ArticleLife sciences2009
The role of translational regulation in ultraviolet C light-induced cyclooxygenase-2 expression.
Article in Life sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- T-Cell Intracellular Antigen 1-Like Protein in Physiology and Pathology.International journal of molecular sciences · 2022Review
- The Bystander Effect of Ultraviolet Radiation and Mediators.Journal of biomedical physics & engineering · 2020Review
- Therapeutic microRNAs targeting the NF-kappa B signaling circuits of cancers.Advanced drug delivery reviews · 2015Review
- Ultraviolet C irradiation induces different expression of cyclooxygenase 2 in NIH 3T3 cells and A431 cells: the roles of COX-2 are different in various cell lines.International journal of molecular sciences · 2012Article
- The roles of nitric oxide synthase and eIF2alpha kinases in regulation of cell cycle upon UVB-irradiation.Cell cycle (Georgetown, Tex.) · 2010Article
- Impact of Silver Nanoparticles on the Ultraviolet Radiation Direct and Bystander Effects on TK6 Cell Line.Journal of medical physicsArticle
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
aimsThe role of ultraviolet C light (UVC)-induced phosphorylation of the eukaryotic initiation factor 2 (eIF2) in the regulation of cyclooxygenase-2 (COX-2) expression at both transcriptional and translational levels is investigated. MAIN
methodsWestern analysis was used to determine COX expressions. Immunoprecipitation after [(35)S]-Met/Cys metabolic labeling was used to determine the rate for COX-2 synthesis and turnover. Quantitative real-time PCR was used to determine COX-2 mRNA levels. Ingenuity Pathways Analysis 6 was used for mapping COX-2 activation network. KEY
findingsUVC induces COX-2 expression in wild-type mouse embryo fibroblasts (MEF(S/S)) and that the inducibility is reduced in MEF(A/A) cells in which the phosphorylation site, Ser-51 in the eIF2alpha, is replaced with a nonphosphorylatable Ala (S51A). UVC-induced transcription of COX-2 is delayed in MEF(A/A) cells, which correlates with NF-kappaB activation as previously reported (Wu, S, Tan, M, Hu, Y, Wang, JL, Scheuner, D, Kaufman, RJ, Ultraviolet light activates NFkappaB through translational inhibition of IkappaBalpha synthesis. The Journal of Biological Chemistry, 279, 34898-34902, 2004). The translational efficiency of COX-2 is higher in MEF(A/A) cells than in MEF(S/S) cells at 4 h, but not at 24 h post-UVC. The translation efficiency is correlated to the ratio of activated COX-2 binding protein HuR/TIAR. In addition, the newly synthesized COX-2 protein is more stable in MEF(A/A) cells than in MEF(S/S) cells. The results demonstrated a complex and dynamic regulation of COX-2 expression. SIGNIFICANCE: UVC induces a prolonged expression of COX-2. While transcriptional regulation of COX-2 expression is intensively studied, the role of translational regulation of COX-2 synthesis upon UVC-irradiation is not yet clear. This study elucidated a novel eIF2alpha phosphorylation-centered network for the regulation of COX-2 expression after UVC-irradiation.
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