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UVB‐induced Epidermal Growth Factor Receptor Phosphorylation is Critical for Downstream Signaling and Keratinocyte Survival ¶
Author(s) -
Peus Dominik,
Vasa Remus A.,
Meves Alexander,
Beyerle Astrid,
Pittelkow Mark R.
Publication year - 2000
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1562/0031-8655(2000)0720135uiegfr2.0.co2
Subject(s) - epidermal growth factor receptor , microbiology and biotechnology , phosphorylation , signal transduction , egfr inhibitors , kinase , epidermal growth factor , chemistry , cancer research , biology , receptor , biochemistry
We have recently shown that UVB radiation activates epidermal growth factor receptor (EGFR)/extracellular regulated kinase 1 and 2 (ERK1/2) and p38 signaling pathways in keratinocytes. However, the functional relevance of these processes for downstream signaling and cell survival remains to be determined. The specific EGFR inhibitor PD153035 markedly decreased UVB‐induced phosphorylation of EGFR, ERK1/2 and shc, whereas p38 activation was unaffected. PD153035 pretreatment followed by UVB reduced clonogenic potential and enhanced peroxide production, apoptosis and cell death. Our data suggest that ligand‐independent phosphorylation of EGFR and likely dependent downstream signaling pathways regulate cellular defense mechanisms important for cell survival following oxidative stress.