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UV‐A‐induced AP‐1 activation requires the Raf/ERK pathway in human NCTC 2544 keratinocytes
Author(s) -
DjavaheriMergny M.,
Dubertret L.
Publication year - 2001
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1034/j.1600-0625.2001.010003204.x
Subject(s) - mapk/erk pathway , kinase , microbiology and biotechnology , effector , singlet oxygen , chemistry , mutant , biology , biochemistry , oxygen , gene , organic chemistry
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.