutes of Health Country: USA Publications
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Factors affecting counteraction by methylamines of urea effects on aldose reductaseM B Burg
National Heart, Lung and Blood Institute, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 96:6517-22. 1999..We conclude that counteraction of urea effects on enzymes by methylamines can depend on ion concentration, pH, the specific methylamine and substrate, and identity of even a single amino acid in the enzyme...
Response of renal inner medullary epithelial cells to osmotic stressMaurice B Burg
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, Bethesda, MD 20892 1603, USA
Comp Biochem Physiol A Mol Integr Physiol 133:661-6. 2002..We conclude that a more gradual increase in osmolality provides time for accumulation of organic osmolytes and activation of heat shock protein, previously known to be important for cell survival...- Macromolecular crowding as a cell volume sensorM B Burg
National Heart, Lung and Blood Institute, Bethesda, Maryland, USA
Cell Physiol Biochem 10:251-6. 2000.... - Renal osmoregulatory transport of compatible organic osmolytesM B Burg
National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892 1603, USA
Curr Opin Nephrol Hypertens 6:430-3. 1997..This transport is osmotically regulated by changes in transcription of the transporters and by post-translational modifications. Most of the original studies were in vitro, but these processes are increasingly being examined in vivo... - Intracellular organic osmolytes: function and regulationMaurice B Burg
Department of Health and Human Services, NHLBI, National Institutes of Health, Bethesda, Maryland 20892 1603, USA
J Biol Chem 283:7309-13. 2008.... - Cellular response to hyperosmotic stressesMaurice B Burg
National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892 1603, USA
Physiol Rev 87:1441-74. 2007.... - Ataxia telangiectasia-mutated, a DNA damage-inducible kinase, contributes to high NaCl-induced nuclear localization of transcription factor TonEBP/OREBPZheng Zhang
Laboratory of Kidney and Electrolyte Metabolism, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
Am J Physiol Renal Physiol 289:F506-11. 2005..In conclusion, activation of ATM contributes to high NaCl-induced nuclear translocation of TonEBP/OREBP... - Betaine transporter cDNA cloning and effect of osmolytes on its mRNA inductionJ D Ferraris
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Am J Physiol 270:C650-4. 1996..Because the aldose reductase gene is controlled in a similar fashion, we surmise that the two genes share a common signal for induction... - Mediator of DNA damage checkpoint 1 (MDC1) contributes to high NaCl-induced activation of the osmoprotective transcription factor TonEBP/OREBPMargarita Kunin
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, Bethesda, Maryland, United States of America
PLoS ONE 5:e12108. 2010..Hypertonicity, such as induced by high NaCl, increases the activity of the transcription factor TonEBP/OREBP whose target genes increase osmoprotective organic osmolytes and heat shock proteins... - Proteomic identification of proteins associated with the osmoregulatory transcription factor TonEBP/OREBP: functional effects of Hsp90 and PARP-1Ye Chen
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Am J Physiol Renal Physiol 292:F981-92. 2007..PARP-1 expression reduces TonEBP/OREBP transcriptional activity and the activity of its transactivating domain. Hsp90 enhances those activities and sustains the increased abundance of TonEBP/OREBP protein in cells exposed to high NaCl... - Distinct regulation of osmoprotective genes in yeast and mammals. Aldose reductase osmotic response element is induced independent of p38 and stress-activated protein kinase/Jun N-terminal kinase in rabbit kidney cellsD Kultz
Laboratory of Kidney and Electrolyte Metabolism, NHLBI, National Institutes of Health, Bethesda, Maryland 20892 0951, USA
J Biol Chem 272:13165-70. 1997..This finding stands in contrast to the requirement for the HOG1 pathway for hyperosmotically induced activation of yeast GPD1... - Phospholipase C-gamma1 is involved in signaling the activation by high NaCl of the osmoprotective transcription factor TonEBP/OREBPCarlos E Irarrazabal
Department of Health and Human Services, Laboratory of Kidney and Electrolyte Metabolism, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892 1603, USA
Proc Natl Acad Sci U S A 107:906-11. 2010.... - Cloning, genomic organization, and osmotic response of the aldose reductase geneJ D Ferraris
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892
Proc Natl Acad Sci U S A 91:10742-6. 1994..Identification and characterization of OREs within this fragment and their associated trans-acting factors should reveal the molecular mechanisms of gene regulation in osmotic stress... - Effects of expression of p53 and Gadd45 on osmotic tolerance of renal inner medullary cellsQi Cai
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892 1603, USA
Am J Physiol Renal Physiol 291:F341-9. 2006.... - Cell cycle delay and apoptosis are induced by high salt and urea in renal medullary cellsL Michea
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892 1603, USA
Am J Physiol Renal Physiol 278:F209-18. 2000..We conclude that elevated NaCl and/or urea reduces the number of proliferating mIMCD3 cells by slowing the transit through the S phase, by cell cycle delay in the G(2)M and G(1), and by inducing apoptotic cell death... - Contribution of SHP-1 protein tyrosine phosphatase to osmotic regulation of the transcription factor TonEBP/OREBPXiaoming Zhou
Division of Nephrology, Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA
Proc Natl Acad Sci U S A 107:7072-7. 2010..Thus, TonEBP/OREBP is extensively regulated by phosphatases, including SHP-1, whose inhibition by high NaCl increases phosphorylation of TonEBP/OREBP at Y143, contributing to the nuclear localization and activation of TonEBP/OREBP... - Activator protein-1 contributes to high NaCl-induced increase in tonicity-responsive enhancer/osmotic response element-binding protein transactivating activityCarlos E Irarrazabal
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health DHHS, 10 Center Drive, Bethesda, MD 20892, USA
J Biol Chem 283:2554-63. 2008..AP-1 reporter only if the AP-1 site is intact. Thus, AP-1 is part of the TonEBP/OREBP enhanceosome, and its role in high NaCl-induced activation of TonEBP/OREBP may require p38 activity... - Elimination of residual metastatic prostate cancer after surgery and adjunctive cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) blockade immunotherapyE D Kwon
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 96:15074-9. 1999.... - Hypertonic stress responseNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Department of Health and Human Services, 10 Center Drive, Building 10, Room 6N260, Bethesda, MD 20892-1603, USA
Mutat Res 569:65-74. 2005..How high NaCl causes the DNA breaks and how the cells survive them is conjectural at this point. We discuss possible answers to these questions, based on current knowledge about induction and processing of DNA breaks... - Increased reactive oxygen species contribute to high NaCl-induced activation of the osmoregulatory transcription factor TonEBP/OREBPXiaoming Zhou
Division of Nephrology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA
Am J Physiol Renal Physiol 289:F377-85. 2005..We conclude that the high NaCl-induced increase in ROS, including superoxide, contributes to activation of TonEBP/OREBP by increasing its transactivation... - c-Abl mediates high NaCl-induced phosphorylation and activation of the transcription factor TonEBP/OREBPMorgan Gallazzini
Laboratory of Kidney and Electrolyte Metabolism, National Heart Lung and Blood Institute, Bethesda, MD 20892 1603
FASEB J 24:4325-35. 2010..Thus, c-Abl is the kinase responsible for high NaCl-induced phosphorylation of TonEBP/OREBP-Y143, which contributes to its increased activity... - Molecular cloning of cDNA coding for kidney aldose reductase. Regulation of specific mRNA accumulation by NaCl-mediated osmotic stressA Garcia-Perez
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892
J Biol Chem 264:16815-21. 1989..The induction of aldose reductase mRNA by osmotic stress was reversible. Our finding of increased abundance of a specific mRNA in direct response to hyperosmotic stress represents the first report of such an effect in animals... - Hyperosmolality causes growth arrest of murine kidney cells. Induction of GADD45 and GADD153 by osmosensing via stress-activated protein kinase 2D Kultz
Laboratory of Kidney and Electrolyte Metabolism, NHLBI, National Institutes of Health, Bethesda, Maryland 20892 1603, USA
J Biol Chem 273:13645-51. 1998.... - Manipulation of T cell costimulatory and inhibitory signals for immunotherapy of prostate cancerE D Kwon
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Room 1N105, Building 9, 9 Memorial Drive, MSC 0951 Bethesda, MD 20892 0951, USA
Proc Natl Acad Sci U S A 94:8099-103. 1997..Additionally, the syngeneic murine model that we introduce provides a comprehensive system for further testing of immune-based treatments for prostate cancer... - Phosphatidylinositol 3-kinase mediates activation of ATM by high NaCl and by ionizing radiation: Role in osmoprotective transcriptional regulationCarlos E Irarrazabal
National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892 1603, USA
Proc Natl Acad Sci U S A 103:8882-7. 2006.... - The saltiness of the sea breaks DNA in marine invertebrates: possible implications for animal evolutionNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
Cell Cycle 5:1320-3. 2006..We speculate that, since DNA breaks cause mutations, salinity might have important background effects on the rate and course of evolution... - Knockout of Ku86 accelerates cellular senescence induced by high NaClNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Aging (Albany NY) 1:245-53. 2009..We conclude that Ku86 deficiency accelerates high NaCl(-) induced cellular senescence,particularly in the renal medulla where NaCl normally is high... - Neuropathy target esterase catalyzes osmoprotective renal synthesis of glycerophosphocholine in response to high NaClMorgan Gallazzini
Laboratory of Kidney and Electrolyte Metabolism, National Heart Lung and Blood Institute, Department of Health and Human Services, Bethesda, MD 20892 1603, USA
Proc Natl Acad Sci U S A 103:15260-5. 2006.... - Tonicity-regulated gene expressionJoan D Ferraris
Laboratory of Kidney and Electrolyte Metabolism, National Heart Lung Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA
Methods Enzymol 428:279-96. 2007..This chapter presents protocols for measuring the transcriptional activity of TonEBP/OREBP and determining its subcellular localization, its binding to OREs, and activity of its transactivation domain... - High NaCl promotes cellular senescenceNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA
Cell Cycle 6:3108-13. 2007..We conclude that high NaCl accelerates cellular senescence and aging, most likely secondary to the DNA breaks and oxidative damage that it causes... - MKP-1 inhibits high NaCl-induced activation of p38 but does not inhibit the activation of TonEBP/OREBP: opposite roles of p38alpha and p38deltaXiaoming Zhou
Division of Nephrology, Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA
Proc Natl Acad Sci U S A 105:5620-5. 2008.... - Analysis of DNA breaks, DNA damage response, and apoptosis produced by high NaClNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Dept of Health and Human Services, 9000 Rockville Pike, Bethesda, MD 20892 1603, USA
Am J Physiol Renal Physiol 295:F1678-88. 2008..We conclude that gammaH2AX induction and MRN activation in response to high NaCl are associated with apoptosis, not DNA repair... - What's new about osmotic regulation of glycerophosphocholineMorgan Gallazzini
Department of Health and Human Services, Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
Physiology (Bethesda) 24:245-9. 2009..We consider the metabolism of glycerophosphocholine, its osmotic regulation, and the recently discovered molecular identity of the enzymes that osmoregulate its abundance... - GDPD5 is a glycerophosphocholine phosphodiesterase that osmotically regulates the osmoprotective organic osmolyte GPCMorgan Gallazzini
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20982, USA
Proc Natl Acad Sci U S A 105:11026-31. 2008..We conclude that GDPD5 is a GPC-PDE that contributes to osmotic regulation of cellular GPC... - DNA damage and osmotic regulation in the kidneyNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, Department of Health and Human Services, Bethesda, MD 20892-1603, USA
Am J Physiol Renal Physiol 289:F2-7. 2005..Furthermore, we consider that the persistent DNA damage may be a sensor of hypertonicity that activates ATM kinase to provide a signal that contributes to protective osmotic regulation... - Ku86 preserves chromatin integrity in cells adapted to high NaClNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, and Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 102:10730-5. 2005..We propose that Ku86 ameliorates the effects of high NaCl-induced DNA breaks in adapted cells by supporting alignment of the broken ends of the DNA and thus maintaining integrity of the fragmented chromatin... - Proliferation and osmotic tolerance of renal inner medullary epithelial cells in vivo and in cell cultureZheng Zhang
Laboratory of Kidney and Electrolyte Metabolism, National Heart Lung and Blood Institute, Bethesda, Maryland 20892, USA
Am J Physiol Renal Physiol 283:F302-8. 2002..We conclude that immortalization and continued DNA replication account for part of the previously observed difference in osmotic tolerance between IM cells in vivo and in cell culture but that other factors must also be involved... - Rate of increase of osmolality determines osmotic tolerance of mouse inner medullary epithelial cellsQi Cai
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892 1603, USA
Am J Physiol Renal Physiol 283:F792-8. 2002..We conclude that gradual changes in osmolality, e.g., in vivo, allow cells to survive much greater changes than do the step changes routinely used in cell culture experiments... - Activity of the TonEBP/OREBP transactivation domain varies directly with extracellular NaCl concentrationJoan D Ferraris
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 99:739-44. 2002..Thus, the 983 C-terminal amino acids of TonEBP/OREBP contain a TAD that is regulated osmotically, apparently by tonicity-dependent phosphorylation... - cAMP-independent role of PKA in tonicity-induced transactivation of tonicity-responsive enhancer/ osmotic response element-binding proteinJoan D Ferraris
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 99:16800-5. 2002.... - Rapid activation of G2/M checkpoint after hypertonic stress in renal inner medullary epithelial (IME) cells is protective and requires p38 kinaseNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, and Gene Response Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 99:184-9. 2002..We propose that the rapid initiation of G(2) delay by p38 kinase after hypertonicity protects the cells by decreasing the level of DNA breaks caused by aberrant mitosis entry... - High NaCl causes Mre11 to leave the nucleus, disrupting DNA damage signaling and repairNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bldg 10, Rm 6N260, Bethesda, MD 20892, USA
Am J Physiol Renal Physiol 285:F266-74. 2003.... - Expression of osmotic stress-related genes in tissues of normal and hyposmotic ratsZheng Zhang
Laboratory of Kidney and Electrolyte Metabolism, National Heart Lung and Blood Institute, Bethesda, MD 20892, USA
Am J Physiol Renal Physiol 285:F688-93. 2003..4) TonEBP abundance and activity are regulated by factors other than tonicity in some tissues... - Greater tolerance of renal medullary cells for a slow increase in osmolality is associated with enhanced expression of HSP70 and other osmoprotective genesQi Cai
National Heart, Lung and Blood Institute, National Institutes of Health, Bldg 10, Rm 6N319, Bethesda, MD 20892 1603, USA
Am J Physiol Renal Physiol 286:F58-67. 2004..We speculate that poorer survival of p2mIME cells with a step than with linear increase in NaCl and urea is accounted for, at least in part, by urea-induced suppression of protective genes, particularly HSP70... - Cells adapted to high NaCl have many DNA breaks and impaired DNA repair both in cell culture and in vivoNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 1603, USA
Proc Natl Acad Sci U S A 101:2317-22. 2004..Thus, both in cell culture and in vivo, although cells adapt to high NaCl, their DNA is damaged and its repair is inhibited... - Living with DNA breaks is an everyday reality for cells adapted to high NaClNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892 1603, USA
Cell Cycle 3:561-3. 2004.... - ATM, a DNA damage-inducible kinase, contributes to activation by high NaCl of the transcription factor TonEBP/OREBPCarlos E Irarrazabal
National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892 1603, USA
Proc Natl Acad Sci U S A 101:8809-14. 2004..In conclusion, signaling via ATM is necessary for full activation of TonEBP/OREBP by high NaCl, but it is not sufficient... - High urea and NaCl carbonylate proteins in renal cells in culture and in vivo, and high urea causes 8-oxoguanine lesions in their DNAZheng Zhang
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 101:9491-6. 2004..iii) In mIMCD3 cells a normal plasma concentration of urea causes carbonylation, and carbonylation increases over the uremic range of urea concentration, indicating that urea can contribute directly to the carbonylation found in uremia... - Drying and salting send different messagesJoan D Ferraris
Laboratory of Kidney and Electrolyte Metabolism, National Heart Lung Blood Institute, National Institutes of Health, Bethesda, MD 20892-1603, USA
J Physiol 558:3. 2004 - High NaCl increases TonEBP/OREBP mRNA and protein by stabilizing its mRNAQi Cai
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892-1603, USA
Am J Physiol Renal Physiol 289:F803-7. 2005..We concluded that 1) hypertonicity stabilizes TonEBP/OREBP mRNA, contributing to its increase, and 2) stabilization depends on the presence of the 5'-UTR... - Mitochondrial dysfunction is an early event in high-NaCl-induced apoptosis of mIMCD3 cellsLuis Michea
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1603, USA
Am J Physiol Renal Physiol 282:F981-90. 2002..Adding urea to 700 mosmol/kgH(2)O does not change NADH or TMRM fluorescence. We conclude that extreme acute hypertonicity causes a mitochondrial dysfunction involved in the initiation of apoptosis... - Direct toxicity of nonsteroidal antiinflammatory drugs for renal medullary cellsG M Rocha
Laboratory of Kidney and Electrolytes Metabolism, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 98:5317-22. 2001..Such effects of APAF might account for renal medullary cell death in vivo and development of uroepithelial tumors from surviving cells that have chromosomal aberrations... - Toxicity of acetaminophen, salicylic acid, and caffeine for first-passage rat renal inner medullary collecting duct cellsQi Cai
Laboratory of Kidney and Electrolytes Metabolism, National Heart, Lung, and Blood Institute Department of Health and Human Services, National Institutes of Health, Bethesda, MD 20892-1603, USA
J Pharmacol Exp Ther 306:35-42. 2003.... - Mitochondrial reactive oxygen species contribute to high NaCl-induced activation of the transcription factor TonEBP/OREBPXiaoming Zhou
Div of Nephrology, Uniformed Services Univ of the Health Sciences, Bethesda, MD 20814, USA
Am J Physiol Renal Physiol 290:F1169-76. 2006..We conclude that high NaCl increases mitochondrial ROS production, which contributes to the activation of TonEBP/OREBP by increasing its transactivating activity... - Cell cycle delay and apoptosis in response to osmotic stressN I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, Bethesda, MD 20892-1603, USA
Comp Biochem Physiol A Mol Integr Physiol 130:411-20. 2001..The possible mechanisms of the protection action of p53 against hypertonic stress are discussed... - Osmotic stress and DNA damageNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
Methods Enzymol 428:241-52. 2007..This chapter also discusses how specifics of the protocols influence the conclusions about types of DNA damage and what the limitations of these methods are for detecting different types of DNA damage... - Three GADD45 isoforms contribute to hypertonic stress phenotype of murine renal inner medullary cellsDevulapalli Chakravarty
The Whitney Laboratory, University of Florida, St Augustine, Florida 32080, USA
Am J Physiol Renal Physiol 283:F1020-9. 2002..These data associate all known GADD45 isoforms with the hypertonicity phenotype of renal IM cells...