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Titolo:
PROLONGED DEPLETION OF AH RECEPTOR WITHOUT ALTERATION OF RECEPTOR MESSENGER-RNA LEVELS AFTER TREATMENT OF CELLS IN CULTURE WITH 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN
Autore:
GIANNONE JV; LI W; PROBST M; OKEY AB;
Indirizzi:
UNIV TORONTO,DEPT PHARMACOL,MED SCI BLDG TORONTO ON M5S 1A8 CANADA UNIV TORONTO,DEPT PHARMACOL TORONTO ON M5S 1A8 CANADA UNIV CALIF LOS ANGELES,MED CTR,CTR HLTH SCI,DEPT PATHOL & LAB MED LOSANGELES CA 90095
Titolo Testata:
Biochemical pharmacology
fascicolo: 4, volume: 55, anno: 1998,
pagine: 489 - 497
SICI:
0006-2952(1998)55:4<489:PDOARW>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
ARYL-HYDROCARBON RECEPTOR; NUCLEAR TRANSLOCATOR PROTEIN; UBIQUITIN-PROTEASOME PATHWAY; MOUSE HEPATOMA-CELLS; DNA-BINDING; DOWN-REGULATION; TOXICITY; PROTEOLYSIS; DEGRADATION; CANCER;
Keywords:
AH RECEPTOR; AH RECEPTOR NUCLEAR TRANSLOCATOR PROTEIN (ARNT); 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN; TCDD; 3-METHYLCHOLANTHRENE; HEPA-1 HEPATOMA CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
28
Recensione:
Indirizzi per estratti:
Citazione:
J.V. Giannone et al., "PROLONGED DEPLETION OF AH RECEPTOR WITHOUT ALTERATION OF RECEPTOR MESSENGER-RNA LEVELS AFTER TREATMENT OF CELLS IN CULTURE WITH 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN", Biochemical pharmacology, 55(4), 1998, pp. 489-497

Abstract

Previous experiments have shown that the total cellular content of the AH receptor (AHR) drops rapidly after exposure of mouse hepatoma cells (Hepa-l) to the potent AHR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD); within 6 hr after treatment, less than 20% of the original cell content of AHR can be detected by radioligand binding or by immunoblotting. The goals of our current study were to determine the duration of receptor depletion following treatment with ligand and to determine ii depletion is due to decreased expression of the Ahr gene that encodes the AHR. We found that depletion of AHR persisted fur at least 7? hr after exposure to TCDD. Treatment with 3-methylcholanthrene caused a transient drop in total cell AHR, but the AHR levels returned to near pretreatment levels within 72 hr after the first exposure. TCDD treatment did not alter the levels of AHR mRNA as assessed by reverse transcription-polymerase chain reaction or slot blot assays. Thus, the decrease in AHR protein cannot be attributed to depression of transcription of the Ahr gene by TCDD. TCDD treatment did not alter the levelsof the dimerization partner of the AHR, the AH receptor nuclear translocator protein (ARNT), or ARNT mRNA. In the presence of TCDD, both the AHR and the ARNT protein can be maintained at high levels in the nucleus if transcription is inhibited with actinomycin-D. In the absence of actinomycin-D, the AHR protein was lost rapidly, but the ARNT protein level in the cell was maintained. Together, these results suggest that the AHR protein is degraded through a selective mechanism that spares the ARNT protein and that the degradation pathway involves a protein that itself has a short half-life. (C) 1998 Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 23:22:45