Journal
CURRENT PHARMACEUTICAL DESIGN
Volume 15, Issue 33, Pages 3844-3852Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/138161209789649420
Keywords
HIF; nuclear factor kappa b; transcription; promoter; reactive oxygen species; hypoxia
Categories
Funding
- DFG [GO709/4-4]
- EU (EUROXY)
- EU (Metoxia)
- Fondation Leducq
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The hypoxia-inducible factor HIF-1 has been shown to be mandatory for the cellular adaptation to hypoxia. In addition, evidence has been provided that HIF-1 can mediate various stress responses and that it may play an important role under inflammatory conditions even independently of hypoxia. HIF-1 is a heterodimer consisting of an subunit which is subject to tight regulation, and beta-subunit, also termed ARNT, which appears to be constitutively expressed. In addition to the complex network controlling the cellular content of HIF-1 alpha at the level of protein stability, recent evidence showed that HIF-1 alpha levels can also be regulated at the mRNA level. In fact, transcriptional regulatory networks seem to be an additional way of controlling HIF-1 alpha levels and may open new therapeutic options to modulate HIF-1 alpha also under non-hypoxic conditions.
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