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In this study, we show that the p42\/p44 MAP kinase cascade, known to phosphorylate HIF\u20101\u03b1, does not modulate the degradation\/stabilization profile of HIF\u20101\u03b1. However, we present evidence that the rate of HIF\u20101\u03b1 degradation depends on the duration of hypoxic stress. We demonstrate that degradation of HIF\u20101\u03b1 is suppressed by: (i) inhibiting general transcription with actinomycin D or (ii) specifically blocking HIF\u20101\u2010dependent transcriptional activity. In keeping with these findings, we postulate that HIF\u20101\u03b1 is targetted to the proteasome via a HIF\u20101\u03b1 proteasome targetting factor (HPTF) which expression is directly under the control of HIF\u20101\u2010mediated transcriptional activity. Although HPTF is not yet molecularly identified, it is clearly distinct from the von Hippel\u2013Lindau protein (pVHL).<\/jats:p>","DOI":"10.1016\/s0014-5793(01)02159-7","type":"journal-article","created":{"date-parts":[[2002,7,25]],"date-time":"2002-07-25T19:52:46Z","timestamp":1027626766000},"page":"85-90","source":"Crossref","is-referenced-by-count":121,"title":["HIF\u20101\u2010dependent transcriptional activity is required for oxygen\u2010mediated HIF\u20101\u03b1 degradation"],"prefix":"10.1002","volume":"491","author":[{"given":"Edurne","family":"Berra","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Darren 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