Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Liver cell-specific transcriptional regulation of connexin32
Autore:
Piechocki, MP; Toti, RM; Fernstrom, MJ; Burk, RD; Ruch, RJ;
Indirizzi:
Med Coll Ohio, Dept Pathol, Toledo, OH 43614 USA Med Coll Ohio Toledo OH USA 43614 Ohio, Dept Pathol, Toledo, OH 43614 USA Albert Einstein Coll Med, Marion Bessin Liver Res Ctr, Bronx, NY 10467 USAAlbert Einstein Coll Med Bronx NY USA 10467 Res Ctr, Bronx, NY 10467 USA
Titolo Testata:
BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION
fascicolo: 1-3, volume: 1491, anno: 2000,
pagine: 107 - 122
SICI:
0167-4781(20000425)1491:1-3<107:LCTROC>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
GAP JUNCTION PROTEIN; DNA-BINDING PROTEIN; RAT-LIVER; MOLECULAR-CLONING; GENE; EXPRESSION; PROMOTER; IDENTIFICATION; ELEMENTS; CDNA;
Keywords:
gap junction; connexin; hepatocyte nuclear factor-1; liver-enriched transcription factor; gene regulation; promoter;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Ruch, RJ Med Coll Ohio, Dept Pathol, 3055 Arlington Ave, Toledo, OH 43614 USA Med Coll Ohio 3055 Arlington Ave Toledo OH USA 43614 OH 43614 USA
Citazione:
M.P. Piechocki et al., "Liver cell-specific transcriptional regulation of connexin32", BBA-GENE ST, 1491(1-3), 2000, pp. 107-122

Abstract

Gap junctional intercellular communication facilitates liver homeostasis and growth control in the liver. The major gap junction protein expressed byhepatocytes is connexin32 (Cx32) and non-parenchymal hepatic cells do not express this gene. We investigated the regulation of Cx32 transcription by trans-activating factors in liver cells. Transient transfection assays using deletions of the rat Cx32 promoter (nt -753 to -33) linked to the luciferase gene were performed in MH1C1 rat hepatoma cells that express endogenousCx32 compared with WB-F344 rat liver epithelial cells that do not. The basal promoter element was located within nt -134 to -33 and was 1.4-fold moreactive in MH1C1 cells than WB-F344 cells whereas the entire promoter fragment (nt -754 to -33) was four-fold more active in MH1C1 cells. Specific nuclear protein-DNA complexes that bound to Sp1 consensus sites within the basal promoter were formed using nuclear extracts from both types of cells. Additional promoter sequences increased promoter activity more strongly in MH1C1 cells than WB-F344 cells and this was correlated with the binding of hepatocyte nuclear factor-1 (HNF-1) to two HNF-1 consensus sites centered at -187 and -736. Expression of HNF-1 and binding to these elements was only observed with MH1C1 cells. Other specific protein-DNA complexes were formed,however, that included YY-1- and NF-1-containing complexes, but these werenot related to promoter activity. Dexamethasone increased Cx32 promoter activity and expression in MH1C1 cells, but had little effect in WB-F344 cells and did not alter protein-DNA complex formation. These data suggest that Sp1 is responsible for Cx32 promoter basal activity, that HNF-1 determines the cell-specific expression of Cx32, and that dexamethasone increases Cx32expression through other mechanisms. (C) 2000 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/01/21 alle ore 05:54:51