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Titolo:
Attenuation of HIF-1 DNA-binding activity limits hypoxia-inducible endothelin-1 expression
Autore:
Camenisch, G; Stroka, DM; Gassmann, M; Wenger, RH;
Indirizzi:
Med Univ Lubeck, Inst Physiol, D-23538 Lubeck, Germany Med Univ Lubeck Lubeck Germany D-23538 Physiol, D-23538 Lubeck, Germany Univ Zurich Irchel, Inst Physiol, CH-8057 Zurich, Switzerland Univ Zurich Irchel Zurich Switzerland CH-8057 H-8057 Zurich, Switzerland Queen Elizabeth Hosp, Liver Labs, Birmingham B15 2TH, W Midlands, England Queen Elizabeth Hosp Birmingham W Midlands England B15 2TH lands, England
Titolo Testata:
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
fascicolo: 2, volume: 443, anno: 2001,
pagine: 240 - 249
SICI:
0031-6768(200111)443:2<240:AOHDAL>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
LACTATE-DEHYDROGENASE-A; PAS DOMAIN PROTEIN-1; GROWTH-FACTOR GENE; FACTOR-I HIF-1; TRANSCRIPTION FACTOR; FACTOR 1-ALPHA; UP-REGULATION; NUCLEAR TRANSLOCATION; RESPONSIVE ELEMENT; RECEPTOR GENE;
Keywords:
angiogenesis; endothelin; hypoxia; vascular endothelial growth factor receptor; vasoconstriction;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
77
Recensione:
Indirizzi per estratti:
Indirizzo: Wenger, RH Med Univ Lubeck, Inst Physiol, Ratzeburger Allee 160, D-23538 Lubeck, Germany Med Univ Lubeck Ratzeburger Allee 160 Lubeck Germany D-23538 y
Citazione:
G. Camenisch et al., "Attenuation of HIF-1 DNA-binding activity limits hypoxia-inducible endothelin-1 expression", PFLUG ARCH, 443(2), 2001, pp. 240-249

Abstract

Hypoxia-inducible factors (HIFs) locate to HIF-binding sites (HBSs) withinthe hypoxia-response elements (HREs) of oxygen-regulated genes. Whereas HIF-1 alpha is expressed ubiquitously, HIF-2 alpha is found primarily in the endothelium, similar to endothelin-1 (ET-1) and fms-like tyrosine kinase 1 (Flt-1), the expression of which is controlled by HREs. We identified an unique sequence alteration in both ET-1 and Flt-1 HBSs not found in other HIF-1 target genes. implying that these HBSs might cause binding of HIF-2 rather than HIF-1. However, electrophoretic mobility shift assays showed HIF-1 and HIF-2 DNA complex formation with the unique ET-1 HBS to be about equal. Both DNA-binding and hypoxic activation of reporter genes using the ET-1 HBS was decreased compared with transferrin and erythropoietin HBSs. The Flt-1 HBS was non-functional when assayed in isolation, suggesting that additional factors are required for hypoxic up-regulation via the reported Flt-1 HRE. Interestingly, HIF-1 activity could be restored fully by point-mutating the ET-1 (but not the Flt-1) HBS, suggesting that the wild-type ET-1 HBS attenuated the full hypoxic response known from other oxygen-regulated genes. Such a mechanism might serve to limit the expression of this potent vasoconstrictor in hypoxia.

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Documento generato il 27/09/20 alle ore 05:32:10