Glucocorticoids repress bcl-X expression in lymphoid cells by recruiting STAT5B to the P4 promoter
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...
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todo:paper_00219258_v281_n45_p33959_RochaViegas2023-10-03T14:23:10Z Glucocorticoids repress bcl-X expression in lymphoid cells by recruiting STAT5B to the P4 promoter Rocha-Viegas, L. Vicent, G.P. Barañao, J.L. Beato, M. Pecci, A. 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 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. Fil:Rocha-Viegas, L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Vicent, G.P. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Barañao, J.L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Pecci, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_00219258_v281_n45_p33959_RochaViegas |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
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 |
| spellingShingle |
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 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 |
| topic_facet |
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 |
| description |
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. |
| format |
JOUR |
| author |
Rocha-Viegas, L. Vicent, G.P. Barañao, J.L. Beato, M. Pecci, A. |
| author_facet |
Rocha-Viegas, L. Vicent, G.P. Barañao, J.L. Beato, M. Pecci, A. |
| author_sort |
Rocha-Viegas, L. |
| title |
Glucocorticoids repress bcl-X expression in lymphoid cells by recruiting STAT5B to the P4 promoter |
| title_short |
Glucocorticoids repress bcl-X expression in lymphoid cells by recruiting STAT5B to the P4 promoter |
| title_full |
Glucocorticoids repress bcl-X expression in lymphoid cells by recruiting STAT5B to the P4 promoter |
| title_fullStr |
Glucocorticoids repress bcl-X expression in lymphoid cells by recruiting STAT5B to the P4 promoter |
| title_full_unstemmed |
Glucocorticoids repress bcl-X expression in lymphoid cells by recruiting STAT5B to the P4 promoter |
| title_sort |
glucocorticoids repress bcl-x expression in lymphoid cells by recruiting stat5b to the p4 promoter |
| url |
http://hdl.handle.net/20.500.12110/paper_00219258_v281_n45_p33959_RochaViegas |
| work_keys_str_mv |
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| _version_ |
1807321274657013760 |