Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-1266
Ameri, K; Hammond, E M; Culmsee, C; Raida, M; Katschinski, D M; Wenger, R H; Wagner, E; Davis, R J; Hai, T; Denko, N; Harris, A L (2007). Induction of activating transcription factor 3 by anoxia is independent of p53 and the hypoxic HIF signalling pathway. Oncogene, 26(2):284-289.
View at publisher
Solid tumors often have an inadequate blood supply, which results in large regions that are subjected to hypoxic or anoxic stress. Hypoxia-inducible factor-1 (HIF-1) is a transcription factor that regulates much of the transcriptional response of cells to hypoxia. Activating transcription factor 3 (ATF3) is another transcription factor that responds to a variety of stresses and is often upregulated in cancer. We investigated the regulation of ATF3 by oxygen deprivation. ATF3 induction occurred most robustly under anoxia, is common, and it is not dependent on presence of HIF-1 or p53, but is sensitive to the inhibition of c-Jun NH2-terminal kinase activation and the antioxidant N-acetylcystein. ATF3 could also be induced by desferrioxamine but not by the mitochondrial poison cyanide or the nonspecific 2-oxoglutarate dioxygenase inhibitor dimethyloxalylglycine. We also show that anoxic ATF3 mRNA is more stable than normoxic mRNA providing a mechanism for this induction. Thus, this study demonstrates that the regulation of ATF3 under anoxia is independent of 2-oxoglutarate dioxygenase, HIF-1 and p53, presumably involving multiple regulatory pathways.
114 downloads since deposited on 11 Feb 2008
16 downloads since 12 months
|Item Type:||Journal Article, refereed|
|Communities & Collections:||04 Faculty of Medicine > Institute of Physiology
07 Faculty of Science > Institute of Physiology
|Dewey Decimal Classification:||570 Life sciences; biology|
|Deposited On:||11 Feb 2008 12:22|
|Last Modified:||05 Apr 2016 12:18|
|Publisher:||Nature Publishing Group|
|Additional Information:||Embargo ending July 11, 2007|
Users (please log in): suggest update or correction for this item
Repository Staff Only: item control page