Paul R Mittelstadt

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint Activating p38 MAPK: new tricks for an old kinase
    Paul R Mittelstadt
    Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Cell Cycle 4:1189-92. 2005
  2. ncbi request reprint The autoimmune suppressor Gadd45alpha inhibits the T cell alternative p38 activation pathway
    Jesus M Salvador
    Gene Response Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nat Immunol 6:396-402. 2005
  3. pmc T cell receptor-mediated activation of p38{alpha} by mono-phosphorylation of the activation loop results in altered substrate specificity
    Paul R Mittelstadt
    Laboratory of Immune Cell Biology, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 284:15469-74. 2009
  4. pmc Lack of the T cell-specific alternative p38 activation pathway reduces autoimmunity and inflammation
    Ludmila Jirmanova
    Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
    Blood 118:3280-9. 2011
  5. ncbi request reprint Alternative p38 activation pathway mediated by T cell receptor-proximal tyrosine kinases
    Jesus M Salvador
    Gene Response Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nat Immunol 6:390-5. 2005
  6. pmc Genetic disruption of p38alpha Tyr323 phosphorylation prevents T-cell receptor-mediated p38alpha activation and impairs interferon-gamma production
    Ludmila Jirmanova
    Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Blood 113:2229-37. 2009
  7. pmc Thymocyte responsiveness to endogenous glucocorticoids is required for immunological fitness
    Paul R Mittelstadt
    Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA
    J Clin Invest 122:2384-94. 2012
  8. pmc Scavenger receptor BI and high-density lipoprotein regulate thymocyte apoptosis in sepsis
    Ling Guo
    From the Department of Pediatrics L G, Z Z, J A, X A L, Graduate Center for Nutritional Sciences Z Z, J A, X A L, and Saha Cardiovascular Research Center D A H, A D, X A L, University of Kentucky College of Medicine, Lexington and Laboratory of Immune Cell Biology, National Cancer Institute P R M, J D A and Lipoprotein Metabolism Section, National Heart, Lung, and Blood Institute S T, A T R, National Institutes of Health, Bethesda, MD
    Arterioscler Thromb Vasc Biol 34:966-75. 2014
  9. pmc Live cell imaging unveils multiple domain requirements for in vivo dimerization of the glucocorticoid receptor
    Diego M Presman
    Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, NIH, Bethesda, Maryland, United States of America Department of Biological Chemistry, School of Sciences FCEN, University of Buenos Aires UBA, Buenos Aires, Argentina IFIBYNE CONICET, School of Sciences FCEN, University of Buenos Aires UBA, Buenos Aires, Argentina
    PLoS Biol 12:e1001813. 2014

Collaborators

  • Jonathan D Ashwell
  • Alan Daugherty
  • Xiang An Li
  • Gordon L Hager
  • Ling Guo
  • Ludmila Jirmanova
  • Jesus M Salvador
  • Diego M Presman
  • Albert J Fornace
  • Lautaro D Alvarez
  • M Florencia Ogara
  • Martín Stortz
  • Thomas A Johnson
  • Sundar Ganesan
  • John R Pooley
  • Valeria Levi
  • Lars Grøntved
  • R Louis Schiltz
  • Gerardo Burton
  • Adali Pecci
  • Nandakumara D Sarma
  • Maria Letizia Giardino Torchia
  • Dragana Jankovic
  • Dandapantula N Sarma
  • Terry D Copeland
  • Galina I Belova
  • Hiroshi Yamaguchi
  • Tad Guszczynski
  • Ettore Appella

Detail Information

Publications9

  1. ncbi request reprint Activating p38 MAPK: new tricks for an old kinase
    Paul R Mittelstadt
    Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Cell Cycle 4:1189-92. 2005
    ..Here we discuss the structural and functional implications of this alternative p38 activation pathway, which may provide a new target for tissue-specific pharmacologic inhibition...
  2. ncbi request reprint The autoimmune suppressor Gadd45alpha inhibits the T cell alternative p38 activation pathway
    Jesus M Salvador
    Gene Response Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nat Immunol 6:396-402. 2005
    ..Thus, constitutive activation of T cell p38 through the alternative pathway is prevented by Gadd45alpha, the absence of which results in p38 activation, T cell hyperproliferation and autoimmunity...
  3. pmc T cell receptor-mediated activation of p38{alpha} by mono-phosphorylation of the activation loop results in altered substrate specificity
    Paul R Mittelstadt
    Laboratory of Immune Cell Biology, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 284:15469-74. 2009
    ..These findings suggest that T cells have evolved a mechanism to utilize p38 in a specialized manner independent of and distinct from the classical p38 MAPK signaling cascade...
  4. pmc Lack of the T cell-specific alternative p38 activation pathway reduces autoimmunity and inflammation
    Ludmila Jirmanova
    Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
    Blood 118:3280-9. 2011
    ..Thus, T cell-specific alternative activation of p38 is an important pathway in T-cell proliferation, Th skewing, and inflammatory autoimmunity, and may be an attractive tissue-specific target for intervention in these processes...
  5. ncbi request reprint Alternative p38 activation pathway mediated by T cell receptor-proximal tyrosine kinases
    Jesus M Salvador
    Gene Response Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nat Immunol 6:390-5. 2005
    ..Thus, phosphorylation of Tyr323 dependent on the tyrosine kinase Lck and mediated by Zap70 serves as an important mechanism for TCR activation of p38 in T cells...
  6. pmc Genetic disruption of p38alpha Tyr323 phosphorylation prevents T-cell receptor-mediated p38alpha activation and impairs interferon-gamma production
    Ludmila Jirmanova
    Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Blood 113:2229-37. 2009
    ..Thus, the Tyr323-dependent pathway and not the classic mitogen-activated protein (MAP) kinase cascade is the physiologic means of p38alpha activation through the TCR and is necessary for normal Th1 function but not Th1 generation...
  7. pmc Thymocyte responsiveness to endogenous glucocorticoids is required for immunological fitness
    Paul R Mittelstadt
    Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA
    J Clin Invest 122:2384-94. 2012
    ....
  8. pmc Scavenger receptor BI and high-density lipoprotein regulate thymocyte apoptosis in sepsis
    Ling Guo
    From the Department of Pediatrics L G, Z Z, J A, X A L, Graduate Center for Nutritional Sciences Z Z, J A, X A L, and Saha Cardiovascular Research Center D A H, A D, X A L, University of Kentucky College of Medicine, Lexington and Laboratory of Immune Cell Biology, National Cancer Institute P R M, J D A and Lipoprotein Metabolism Section, National Heart, Lung, and Blood Institute S T, A T R, National Institutes of Health, Bethesda, MD
    Arterioscler Thromb Vasc Biol 34:966-75. 2014
    ..Thymocyte apoptosis is a major event in sepsis; however, how this process is regulated remains poorly understood...
  9. pmc Live cell imaging unveils multiple domain requirements for in vivo dimerization of the glucocorticoid receptor
    Diego M Presman
    Laboratory of Receptor Biology and Gene Expression, National Cancer Institute, NIH, Bethesda, Maryland, United States of America Department of Biological Chemistry, School of Sciences FCEN, University of Buenos Aires UBA, Buenos Aires, Argentina IFIBYNE CONICET, School of Sciences FCEN, University of Buenos Aires UBA, Buenos Aires, Argentina
    PLoS Biol 12:e1001813. 2014
    ..Finally, the state of dimerization affected DNA binding only to a subset of GR binding sites. These results have major implications on future searches for therapeutic glucocorticoids with reduced side effects. ..