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Abstract:

The bcl-X gene plays a critical role in apoptosis. Six different isoforms generated by tissue-specific promoter usage and alternative splicing were described. Some of them exert opposite effects on cell death. In mammary epithelial cells glucocorticoids induce bcl-X expression and increase the ratio bcl-XL (antiapoptotic)/bcl-XS (apoptotic) by activating P4 promoter, which contains two hormone response elements. Here we show that, on mouse thymocytes and T lymphocyte derivative S49 cells, glucocorticoids inhibited transcription from P4 and decreased the ratio bcl-X L/bcl-XS favoring apoptosis. Upon hormonal treatment, glucocorticoid receptor (GR), steroid receptor coactivator-1, and RNA polymerase II were transiently recruited to P4 promoter, whereas STAT5B was also recruited but remained bound. Concomitant with the release of GR, silencing mediator for retinoic acid receptor and thyroid hormone receptor and histone deacetylase 3 were recruited, histone H3 was deacetylated, and RNA polymerase II left the promoter. Inhibition of STAT5 activity reverted glucocorticoid repression to activation of transcription and was accompanied by stable recruitment of GR and RNA polymerase II to P4. © 2006 by The American Society for Biochemistry and Molecular Biology, Inc.

Registro:

Documento: Artículo
Título:Glucocorticoids repress bcl-X expression in lymphoid cells by recruiting STAT5B to the P4 promoter
Autor:Rocha-Viegas, L.; Vicent, G.P.; Barañao, J.L.; Beato, M.; Pecci, A.
Filiación:Departamento de Química Biológica, Inst. de Fisiol., Biol. Molec. Y Neurociencias (IFIBYNE)-Consejo Nac. de Invest. Cient. Y Tec., Pab. II, C1428EGA Buenos Aires, Argentina
Departamento de Fisiología, Biología Molecular Y Celular, Inst. de Fisiol., Biol. Molec. Y Neurociencias (IFIBYNE)-Consejo Nac. de Invest. Cient. Y Tec., Ciudad Universitaria, Intendente Guiraldes 2160, Pab. II, C1428EGA Buenos Aires, Argentina
Centre de Regulació Genòmica, Universitat Pompeu Fabra, Passeig Marítim, 37-49, 08003 Barcelona, Spain
Palabras clave:Derivatives; Enzyme inhibition; Genes; Hormones; RNA; Tissue; Cell death; Hormonal treatment; Lymphoid cells; Thymocytes; Cells; dexamethasone; glucocorticoid; glucocorticoid receptor; histone deacetylase 3; histone H3; protein bcl x; retinoic acid receptor; RNA polymerase II; STAT5b protein; steroid receptor coactivator 1; thyroid hormone receptor; acetylation; animal cell; animal experiment; article; controlled study; gene activity; gene expression; gene silencing; hormone inhibition; lymphoid cell; male; mouse; nonhuman; priority journal; promoter region; protein DNA binding; protein DNA interaction; T lymphocyte; thymocyte; transcription regulation; Acetylation; Animals; Apoptosis; bcl-X Protein; Cercopithecus aethiops; Chromatin Immunoprecipitation; COS Cells; Dexamethasone; Electrophoretic Mobility Shift Assay; Gene Expression Regulation; Histone Acetyltransferases; Histones; Hormone Antagonists; Lymphocytes; Male; Mice; Mifepristone; Plasmids; Promoter Regions (Genetics); Receptors, Glucocorticoid; Reverse Transcriptase Polymerase Chain Reaction; RNA Polymerase II; RNA, Messenger; STAT5 Transcription Factor; Thymus Gland; Transcription Factors; Transcription, Genetic
Año:2006
Volumen:281
Número:45
Página de inicio:33959
Página de fin:33970
DOI: http://dx.doi.org/10.1074/jbc.M602408200
Título revista:Journal of Biological Chemistry
Título revista abreviado:J. Biol. Chem.
ISSN:00219258
CODEN:JBCHA
CAS:dexamethasone, 50-02-2; bcl-X Protein; Dexamethasone, 50-02-2; Histone Acetyltransferases, EC 2.3.1.48; Histones; Hormone Antagonists; Mifepristone, 84371-65-3; nuclear receptor coactivator 1, EC 2.3.1.48; Receptors, Glucocorticoid; RNA Polymerase II, EC 2.7.7.-; RNA, Messenger; STAT5 Transcription Factor; STAT5B protein, human; Transcription Factors
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Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219258_v281_n45_p33959_RochaViegas

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Citas:

---------- APA ----------
Rocha-Viegas, L., Vicent, G.P., Barañao, J.L., Beato, M. & Pecci, A. (2006) . Glucocorticoids repress bcl-X expression in lymphoid cells by recruiting STAT5B to the P4 promoter. Journal of Biological Chemistry, 281(45), 33959-33970.
http://dx.doi.org/10.1074/jbc.M602408200
---------- CHICAGO ----------
Rocha-Viegas, L., Vicent, G.P., Barañao, J.L., Beato, M., Pecci, A. "Glucocorticoids repress bcl-X expression in lymphoid cells by recruiting STAT5B to the P4 promoter" . Journal of Biological Chemistry 281, no. 45 (2006) : 33959-33970.
http://dx.doi.org/10.1074/jbc.M602408200
---------- MLA ----------
Rocha-Viegas, L., Vicent, G.P., Barañao, J.L., Beato, M., Pecci, A. "Glucocorticoids repress bcl-X expression in lymphoid cells by recruiting STAT5B to the P4 promoter" . Journal of Biological Chemistry, vol. 281, no. 45, 2006, pp. 33959-33970.
http://dx.doi.org/10.1074/jbc.M602408200
---------- VANCOUVER ----------
Rocha-Viegas, L., Vicent, G.P., Barañao, J.L., Beato, M., Pecci, A. Glucocorticoids repress bcl-X expression in lymphoid cells by recruiting STAT5B to the P4 promoter. J. Biol. Chem. 2006;281(45):33959-33970.
http://dx.doi.org/10.1074/jbc.M602408200