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Abstract:

Transcription from the mouse mammary tumor virus (MMTV) promoter can be induced by glucocorticoids or progestins. Progesterone treatment of cultured cells carrying an integrated single copy of an MMTV transgene leads to recruitment of progesterone receptor (PR), SWI/SNF, and SNF2h-related complexes to MMTV promoter. Recruitment is accompanied by selective displacement of histones H2A and H2B from the nucleosome B. In nucleosomes assembled on promoter sequences, SWI/SNF displaces histones H2A and H2B from MMTV nucleosome B, but not from other MMTV nucleosomes or from an rDNA promoter nucleosome. Thus, the outcome of nucleosome remodeling by purified SWI/SNF depends on the DNA sequence. On the other hand, 5 min after hormone treatment, the cytoplasmic signaling cascade Src/Ras/Erk is activated via an interaction of PR with the estrogen receptor, which activates Src. As a consequence of Erk activation PR is phosphorylated, Msk1 is activated, and a ternary complex PR-Erk-Msk1 is recruited to MMTV nucleosome B. Msk1 phosphorylates H3 at serine 10, which is followed by acetylation at lysine 14, displacement of HP1γ, and recruitment of Brg1, PCAF, and RNA polymerase II. Blocking Erk activation or Msk1 activity prevents induction of the MMTV transgene. Thus, the rapid nongenomic effects of progestins are essential for their transcriptional effects on certain progestin target genes. In rat endometrial stromal cells, picomolar concentrations of progestins trigger the cross talk of PR with ERβ that activates the Erk and Akt kinase pathways leading to cell proliferation in the absence of direct transcriptional effects of the ligand-activated PR. Thus, depending on the cellular context rapid kinase activation and transcriptional effect play different roles in the physiological response to progestins. © 2006 New York Academy of Sciences.

Registro:

Documento: Artículo
Título:Chromatin remodeling and control of cell proliferation by progestins via cross talk of progesterone receptor with the estrogen receptors and kinase signaling pathways
Autor:Vicent, G.P.; Ballaré, C.; Zaurin, R.; Saragüeta, P.; Beato, M.
Filiación:Centre de Regulació Genòmica (CRG), Universitat Pompeu Fabra (UPF), PRBB, Dr Aiguader 88, 08003 Barcelona, Spain
Instituto de Biología Y Medicina Experimental, CONICET, Universidad de Buenos Aires, 1428 Buenos Aires, Argentina
Center for Genomic Regulation (C.R.G.), PRBB, Dr Aiguader 88, E-08003 Barcelona, Spain
Palabras clave:Chromatin; Histone H1; Kinases; Mouse mammary tumor virus; Progesterone receptor; Transcriptional regulation; adenosine triphosphate; cell nucleus receptor; DNA directed RNA polymerase III; estrogen receptor; gestagen; heterochromatin protein 1; histone acetyltransferase PCAF; histone H2A; histone H2B; histone H3; lysine; mitogen activated protein kinase; phosphotransferase; progesterone; progesterone receptor; protein kinase B; protein tyrosine kinase; Ras protein; regulator protein; ribosome DNA; steroid receptor; estrogen receptor; gestagen; progesterone receptor; protein kinase; binding kinetics; cell proliferation; chromatin assembly and disassembly; chromosome analysis; concentration (parameters); conference paper; cytoplasm; DNA sequence; endometrium cell; enzyme activation; enzyme activity; enzyme phosphorylation; gene sequence; hormonal regulation; human; minichromosome; mitosis inhibition; molecular interaction; Mouse mammary tumor oncovirus; nonhuman; nucleosome; outcome assessment; promoter region; protein protein interaction; protein purification; signal transduction; transcription regulation; transgene; animal; drug effect; gene expression regulation; genetics; metabolism; mouse; Mouse mammary tumor oncovirus; rat; review; Mouse mammary tumor virus; Rattus; Animals; Cell Proliferation; Chromatin Assembly and Disassembly; Gene Expression Regulation; Mammary Tumor Virus, Mouse; Mice; Progestins; Promoter Regions (Genetics); Protein Kinases; Rats; Receptors, Estrogen; Receptors, Progesterone; Signal Transduction
Año:2006
Volumen:1089
Página de inicio:59
Página de fin:72
DOI: http://dx.doi.org/10.1196/annals.1386.025
Título revista:Annals of the New York Academy of Sciences
Título revista abreviado:Ann. New York Acad. Sci.
ISSN:00778923
CODEN:ANYAA
CAS:adenosine triphosphate, 15237-44-2, 56-65-5, 987-65-5; lysine, 56-87-1, 6899-06-5, 70-54-2; mitogen activated protein kinase, 142243-02-5; phosphotransferase, 9031-09-8, 9031-44-1; progesterone, 57-83-0; protein kinase B, 148640-14-6; protein tyrosine kinase, 80449-02-1; protein kinase, 9026-43-1; Progestins; Protein Kinases, EC 2.7.1.37; Receptors, Estrogen; Receptors, Progesterone
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00778923_v1089_n_p59_Vicent

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Citas:

---------- APA ----------
Vicent, G.P., Ballaré, C., Zaurin, R., Saragüeta, P. & Beato, M. (2006) . Chromatin remodeling and control of cell proliferation by progestins via cross talk of progesterone receptor with the estrogen receptors and kinase signaling pathways. Annals of the New York Academy of Sciences, 1089, 59-72.
http://dx.doi.org/10.1196/annals.1386.025
---------- CHICAGO ----------
Vicent, G.P., Ballaré, C., Zaurin, R., Saragüeta, P., Beato, M. "Chromatin remodeling and control of cell proliferation by progestins via cross talk of progesterone receptor with the estrogen receptors and kinase signaling pathways" . Annals of the New York Academy of Sciences 1089 (2006) : 59-72.
http://dx.doi.org/10.1196/annals.1386.025
---------- MLA ----------
Vicent, G.P., Ballaré, C., Zaurin, R., Saragüeta, P., Beato, M. "Chromatin remodeling and control of cell proliferation by progestins via cross talk of progesterone receptor with the estrogen receptors and kinase signaling pathways" . Annals of the New York Academy of Sciences, vol. 1089, 2006, pp. 59-72.
http://dx.doi.org/10.1196/annals.1386.025
---------- VANCOUVER ----------
Vicent, G.P., Ballaré, C., Zaurin, R., Saragüeta, P., Beato, M. Chromatin remodeling and control of cell proliferation by progestins via cross talk of progesterone receptor with the estrogen receptors and kinase signaling pathways. Ann. New York Acad. Sci. 2006;1089:59-72.
http://dx.doi.org/10.1196/annals.1386.025