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Titolo:
Identification of a critical Sp1 site within the endoglin promoter and itsinvolvement in the transforming growth factor-beta stimulation
Autore:
Botella, LM; Sanchez-Elsner, T; Rius, C; Corbi, A; Bernabeu, C;
Indirizzi:
CSIC, Ctr Invest Biol, E-28006 Madrid, Spain CSIC Madrid Spain E-28006CSIC, Ctr Invest Biol, E-28006 Madrid, Spain
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 37, volume: 276, anno: 2001,
pagine: 34486 - 34494
SICI:
0021-9258(20010914)276:37<34486:IOACSS>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
HEREDITARY HEMORRHAGIC TELANGIECTASIA; TRANSCRIPTION FACTOR SP1; SMAD-BINDING-ELEMENT; TGF-BETA; DNA-BINDING; ENDOTHELIAL-CELLS; FUNCTIONAL INTERACTIONS; EXPRESSION ANALYSIS; CELLULAR-RESPONSES; HEART DEVELOPMENT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
60
Recensione:
Indirizzi per estratti:
Indirizzo: Bernabeu, C CSIC, Ctr Invest Biol, Velazquez 144, E-28006 Madrid, Spain CSIC Velazquez 144 Madrid Spain E-28006 E-28006 Madrid, Spain
Citazione:
L.M. Botella et al., "Identification of a critical Sp1 site within the endoglin promoter and itsinvolvement in the transforming growth factor-beta stimulation", J BIOL CHEM, 276(37), 2001, pp. 34486-34494

Abstract

Endoglin, a component of the transforming growth factor-beta (TGF-beta) receptor complex expressed on endothelial cells, is involved in cardiovascular morphogenesis and vascular remodeling, as exemplified by the fact that the endoglin gene is the target for the autosomal dominant disorder known as hereditary hemorrhagic telangiectasia type 1. Since haploinsufficiency is the underlying mechanism for hereditary hemorrhagic telangiectasia type 1, understanding the regulation of endoglin gene expression appears to be a crucial step to correct the disease. In this study we have identified an Sp1 site at -37 as a critical element for the basal transcription of the endoglin TATA-less promoter. Since endoglin promoter activity is stimulated by TGF-beta and this stimulation is located at the Spl-containing proximal region, we have investigated the possible involvement of Spl in the TGF-beta -mediated induction. Mutation of the Sp1-binding sequence, or addition of the Spl inhibitor WP631, abolished both the basal transcription activity and theTGF-beta responsiveness of the endoglin promoter. Binding of Sp1 and Smad3to the proximal promoter region -50/-29 was evidenced by electrophoretic mobility shift assays and DNA affinity precipitation studies. Furthermore, synergistic cooperation on the promoter activity between Sp1 and TGF-beta orSmad3 could be demonstrated by co-transfection experiments of reporter promoter constructs. The molecular mechanism underlying this cooperation appears to involve a direct physical interaction between Sp1 and Smad3/Smad4.

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Documento generato il 05/12/20 alle ore 14:11:49