http://www.cnr.it/ontology/cnr/individuo/prodotto/ID20934
Selective transcription and cellular proliferation induced by PDGF require histone deacetylase activity (Articolo in rivista)
- Type
- Label
- Selective transcription and cellular proliferation induced by PDGF require histone deacetylase activity (Articolo in rivista) (literal)
- Anno
- 2006-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/j.bbrc.2006.03.013 (literal)
- Alternative label
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Catania A. Iavarone C., Carlomagno M.S. and Chiariello M. (literal)
- Pagina inizio
- Pagina fine
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Note
- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Dipartimento di Biologia e Patologia Cellulare e Molecolare, Universita` degli Studi di Napoli ''Federico II,'' Italy
Istituto di Endocrinologia e Oncologia Sperimentale, CNR, Italy (literal)
- Titolo
- Selective transcription and cellular proliferation induced by PDGF require histone deacetylase activity (literal)
- Abstract
- Histone deacetylases (HDACs) are key regulatory enzymes involved in the control of gene expression and their inhibition by specific drugs has been widely correlated to cell cycle arrest, terminal differentiation, and apoptosis. Here, we investigated whether HDAC activ- ity was required for PDGF-dependent signal transduction and cellular proliferation. Exposure of PDGF-stimulated NIH3T3 fibroblasts to the HDAC inhibitor trichostatin A (TSA) potently repressed the expression of a group of genes correlated to PDGF-dependent cel- lular growth and pro-survival activity. Moreover, we show that TSA interfered with STAT3-dependent transcriptional activity induced by PDGF. Still, neither phosphorylation nor nuclear translocation and DNA-binding in vitro and in vivo of STAT3 were affected by using TSA to interfere with PDGF stimulation. Finally, TSA treatment resulted in the suppression of PDGF-dependent cellular prolif- eration without affecting cellular survival of NIH3T3 cells. Our data indicate that inhibition of HDAC activity antagonizes the mitogenic effect of PDGF, suggesting that these drugs may specifically act on the expression of STAT-dependent, PDGF-responsive genes. (literal)
- Prodotto di
- Autore CNR
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi