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Glucocorticoids repress bcl-X expression in lymphoid cells by recruiting STAT5B to the P4 promoter.
J Biol Chem. 2006 Nov 10; 281(45):33959-70.JB

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-X(L) (antiapoptotic)/bcl-X(S) (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-X(S) 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.

Authors+Show Affiliations

Departamento de Fisiología, Biología Molecular y Celular, Instituto de Fisiología, Biología Molecular y Neurociencias-CONICET, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Argentina.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16959781

Citation

Rocha-Viegas, Luciana, et al. "Glucocorticoids Repress bcl-X Expression in Lymphoid Cells By Recruiting STAT5B to the P4 Promoter." The Journal of Biological Chemistry, vol. 281, no. 45, 2006, pp. 33959-70.
Rocha-Viegas L, Vicent GP, Barañao JL, et al. Glucocorticoids repress bcl-X expression in lymphoid cells by recruiting STAT5B to the P4 promoter. J Biol Chem. 2006;281(45):33959-70.
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. The Journal of Biological Chemistry, 281(45), 33959-70.
Rocha-Viegas L, et al. Glucocorticoids Repress bcl-X Expression in Lymphoid Cells By Recruiting STAT5B to the P4 Promoter. J Biol Chem. 2006 Nov 10;281(45):33959-70. PubMed PMID: 16959781.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glucocorticoids repress bcl-X expression in lymphoid cells by recruiting STAT5B to the P4 promoter. AU - Rocha-Viegas,Luciana, AU - Vicent,Guillermo P, AU - Barañao,José L, AU - Beato,Miguel, AU - Pecci,Adali, Y1 - 2006/09/07/ PY - 2006/9/9/pubmed PY - 2006/12/22/medline PY - 2006/9/9/entrez SP - 33959 EP - 70 JF - The Journal of biological chemistry JO - J Biol Chem VL - 281 IS - 45 N2 - 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-X(L) (antiapoptotic)/bcl-X(S) (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-X(S) 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. SN - 0021-9258 UR - https://www.unboundmedicine.com/medline/citation/16959781/Glucocorticoids_repress_bcl_X_expression_in_lymphoid_cells_by_recruiting_STAT5B_to_the_P4_promoter_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0021-9258(20)70581-8 DB - PRIME DP - Unbound Medicine ER -