Laura E Nagy

Summary

Affiliation: Case Western Reserve University
Country: USA

Publications

  1. ncbi Molecular aspects of alcohol metabolism: transcription factors involved in early ethanol-induced liver injury
    Laura E Nagy
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44106 4906, USA
    Annu Rev Nutr 24:55-78. 2004
  2. ncbi Stabilization of tumor necrosis factor-alpha mRNA in macrophages in response to chronic ethanol exposure
    Laura E Nagy
    Department of Nutrition, Case Western Reserve University, 2123 Abington Road, Room 201, Cleveland, OH 44106 4906, USA
    Alcohol 33:229-33. 2004
  3. ncbi Ethanol and membrane protein trafficking: diverse mechanisms of ethanol action
    Laura E Nagy
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44106 4906, USA
    Alcohol Clin Exp Res 26:287-93. 2002
  4. ncbi Recent insights into the role of the innate immune system in the development of alcoholic liver disease
    Laura E Nagy
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44106 4906, USA
    Exp Biol Med (Maywood) 228:882-90. 2003
  5. ncbi Complement and alcoholic liver disease: role of C1q in the pathogenesis of ethanol-induced liver injury in mice
    Jessica I Cohen
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44195, USA
    Gastroenterology 139:664-74, 674.e1. 2010
  6. ncbi Short-term treatment of RAW264.7 macrophages with adiponectin increases tumor necrosis factor-alpha (TNF-alpha) expression via ERK1/2 activation and Egr-1 expression: role of TNF-alpha in adiponectin-stimulated interleukin-10 production
    Pil Hoon Park
    Department of Pathobiology, Cleveland Clinic Foundation, Cleveland, OH 44195, USA
    J Biol Chem 282:21695-703. 2007
  7. ncbi Chronic ethanol and triglyceride turnover in white adipose tissue in rats: inhibition of the anti-lipolytic action of insulin after chronic ethanol contributes to increased triglyceride degradation
    Li Kang
    Department of Biochemistry, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Biol Chem 282:28465-73. 2007
  8. ncbi Chronic ethanol feeding increases activation of NADPH oxidase by lipopolysaccharide in rat Kupffer cells: role of increased reactive oxygen in LPS-stimulated ERK1/2 activation and TNF-alpha production
    Varsha Thakur
    Department of Nutrition, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106-4906, USA
    J Leukoc Biol 79:1348-56. 2006
  9. ncbi Stimulation of macrophage TNFalpha production by orthopaedic wear particles requires activation of the ERK1/2/Egr-1 and NF-kappaB pathways but is independent of p38 and JNK
    Michelle A Beidelschies
    Department of Physiology and Biophysics, Case Medical Center, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Cell Physiol 217:652-66. 2008
  10. ncbi Lipopolysaccharide stimulation of ERK1/2 increases TNF-alpha production via Egr-1
    Liang Shi
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44106 4906, USA
    Am J Physiol Cell Physiol 282:C1205-11. 2002

Collaborators

Detail Information

Publications52

  1. ncbi Molecular aspects of alcohol metabolism: transcription factors involved in early ethanol-induced liver injury
    Laura E Nagy
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44106 4906, USA
    Annu Rev Nutr 24:55-78. 2004
    ....
  2. ncbi Stabilization of tumor necrosis factor-alpha mRNA in macrophages in response to chronic ethanol exposure
    Laura E Nagy
    Department of Nutrition, Case Western Reserve University, 2123 Abington Road, Room 201, Cleveland, OH 44106 4906, USA
    Alcohol 33:229-33. 2004
    ..Taken together, the results from these studies identify the regulation of TNF-alpha mRNA stability as a novel mechanism by which chronic exposure to ethanol increases the expression of TNF-alpha...
  3. ncbi Ethanol and membrane protein trafficking: diverse mechanisms of ethanol action
    Laura E Nagy
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44106 4906, USA
    Alcohol Clin Exp Res 26:287-93. 2002
    ..Casey; (3) Ethanol and L1 mediated neurite outgrowth: receptor recycling and L1 signal transduction, by Cynthia F. Bearer; and (4) Ethanol and glucose transport, GLUT4 vesicle trafficking, by Laura E. Nagy...
  4. ncbi Recent insights into the role of the innate immune system in the development of alcoholic liver disease
    Laura E Nagy
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44106 4906, USA
    Exp Biol Med (Maywood) 228:882-90. 2003
    ..Enhanced activation of these TLR-4 dependent signaling pathways after chronic ethanol likely contributes to the development of alcoholic liver disease...
  5. ncbi Complement and alcoholic liver disease: role of C1q in the pathogenesis of ethanol-induced liver injury in mice
    Jessica I Cohen
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44195, USA
    Gastroenterology 139:664-74, 674.e1. 2010
    ..Because ethanol exposure increases hepatocellular apoptosis, we hypothesized that ethanol-induced apoptosis would lead to activation of complement via the classical pathway...
  6. ncbi Short-term treatment of RAW264.7 macrophages with adiponectin increases tumor necrosis factor-alpha (TNF-alpha) expression via ERK1/2 activation and Egr-1 expression: role of TNF-alpha in adiponectin-stimulated interleukin-10 production
    Pil Hoon Park
    Department of Pathobiology, Cleveland Clinic Foundation, Cleveland, OH 44195, USA
    J Biol Chem 282:21695-703. 2007
    ....
  7. ncbi Chronic ethanol and triglyceride turnover in white adipose tissue in rats: inhibition of the anti-lipolytic action of insulin after chronic ethanol contributes to increased triglyceride degradation
    Li Kang
    Department of Biochemistry, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Biol Chem 282:28465-73. 2007
    ..Furthermore, this enhanced rate of lipolysis was due to a suppression of the anti-lipolytic effects of insulin in adipocytes after chronic ethanol feeding...
  8. ncbi Chronic ethanol feeding increases activation of NADPH oxidase by lipopolysaccharide in rat Kupffer cells: role of increased reactive oxygen in LPS-stimulated ERK1/2 activation and TNF-alpha production
    Varsha Thakur
    Department of Nutrition, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106-4906, USA
    J Leukoc Biol 79:1348-56. 2006
    ..Further, ERK1/2 is an important target of NADPH oxidase-derived ROS in Kupffer cells, contributing to enhanced LPS-stimulated TNF-alpha production by Kupffer cells after chronic ethanol feeding...
  9. ncbi Stimulation of macrophage TNFalpha production by orthopaedic wear particles requires activation of the ERK1/2/Egr-1 and NF-kappaB pathways but is independent of p38 and JNK
    Michelle A Beidelschies
    Department of Physiology and Biophysics, Case Medical Center, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Cell Physiol 217:652-66. 2008
    ....
  10. ncbi Lipopolysaccharide stimulation of ERK1/2 increases TNF-alpha production via Egr-1
    Liang Shi
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44106 4906, USA
    Am J Physiol Cell Physiol 282:C1205-11. 2002
    ..These results delineate the role of ERK1/2 activation of Egr-1 activity in mediating LPS-induced increases in TNF-alpha mRNA expression in macrophages...
  11. ncbi Chronic ethanol-induced insulin resistance is associated with macrophage infiltration into adipose tissue and altered expression of adipocytokines
    Li Kang
    Department of Biochemistry, Case Western Reserve University, Cleveland, Ohio, USA
    Alcohol Clin Exp Res 31:1581-8. 2007
    ....
  12. ncbi An early complement-dependent and TLR-4-independent phase in the pathogenesis of ethanol-induced liver injury in mice
    Sanjoy Roychowdhury
    Department of Pathobiology, Cleveland Clinic Foundation, Cleveland, OH, USA
    Hepatology 49:1326-34. 2009
    ..CONCLUSION: We have identified a complement- and macrophage-dependent, but TLR-4 independent, phase in the pathogenesis of ethanol-induced liver injury...
  13. ncbi Ethanol-induced oxidative stress via the CYP2E1 pathway disrupts adiponectin secretion from adipocytes
    Hui Tang
    Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA
    Alcohol Clin Exp Res 36:214-22. 2012
    ..Here, we investigated the role of cytochrome P450 2E1 (CYP2E1) and oxidative stress in the mechanism for impaired adiponectin secretion from adipocytes in response to ethanol...
  14. ncbi Regulation of macrophage activation in alcoholic liver disease
    Varsha Thakur
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44106 4906, USA
    J Gastroenterol Hepatol 22:S53-6. 2007
    ....
  15. ncbi Chronic alcohol exposure increases circulating bioactive oxidized phospholipids
    Lili Yang
    Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio 44195, USA
    J Biol Chem 285:22211-20. 2010
    ..Suppressing hepatic inflammation, not ethanol catabolism, reduces circulating inflammatory and apoptotic agonists...
  16. ncbi Formation of gamma-ketoaldehyde-protein adducts during ethanol-induced liver injury in mice
    Sanjoy Roychowdhury
    Department of Pathobiology, Cleveland Clinic, Cleveland, OH 44195, USA
    Free Radic Biol Med 47:1526-38. 2009
    ..In summary, ethanol feeding enhanced gamma-ketoaldehyde-protein adduct production via a TNFR1/CYP2E1-dependent, but cyclooxygenase-independent, mechanism in mouse liver...
  17. ncbi Methods to investigate the effects of chronic ethanol on adipocytes
    Becky M Sebastian
    Department of Pathobiology, Cleveland Clinic, Cleveland, OH, USA
    Methods Mol Biol 447:357-66. 2008
    ..Included in this chapter are protocols for studying the effect of chronic ethanol feeding on these adipocyte functions...
  18. ncbi Chronic ethanol exposure increases the binding of HuR to the TNFalpha 3'-untranslated region in macrophages
    Megan R McMullen
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44106 4906, USA
    J Biol Chem 278:38333-41. 2003
    ..Taken together, these data demonstrate that increased binding of HuR to the TNFalpha 3'-UTR contributes to increased LPS-stimulated TNFalpha expression in macrophages after chronic ethanol exposure...
  19. ncbi Molecular mechanism for adiponectin-dependent M2 macrophage polarization: link between the metabolic and innate immune activity of full-length adiponectin
    Palash Mandal
    Department of Pathobiology, Cleveland Clinic, Cleveland, Ohio 44195, USA
    J Biol Chem 286:13460-9. 2011
    ....
  20. ncbi Differential contributions of C3, C5, and decay-accelerating factor to ethanol-induced fatty liver in mice
    Michele T Pritchard
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44905, USA
    Gastroenterology 132:1117-26. 2007
    ..The complement pathway is an important component of the innate and adaptive immune response. Here we tested the hypothesis that activation of complement is required for development of ethanol-induced fatty liver...
  21. ncbi Anti-inflammatory pathways and alcoholic liver disease: role of an adiponectin/interleukin-10/heme oxygenase-1 pathway
    Palash Mandal
    Department of Pathobiology and Gastroenterology, Cleveland Clinic, Lerner Research Institute NE 40, 9500 Euclid Avenue, Cleveland, OH 44195, USA
    World J Gastroenterol 16:1330-6. 2010
    ....
  22. ncbi Suppression of lipopolysaccharide-stimulated tumor necrosis factor-alpha production by adiponectin is mediated by transcriptional and post-transcriptional mechanisms
    Pil Hoon Park
    Department of Pathobiology, Cleveland Clinic, Cleveland, Ohio 44195, USA
    J Biol Chem 283:26850-8. 2008
    ..gAcrp treatment profoundly suppressed the ability of LPS to increase TNF-alpha transcription and reduced the stimulus-induced stabilization of TNF-alpha mRNA in response to LPS...
  23. ncbi Adiponectin and heme oxygenase-1 suppress TLR4/MyD88-independent signaling in rat Kupffer cells and in mice after chronic ethanol exposure
    Palash Mandal
    Department of Pathobiology, Cleveland Clinic, Cleveland, OH 44195, USA
    J Immunol 185:4928-37. 2010
    ..These data suggest that induction of HO-1 may be a useful therapeutic strategy in alcoholic liver disease...
  24. ncbi Adiponectin normalizes LPS-stimulated TNF-alpha production by rat Kupffer cells after chronic ethanol feeding
    Varsha Thakur
    Department of Nutrition, Case Western Reserve University, Rm 201, 2123 Abington Road, Cleveland, OH 44106 4906, USA
    Am J Physiol Gastrointest Liver Physiol 290:G998-1007. 2006
    ..Suppression of LPS-stimulated ERK1/2 signaling by low concentrations of gAcrp was associated with normalization of TNF-alpha production by Kupffer cells after chronic ethanol exposure...
  25. ncbi Endothelin-1-stimulated glucose uptake is desensitized by tumor necrosis factor-alpha in 3T3-L1 adipocytes
    Nadia Rachdaoui
    Department of Nutrition, Case Western Reserve University, Cleveland, OH 44106, USA
    Am J Physiol Endocrinol Metab 285:E545-51. 2003
    ....
  26. ncbi Isolation of Kupffer cells from rats fed chronic ethanol
    Megan R McMullen
    Department Pathobiology, Cleveland Clinic, Cleveland, OH, USA
    Methods Mol Biol 447:199-212. 2008
    ..The isolation and culture of Kupffer cells is an important technique with which one can elucidate the mechanisms that contribute to alcoholic liver injury...
  27. ncbi Taurine supplementation prevents ethanol-induced decrease in serum adiponectin and reduces hepatic steatosis in rats
    Xiaocong Chen
    Department of Nutrition, Case Western Reserve University, Cleveland, OH, USA
    Hepatology 49:1554-62. 2009
    ..Taken together, these data demonstrate that taurine has important protective effects against ethanol-induced tissue injury in both adipose and liver tissue...
  28. ncbi Regulation of Kupffer cell activity during chronic ethanol exposure: role of adiponectin
    Pil-Hoon Park
    Department of Nutrition, Case Western Reserve University, Cleveland and Departments of Gastroenterology and Pathobiology, Cleveland Clinic Foundation, Cleveland, Ohio 44106-4906, USA
    J Gastroenterol Hepatol 21:S30-3. 2006
    ..These studies suggest that the hepato-protective activity of adiponectin is due, at least in part, to a direct anti-inflammatory effect of adiponectin on Kupffer cells...
  29. ncbi Early growth response-1 transcription factor is essential for ethanol-induced fatty liver injury in mice
    Megan R McMullen
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44106 4906, USA
    Gastroenterology 128:2066-76. 2005
    ..Furthermore, because TNF-alpha contributes to alcoholic liver injury, we tested the hypothesis that Egr-1 is required for the development of ethanol-induced fatty liver injury in wild type and egr-1 -/- mice...
  30. ncbi Decreased insulin-dependent glucose transport by chronic ethanol feeding is associated with dysregulation of the Cbl/TC10 pathway in rat adipocytes
    Becky M Sebastian
    Dept of Nutrition, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106 4906, USA
    Am J Physiol Endocrinol Metab 289:E1077-84. 2005
    ....
  31. ncbi Identification of a cytochrome P4502E1/Bid/C1q-dependent axis mediating inflammation in adipose tissue after chronic ethanol feeding to mice
    Becky M Sebastian
    Liver Disease Research Center, Department of Pathobiology, Cleveland Clinic, Cleveland, Ohio 44195, USA
    J Biol Chem 286:35989-97. 2011
    ..Taken together, these data identify a novel mechanism for the development of adipose tissue inflammation that likely contributes to the pathophysiological effects of ethanol...
  32. ncbi Exogenous thioredoxin prevents ethanol-induced oxidative damage and apoptosis in mouse liver
    Jessica I Cohen
    Department of Nutrition, Case Western Reserve University, Cleveland, OH, USA
    Hepatology 49:1709-17. 2009
    ..rhTrx treatment prevented these increases. In summary, rhTrx attenuated ethanol-induced increases in markers of oxidative stress, inflammatory cytokine expression, and apoptosis...
  33. ncbi Mechanisms for the anti-inflammatory effects of adiponectin in macrophages
    Honglian Huang
    Department of Pathobiology, Cleveland Clinic, Cleveland, OH 44195, USA
    J Gastroenterol Hepatol 23:S50-3. 2008
    ..Increased IL-10 expression was ultimately required for the suppression of TLR4-mediated signaling by gAcrp...
  34. ncbi Chronic ethanol increases lipopolysaccharide-stimulated Egr-1 expression in RAW 264.7 macrophages: contribution to enhanced tumor necrosis factor alpha production
    Liang Shi
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44106 4906, USA
    J Biol Chem 277:14777-85. 2002
    ..These results demonstrate that enhanced LPS-dependent activation of Egr-1 contributes to increased TNFalpha production after chronic ethanol exposure...
  35. ncbi Isolevuglandins covalently modify phosphatidylethanolamines in vivo: detection and quantitative analysis of hydroxylactam adducts
    Wei Li
    Department of Chemistry, Case Western Reserve University, Cleveland, OH 44106, USA
    Free Radic Biol Med 47:1539-52. 2009
    ..4+/-0.1 ng/ml, n=15). Just as LG/isoLG-protein adducts provide a dosimeter of oxidative injury, this study suggests that LG/isoLG-PE-hydroxylactams are potential biomarkers for assessing risk for oxidative stress-stimulated diseases...
  36. ncbi Role of complement in ethanol-induced liver injury
    Michele T Pritchard
    Department of Pathobiology, Cleveland Clinic, Cleveland, OH 44195, USA
    Adv Exp Med Biol 632:175-86. 2008
    ....
  37. ncbi Early growth response-1 contributes to galactosamine/lipopolysaccharide-induced acute liver injury in mice
    Michele T Pritchard
    Dept of Pathobiology, Cleveland Clinic, 9500 Euclid Ave NE40, Cleveland, OH 44195, USA
    Am J Physiol Gastrointest Liver Physiol 293:G1124-33. 2007
    ..These data demonstrate that Egr-1 plays an important role in acceleration of hepatic inflammation, apoptosis, and subsequent mortality in GalN/LPS-induced acute liver injury...
  38. ncbi Chronic ethanol feeding impairs endothelin-1-stimulated glucose uptake via decreased G alpha 11 expression in rat adipocytes
    Nadia Rachdaoui
    Dept of Nutrition, Case Western Reserve University, 2123 Abington Rd, Rm 201, Cleveland, OH 44106 4906, USA
    Am J Physiol Endocrinol Metab 285:E303-10. 2003
    ....
  39. ncbi Chronic ethanol feeding suppresses beta-adrenergic receptor-stimulated lipolysis in adipocytes isolated from epididymal fat
    Li Kang
    Department of Nutrition, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, Ohio 44106-4906, USA
    Endocrinology 147:4330-8. 2006
    ....
  40. ncbi Inhibition of apoptosis protects mice from ethanol-mediated acceleration of early markers of CCl(4) -induced fibrosis but not steatosis or inflammation
    Sanjoy Roychowdhury
    Center for Liver Disease Research, Departments of Pathobiology, Case Western Reserve University, Cleveland, Ohio, USA
    Alcohol Clin Exp Res 36:1139-47. 2012
    ....
  41. ncbi Early growth response-1 attenuates liver injury and promotes hepatoprotection after carbon tetrachloride exposure in mice
    Michele T Pritchard
    Department of Pathobiology, Cleveland Clinic, Cleveland, OH 44195, USA
    J Hepatol 53:655-62. 2010
    ..Here, we tested the hypothesis that Egr-1 is beneficial after toxic liver injury...
  42. ncbi Chronic ethanol feeding to rats decreases adiponectin secretion by subcutaneous adipocytes
    Xiaocong Chen
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio, USA
    Am J Physiol Endocrinol Metab 292:E621-8. 2007
    ..In conclusion, chronic ethanol feeding impaired adiponectin secretion by subcutaneous and retroperitoneal adipocytes; impaired secretion likely contributes to decreased adiponectin concentrations after chronic ethanol feeding...
  43. ncbi Hepatic fibrosis is enhanced and accompanied by robust oval cell activation after chronic carbon tetrachloride administration to Egr-1-deficient mice
    Michele T Pritchard
    Department of Pathobiology NE40, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA
    Am J Pathol 176:2743-52. 2010
    ..Taken together, these data reveal novel roles for Egr-1 as a negative regulator of both CCl(4)-induced hepatic fibrosis and the oval cell response...
  44. ncbi Early growth response (EGR)-1 is required for timely cell-cycle entry and progression in hepatocytes after acute carbon tetrachloride exposure in mice
    Michele T Pritchard
    Department of Pathobiology, Cleveland Clinic, Case Western Reserve University, Ohio 44106, USA
    Am J Physiol Gastrointest Liver Physiol 300:G1124-31. 2011
    ..These data support the hypothesis that Egr-1 provides hepatoprotection in the CCl(4)-injured liver, attributable, in part, to timely cell-cycle induction and progression...
  45. ncbi ERK1/2 and Egr-1 contribute to increased TNF-alpha production in rat Kupffer cells after chronic ethanol feeding
    Raj Kishore
    Department of Nutrition, Case Western Reserve University, Cleveland, Ohio 44106 4906, USA
    Am J Physiol Gastrointest Liver Physiol 282:G6-15. 2002
    ..Together, these data suggest that enhanced activation of ERK1/2 and Egr-1 contributes to increased TNF-alpha production after chronic ethanol feeding...
  46. ncbi Pathogenesis of alcoholic liver disease: interactions between parenchymal and non-parenchymal cells
    Jessica I Cohen
    Department of Pathobiology, Cleveland Clinic, Cleveland, Ohio 44195, USA
    J Dig Dis 12:3-9. 2011
    ..In this review we provide an overview of the complex interactions between parenchymal and non-parenchymal cells in the liver during the progression of ethanol-induced liver injury...
  47. ncbi Redox signaling and the innate immune system in alcoholic liver disease
    Jessica I Cohen
    Department of Pathobiology, Cleveland Clinic, Cleveland, Ohio 44195, USA
    Antioxid Redox Signal 15:523-34. 2011
    ..These data illustrate that ethanol-induced oxidative stress and activation of the innate immune system interact dynamically during ethanol exposure, exacerbating ethanol-induced liver injury...
  48. ncbi Caspase-1 as a central regulator of high fat diet-induced non-alcoholic steatohepatitis
    Laura J Dixon
    Department of Molecular Medicine, Case Western Reserve University, Cleveland, Ohio, United States of America
    PLoS ONE 8:e56100. 2013
    ..Specifically, mice deficient in caspase-1 are protected from high fat-induced hepatic steatosis, inflammation and early fibrogenesis. These data point to the inflammasome as an important therapeutic target for NASH...
  49. ncbi Nutritional control of mRNA stability is mediated by a conserved AU-rich element that binds the cytoplasmic shuttling protein HuR
    Ibrahim Yaman
    Departments of Nutrition and Biochemistry, Case Western Reserve University School of Medicine, Cleveland, Ohio, 44106-4906, USA
    J Biol Chem 277:41539-46. 2002
    ..It is proposed that an adaptive response of cells to nutritional stress results in increased mRNA stability mediated by HuR binding to the NS-ARE...
  50. ncbi Activation of cyclic-AMP response element binding protein contributes to adiponectin-stimulated interleukin-10 expression in RAW 264.7 macrophages
    Pil Hoon Park
    Department of Pathobiology, Cleveland Clinic, OH 44195, USA
    J Leukoc Biol 83:1258-66. 2008
    ..Taken together, these data identify gAcrp-stimulated phospho-CREB as a key transcription factor responsible for gAcrp-induced IL-10 promoter activation...
  51. ncbi Acute and chronic ethanol exposure. Preface
    Laura E Nagy
    Cleveland Clinic, USA
    Methods Mol Biol 447:v-vi. 2008
  52. ncbi Acute and chronic alcohol abuse modulate immunity
    Lou Ann S Brown
    Department of Pediatrics, Emory University, Atlanta, Georgia, USA
    Alcohol Clin Exp Res 30:1624-31. 2006
    ..Nagy, and (8) Hepatitis C Virus Infection and Alcohol Use by Gyongyi Szabo. Meeting coorganizers were Elizabeth J. Kovacs, Lou Ann S. Brown, Thomas R. Jerrells, and Robert T. Cook...