{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T01:24:18Z","timestamp":1789953858178,"version":"4.0.1"},"reference-count":30,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2018,3,8]],"date-time":"2018-03-08T00:00:00Z","timestamp":1520467200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Photochem &amp; Photobiology"],"published-print":{"date-parts":[[2018,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>A single exposure of normal human melanocytes (<jats:styled-content style=\"fixed-case\">NHM<\/jats:styled-content>s) to ultraviolet B (<jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>) radiation induces a distinct increase in the expression of c\u2010<jats:styled-content style=\"fixed-case\">KIT<\/jats:styled-content> and endothelin B receptor (<jats:styled-content style=\"fixed-case\">EDNRB<\/jats:styled-content>) and upregulates the expression of microphthalmia\u2010associated transcription factor (<jats:styled-content style=\"fixed-case\">MITF<\/jats:styled-content>). In this review, we clarify the signaling mechanisms by which <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content> stimulates the expression of <jats:styled-content style=\"fixed-case\">MITF<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">NHM<\/jats:styled-content>s, thus leading to upregulation of those two important melanogenic receptors. The increased expression of <jats:styled-content style=\"fixed-case\">MITF<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>\u2010exposed <jats:styled-content style=\"fixed-case\">NHM<\/jats:styled-content>s is accompanied by a markedly stimulated and prolonged phosphorylation of p38\/<jats:styled-content style=\"fixed-case\">CREB<\/jats:styled-content>. The <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>\u2010stimulated expression of c\u2010<jats:styled-content style=\"fixed-case\">KIT<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">EDNRB<\/jats:styled-content> could be completely abolished by a p38 inhibitor concomitant with a reduced phosphorylation of <jats:styled-content style=\"fixed-case\">CREB<\/jats:styled-content> and a downregulation of <jats:styled-content style=\"fixed-case\">MITF<\/jats:styled-content> expression. The <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content> exposure of <jats:styled-content style=\"fixed-case\">NHM<\/jats:styled-content>s stimulates the phosphorylation of p38 and c\u2010jun N\u2010terminal kinase, but not <jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>, followed by the increased phosphorylation of <jats:styled-content style=\"fixed-case\">MSK<\/jats:styled-content>1 and subsequently <jats:styled-content style=\"fixed-case\">CREB<\/jats:styled-content>. Postirradiation treatment with the <jats:styled-content style=\"fixed-case\">MSK<\/jats:styled-content>1 inhibitor H89 significantly downregulates the increased <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> and protein expression of <jats:styled-content style=\"fixed-case\">MITF<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> EDNRB<\/jats:styled-content> and c\u2010<jats:styled-content style=\"fixed-case\">KIT<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>\u2010exposed <jats:styled-content style=\"fixed-case\">NHM<\/jats:styled-content>s. Our findings indicate for the first time that the increased expression of <jats:styled-content style=\"fixed-case\">MITF<\/jats:styled-content> that leads to the upregulation of melanocyte\u2010specific proteins in <jats:styled-content style=\"fixed-case\">UVB<\/jats:styled-content>\u2010exposed <jats:styled-content style=\"fixed-case\">NHM<\/jats:styled-content>s is mediated via activation of the p38\/<jats:styled-content style=\"fixed-case\">MSK<\/jats:styled-content>1\/<jats:styled-content style=\"fixed-case\">CREB<\/jats:styled-content> axis but not the <jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">RSK<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">CREB<\/jats:styled-content> axis.<\/jats:p>","DOI":"10.1111\/php.12848","type":"journal-article","created":{"date-parts":[[2017,10,4]],"date-time":"2017-10-04T19:32:45Z","timestamp":1507145565000},"page":"421-431","source":"Crossref","is-referenced-by-count":23,"title":["Signaling Cascades Activated by <scp>UVB<\/scp> in Human Melanocytes Lead to the Increased Expression of Melanocyte Receptors, Endothelin B Receptor and c\u2010<scp>KIT<\/scp>"],"prefix":"10.1111","volume":"94","author":[{"given":"Shuko","family":"Terazawa","sequence":"first","affiliation":[{"name":"Research Institute for Biological Functions Chubu University Aichi Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Genji","family":"Imokawa","sequence":"additional","affiliation":[{"name":"Research Institute for Biological Functions Chubu University Aichi Japan"},{"name":"Center for Bioscience Research &amp; Education Utsunomiya University Tochigi Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2018,3,8]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.3390\/ijms15058293"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0749.2003.00126.x"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0128678"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00403-009-1007-x"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1747.2001.01290.x"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9440(10)63260-9"},{"key":"e_1_2_6_8_1","first-page":"58","article-title":"Novel mutations and deletions of the KIT (steel factor receptor) gene in human piebaldism","volume":"56","author":"Ezoe K.","year":"1995","journal-title":"Am. 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