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NF-κB-regulated transcriptional control of CLCA in a differentiated mouse keratinocyte line.
https://fdc.repo.nii.ac.jp/records/47
https://fdc.repo.nii.ac.jp/records/4715c8e01d-757d-41fc-9411-dfdeeb282ce5
名前 / ファイル | ライセンス | アクション |
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甲第270号_論文(廣松) (2.8 MB)
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要旨 (313.7 kB)
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審査結果の要旨 (291.5 kB)
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Item type | 学位論文 / Thesis or Dissertation(1) | |||||||||||||||
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公開日 | 2015-07-22 | |||||||||||||||
タイトル | ||||||||||||||||
言語 | en | |||||||||||||||
タイトル | NF-κB-regulated transcriptional control of CLCA in a differentiated mouse keratinocyte line. | |||||||||||||||
言語 | ||||||||||||||||
言語 | eng | |||||||||||||||
キーワード | ||||||||||||||||
主題 | 転写制御 | |||||||||||||||
キーワード | ||||||||||||||||
主題 | ケラチノサイト | |||||||||||||||
キーワード | ||||||||||||||||
言語 | en | |||||||||||||||
主題 | CLCA | |||||||||||||||
キーワード | ||||||||||||||||
言語 | en | |||||||||||||||
主題 | NF-kB | |||||||||||||||
キーワード | ||||||||||||||||
言語 | en | |||||||||||||||
主題 | transcriptioal control | |||||||||||||||
キーワード | ||||||||||||||||
言語 | en | |||||||||||||||
主題 | keratinocyte | |||||||||||||||
資源タイプ | ||||||||||||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_db06 | |||||||||||||||
資源タイプ | doctoral thesis | |||||||||||||||
アクセス権 | ||||||||||||||||
アクセス権 | open access | |||||||||||||||
アクセス権URI | http://purl.org/coar/access_right/c_abf2 | |||||||||||||||
著者 |
Hiromatsu, Ryo
× Hiromatsu, Ryo
× Hatta, Mitsutoki
× Okamura, Kazuhiko
× Sakagami, Ryuji
× Yamazaki, Jun
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抄録 | ||||||||||||||||
内容記述タイプ | Abstract | |||||||||||||||
内容記述 | BACKGROUND: CLCA was postulated to be a calcium-activated chloride channel accessory protein. Recent reports indicate that CLCA isoforms are likely to be expressed in different layers of the stratified epithelium of the skin. OBJECTIVE: The present study investigated the transcriptional mechanism by which murine CLCA2 (mCLCA2) is expressed in the transformed keratinocyte line Pam212 that can differentiate. METHODS: A luciferase reporter assay, chromatin immunoprecipitation (ChIP) assay, reverse transcription-PCR, and immunocytochemistry were performed using Pam212 cells. RESULTS: Promoter activity of mCLCA2 was inhibited profoundly by site-directed mutagenesis of a putative nuclear factor-κB (NF-κB) binding site and by treatment with siRNA against p65. ChIP and transcription factor assays showed the specific association of endogenously activated p65 protein with the NF-κB binding domain. As confirmed by the nuclear translocation of p65, tumor necrosis factor α and caffeic acid phenethyl ester (CAPE) increased and decreased mCLCA2 promoter activity, respectively, but exhibited modest effects on endogenous mCLCA2 expression in cells in culture medium containing 0.05 mM Ca(2+). When the Ca(2+) concentration was raised to 1.0mM, the mRNA and protein levels of mCLCA2 increased as well as those of the differentiation markers keratin 1 (K1) and K10. CAPE profoundly suppressed only the Ca(2+)-triggered expression of mCLCA2, not K1 or K10. Immunohistochemistry of native skin and organotypic 3D cultures confirmed the distribution of the CLCA2 homolog in differentiated cells. CONCLUSION: The present study revealed for the first time that basal NF-κB activity is involved in the Ca(2+)-dependent regulation of mCLCA2 expression in a mouse keratinocyte line. |
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学位名 | ||||||||||||||||
学位名 | 博士(歯学) | |||||||||||||||
学位授与大学 | ||||||||||||||||
学位授与機関識別子 | 37114 | |||||||||||||||
学位授与機関名 | 福岡歯科大学 | |||||||||||||||
学位授与年度 | ||||||||||||||||
内容記述 | 2014年度 | |||||||||||||||
学位授与年月日 | ||||||||||||||||
学位授与年月日 | 2015-03-14 | |||||||||||||||
報告番号 | ||||||||||||||||
学位授与番号 | 甲第270号 | |||||||||||||||
情報源 | ||||||||||||||||
関連名称 | J Dermatol Sci. 2015 Jun;78(3):189-96. doi: 10.1016/j.jdermsci.2015.03.007. Epub 2015 Mar 18. | |||||||||||||||
関連サイト | ||||||||||||||||
識別子タイプ | URI | |||||||||||||||
関連識別子 | http://www.sciencedirect.com/science/article/pii/S0923181115000857 | |||||||||||||||
関連名称 | ScienceDirect | |||||||||||||||
著者版フラグ | ||||||||||||||||
出版タイプ | VoR | |||||||||||||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 |