Redox regulation of the hypoxia-inducible factor.
- Others:
- Institut de signalisation, biologie du développement et cancer (ISBDC) ; Université Nice Sophia Antipolis (1965 - 2019) (UNS) ; COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA)
- Transduction du signal et oncogénèse ; Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)
Description
Reactive oxygen species (ROS) have long been considered only as cyto- and genotoxic. However, there is now compelling evidence that ROS also act as second messengers in response to various stimuli, such as growth factors, hormones and cytokines. The hypoxia-inducible transcription factor (HIF) is a master regulator of oxygen-sensitive gene expression. More recently, HIF has also been shown to respond to non-hypoxic stimuli. Interestingly, recent reports indicate that ROS regulate HIF stability and transcriptional activity in well-oxygenated cells, as well as under hypoxic conditions. Consequently, ROS appear to be key players in regulating HIF-dependent pathways under both normal and pathological circumstances. This review summarizes the current understanding of the role of ROS in the regulation of the mammalian HIF system.
Additional details
- URL
- https://hal.archives-ouvertes.fr/hal-00321043
- URN
- urn:oai:HAL:hal-00321043v1
- Origin repository
- UNICA