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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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UV-A-induced AP-1 activation requires the Raf/ ERK pathway in human NCTC 2544 keratinocytes.

UV-A irradiation causes a dose-dependent activation of ERK in human NCTC 2544 keratinocytes. The specific inhibition of either ERK activity or Raf kinase activity impedes the activation of AP-1 DNA binding induced by UV-A. In addition, UV-A raises AP-1 promoter transcriptional activity, which is downregulated in NCTC 2544 cells expressing an inactive mutant of Raf-1. We found that singlet oxygen might be one of the mediators in both UV-A-induced AP-1 DNA binding and transcriptional activity. These results strongly suggest that UV-A-induced AP-1 activity requires the Raf-ERK pathway and imply a singlet oxygen effector.[1]

References

  1. UV-A-induced AP-1 activation requires the Raf/ERK pathway in human NCTC 2544 keratinocytes. Djavaheri-Mergny, M., Dubertret, L. Exp. Dermatol. (2001) [Pubmed]
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