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Titolo:
Interactions between aryl hydrocarbon receptor (AhR) and hypoxia signalingpathways
Autore:
Nie, MH; Blankenship, AL; Giesy, JP;
Indirizzi:
Michigan State Univ, Natl Food Safety & Toxicol Ctr, Dept Zool, E Lansing,MI 48824 USA Michigan State Univ E Lansing MI USA 48824 t Zool, E Lansing,MI 48824 USA Michigan State Univ, Inst Environm Toxicol, E Lansing, MI 48824 USA Michigan State Univ E Lansing MI USA 48824 xicol, E Lansing, MI 48824 USA ENTRIX Inc, E Lansing, MI USA ENTRIX Inc E Lansing MI USAENTRIX Inc, E Lansing, MI USA
Titolo Testata:
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
fascicolo: 1-2, volume: 10, anno: 2001,
pagine: 17 - 27
SICI:
1382-6689(200105/06)10:1-2<17:IBAHR(>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCIBLE FACTOR 1-ALPHA; NUCLEAR TRANSLOCATOR PROTEIN; ENDOTHELIAL GROWTH-FACTOR; UBIQUITIN-PROTEASOME PATHWAY; ARNT TRANSCRIPTION FACTOR; DNA-BINDING; GENE-EXPRESSION; DIOXIN RECEPTOR; GUINEA-PIG; FACTOR-I;
Keywords:
Ah receptor; ARNT; HIF-1 alpha; in vitro; hypoxia; PAS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
81
Recensione:
Indirizzi per estratti:
Indirizzo: Giesy, JP Michigan State Univ, Natl Food Safety & Toxicol Ctr, Dept Zool, E Lansing,MI 48824 USA Michigan State Univ E Lansing MI USA 48824 Lansing,MI 48824 USA
Citazione:
M.H. Nie et al., "Interactions between aryl hydrocarbon receptor (AhR) and hypoxia signalingpathways", ENV TOX PH, 10(1-2), 2001, pp. 17-27

Abstract

Most if not all of the toxic responses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are mediated through the AhR, which requires ARNT to regulate gene expression. ARNT is also required by HIF-1 alpha to enhance the expression of various genes in response to hypoxia. Since both the AhR and hypoxia transcriptional pathways require ARNT, some of the effects of TCDD and similar types of ligands could be explained by interaction between the AhR and hypoxia pathways involving ARNT. The studies on which we report here were conducted to lest the hypothesis that there is cross talk between AhR- and HIF-1-mediated transcription pathways. TCDD significantly reduced the hypoxia-mediated reporter gene activity in B-1 cells. Reciprocally, the hypoxia response inducers desferrioxamine or CoCl2 inhibited AhR-mediated CYP1A1 enzyme activity in B-1 and Hepa 1 cells, and the AhR-mediated luciferase reporter gene activity in H1L1.1c2 cells. The inhibition of AhR-mediated transcription by hypoxia inducers, however, was not observed in H4IIE-luc cells. The interaction between the AhR- and HIF-1-mediated transcription can be attributed to changes in DNA binding activities. TCDD-induced protein binding to dioxin responsive element (DRE) was diminished by desferrioxamine, and TCDD reduced the binding activity to HIF-1 binding site in desferrioxamine-treated Hepa 1 cells. This mutual repression may provide an underlying mechanism for many TCDD-induced toxic responses. The results reported here indicate that there is cross talk between ARNT-requiring pathways. Since ARNT ispossibly required by a number of pathways, this type of interaction may explain some of the pleiotropic effects caused by TCDD. (C) 2001 Elsevier Science B.V. All rights reserved.

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Documento generato il 04/04/20 alle ore 11:03:52