@article{oai:kanazawa-u.repo.nii.ac.jp:00027444,
 author = {Enkhtuya, Radnaa and Sato, Tokiharu and Wakasugi, Mitsuo and Tuvshintugs, Baljinnyam and Miyata, Hirofumi and Sakurai, Takeshi and Matsunaga, Tsukasa and Yoshioka, Katsuji},
 issue = {4},
 journal = {Genes to Cells},
 month = {Apr},
 note = {The ultraviolet B (UVB) component of sunlight can cause severe damage to skin cells and even induce skin cancer. Growing evidence indicates that the UVB-induced signaling network is complex and involves diverse cellular processes. In this study, we investigated the role of c-Jun NH2-terminal kinase-associated leucine zipper protein (JLP), a scaffold protein for mitogen-activated protein kinase (MAPK) signaling cascades, in UVB-induced apoptosis. We found that UVB-induced skin epidermal apoptosis was prevented in Jlp knockout (KO) as well as in keratinocyte-specific Jlp KO mice. Analysis of the repair of UVB-induced DNA damage over time showed no evidence for the involvement of JLP in this process. In contrast, UVB-stimulated p38 MAPK activation in the skin was impaired in both Jlp KO and keratinocyte-specific Jlp KO mice. Moreover, topical treatment of UVB-irradiated mouse skin with a p38 inhibitor significantly suppressed the epidermal apoptosis in wild-type mice, but not in Jlp KO mice. Our findings suggest that JLP in skin basal keratinocytes plays an important role in UVB-induced apoptosis by modulating p38 MAPK signaling pathways. This is the first study to show a critical role for JLP in an in vivo response to environmental stimulation. © 2014 by the Molecular Biology Society of Japan and Wiley Publishing Asia Pty Ltd.},
 pages = {350--358},
 title = {The scaffold protein JLP plays a key role in regulating ultraviolet B-induced apoptosis in mice},
 volume = {19},
 year = {2014}
}