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Titolo:
REGULATION OF CLUSTERIN GENE-EXPRESSION BY TRANSFORMING-GROWTH-FACTOR-BETA
Autore:
JIN G; HOWE PH;
Indirizzi:
CLEVELAND CLIN FDN,DEPT CELL BIOL NC1,LERNER RES INST,9500 EUCLID AVECLEVELAND OH 44195 CLEVELAND CLIN FDN,DEPT CELL BIOL NC1,LERNER RES INST CLEVELAND OH 44195 CASE WESTERN RESERVE UNIV,SCH MED,DEPT PHYSIOL & BIOPHYS CLEVELAND OH44106
Titolo Testata:
The Journal of biological chemistry
fascicolo: 42, volume: 272, anno: 1997,
pagine: 26620 - 26626
SICI:
0021-9258(1997)272:42<26620:ROCGBT>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; TGF-BETA; APOLIPOPROTEIN J/CLUSTERIN; MESSENGER-RNA; TRANSCRIPTIONAL ACTIVATION; SIGNAL-TRANSDUCTION; BINDING SEQUENCE; CELLS; RECEPTORS; ELEMENTS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
63
Recensione:
Indirizzi per estratti:
Citazione:
G. Jin e P.H. Howe, "REGULATION OF CLUSTERIN GENE-EXPRESSION BY TRANSFORMING-GROWTH-FACTOR-BETA", The Journal of biological chemistry, 272(42), 1997, pp. 26620-26626

Abstract

Transforming growth factor beta (TGF beta) induces the expression of a wide variety of genes in many cell types. Our previous studies have shown that TGF beta stimulates both clusterin mRNA and protein levels,and induces its accumulation in the nucleus of CCL64 cells. To further investigate the molecular mechanism of clusterin mRNA induction by TGF beta, we created a 1.3-kilobase rat clusterin promoter/luciferase reporter construct. We demonstrate that TGF beta enhances luciferase activity 2.5-6fold in transient transfection assays of epithelial, endothelial, and fibroblast cell lines. Deletional analysis reveals that anAP-1-binding site (5'-TGAGTCA) in the minimal promoter region is necessary for initiating transactivation by TGF beta. A single T to G basemutation in the AP-1 site (5'-TGAGGCA) abolishes TGF beta-induced clusterin promoter transactivation. In transcription factor decoy experiments, 23-mer oligonucleotides of wild type AP-1 reduce TGF beta induction of clusterin mRNA levels and promoter transactivation, while all oligonucleotide containing the mutated AP-1 site has no effect. Two specific protein kinase C inhibitors, GF109203X and calphostin C, block TGF beta-induced clusterin mRNA levels and promoter transactivation. Together these results indicate that TGF beta regulates clusterin gene expression through an AP-1 site and its cognate transcription factor AP-1, and requires the involvement of protein kinase C.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 13:04:23