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Campo DC | Valor | Lengua/Idioma |
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dc.provenance | Facultad de Ciencias Exactas y Naturales de la UBA | - |
dc.contributor | <div class="autor_fcen" id="4984">Liberman, A.C.</div> | - |
dc.contributor | Antunica-Noguerol, M. | - |
dc.contributor | Ferraz-de-Paula, V. | - |
dc.contributor | Palermo-Neto, J. | - |
dc.contributor | <div class="autor_fcen" id="1656">Castro, C.N.</div> | - |
dc.contributor | <div class="autor_fcen" id="2675">Druker, J.</div> | - |
dc.contributor | Holsboer, F. | - |
dc.contributor | Perone, M.J. | - |
dc.contributor | Gerlo, S. | - |
dc.contributor | de Bosscher, K. | - |
dc.contributor | Haegeman, G. | - |
dc.contributor | Arzt, E. | - |
dc.creator | <div class="autor_fcen" id="4984">Liberman, A.C.</div> | - |
dc.creator | Antunica-Noguerol, M. | - |
dc.creator | Ferraz-de-Paula, V. | - |
dc.creator | Palermo-Neto, J. | - |
dc.creator | <div class="autor_fcen" id="1656">Castro, C.N.</div> | - |
dc.creator | <div class="autor_fcen" id="2675">Druker, J.</div> | - |
dc.creator | Holsboer, F. | - |
dc.creator | Perone, M.J. | - |
dc.creator | Gerlo, S. | - |
dc.creator | de Bosscher, K. | - |
dc.creator | Haegeman, G. | - |
dc.creator | Arzt, E. | - |
dc.date.accessioned | 2018-05-04T22:04:30Z | - |
dc.date.accessioned | 2018-05-28T15:49:17Z | - |
dc.date.available | 2018-05-04T22:04:30Z | - |
dc.date.available | 2018-05-28T15:49:17Z | - |
dc.date.issued | 2012 | - |
dc.identifier.uri | http://10.0.0.11:8080/jspui/handle/bnmm/68626 | - |
dc.description | Background: Compound A (CpdA) is a dissociating non-steroidal glucocorticoid receptor (GR) ligand which has anti-inflammatory properties exerted by down-modulating proinflammatory gene expression. By favouring GR monomer formation, CpdA does not enhance glucocorticoid (GC) response element-driven gene expression, resulting in a reduced side effect profile as compared to GCs. Considering the importance of Th1/Th2 balance in the final outcome of immune and inflammatory responses, we analyzed how selective GR modulation differentially regulates the activity of T-bet and GATA-3, master drivers of Th1 and Th2 differentiation, respectively. Results: Using Western analysis and reporter gene assays, we show in murine T cells that, similar to GCs, CpdA inhibits T-bet activity via a transrepressive mechanism. Different from GCs, CpdA induces GATA-3 activity by p38 MAPK-induction of GATA-3 phosphorylation and nuclear translocation. CpdA effects are reversed by the GR antagonist RU38486, proving the involvement of GR in these actions. ELISA assays demonstrate that modulation of T-bet and GATA-3 impacts on cytokine production shown by a decrease in IFN-γ and an increase in IL-5 production, respectively. Conclusions: Taken together, through their effect favoring Th2 over Th1 responses, particular dissociated GR ligands, for which CpdA represents a paradigm, hold potential for the application in Th1-mediated immune disorders. © 2012 Liberman et al. | - |
dc.description | Fil:Liberman, A.C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. | - |
dc.description | Fil:Castro, C.N. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. | - |
dc.description | Fil:Druker, J. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. | - |
dc.format | application/pdf | - |
dc.language | eng | - |
dc.rights | info:eu-repo/semantics/openAccess | - |
dc.rights | http://creativecommons.org/licenses/by/2.5/ar | - |
dc.source | PLoS ONE 2012;7(4) | - |
dc.source.uri | http://digital.bl.fcen.uba.ar/Download/paper/paper_19326203_v7_n4_p_Liberman.pdf | - |
dc.subject | compound A | - |
dc.subject | dexamethasone | - |
dc.subject | gamma interferon | - |
dc.subject | glucocorticoid receptor | - |
dc.subject | interleukin 5 | - |
dc.subject | mifepristone | - |
dc.subject | transcription factor GATA 3 | - |
dc.subject | unclassified drug | - |
dc.subject | 2 (4 acetoxyphenyl) 2 chloro N methyl ethylammonium chloride | - |
dc.subject | 2-(4-acetoxyphenyl)-2-chloro-N-methyl-ethylammonium chloride | - |
dc.subject | aziridine derivative | - |
dc.subject | gamma interferon | - |
dc.subject | Gata3 protein, mouse | - |
dc.subject | glucocorticoid receptor | - |
dc.subject | mifepristone | - |
dc.subject | quaternary ammonium derivative | - |
dc.subject | T box transcription factor | - |
dc.subject | T box transcription factor TBX21 | - |
dc.subject | T-box transcription factor TBX21 | - |
dc.subject | transcription factor GATA 3 | - |
dc.subject | animal cell | - |
dc.subject | article | - |
dc.subject | cell differentiation | - |
dc.subject | controlled study | - |
dc.subject | cytokine production | - |
dc.subject | dimerization | - |
dc.subject | enzyme linked immunosorbent assay | - |
dc.subject | gene expression | - |
dc.subject | immune response | - |
dc.subject | immunocompetent cell | - |
dc.subject | ligand binding | - |
dc.subject | mouse | - |
dc.subject | nonhuman | - |
dc.subject | protein expression | - |
dc.subject | protein phosphorylation | - |
dc.subject | reporter gene | - |
dc.subject | spleen cell | - |
dc.subject | Th1 cell | - |
dc.subject | Th2 cell | - |
dc.subject | animal | - |
dc.subject | Bagg albino mouse | - |
dc.subject | biosynthesis | - |
dc.subject | drug antagonism | - |
dc.subject | drug effect | - |
dc.subject | drug potentiation | - |
dc.subject | immunology | - |
dc.subject | spleen | - |
dc.subject | T lymphocyte | - |
dc.subject | Th1 Th2 balance | - |
dc.subject | Murinae | - |
dc.subject | Animals | - |
dc.subject | Aziridines | - |
dc.subject | GATA3 Transcription Factor | - |
dc.subject | Interferon-gamma | - |
dc.subject | Mice | - |
dc.subject | Mice, Inbred BALB C | - |
dc.subject | Mifepristone | - |
dc.subject | Quaternary Ammonium Compounds | - |
dc.subject | Receptors, Glucocorticoid | - |
dc.subject | Spleen | - |
dc.subject | T-Box Domain Proteins | - |
dc.subject | T-Lymphocytes | - |
dc.subject | Th1 Cells | - |
dc.subject | Th1-Th2 Balance | - |
dc.subject | Th2 Cells | - |
dc.title | Compound a, a dissociated glucocorticoid receptor modulator, inhibits t-bet (th1) and induces gata-3 (th2) activity in immune cells | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:ar-repo/semantics/artículo | - |
dc.type | info:eu-repo/semantics/publishedVersion | - |
Aparece en las colecciones: | FCEN - Facultad de Ciencias Exactas y Naturales. UBA |
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