Sp6 regulation of Rock1 promoter activity in dental epithelial cells
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- Dwi Yanuaryska Ryna
- Department of Molecular Biology, Institute of Health Biosciences, the University of Tokushima Graduate School
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- Miyoshi Keiko
- Department of Molecular Biology, Institute of Health Biosciences, the University of Tokushima Graduate School
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- Adiningrat Arya
- Department of Molecular Biology, Institute of Health Biosciences, the University of Tokushima Graduate School
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- Horiguchi Taigo
- Department of Molecular Biology, Institute of Health Biosciences, the University of Tokushima Graduate School
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- Tanimura Ayako
- Department of Molecular Biology, Institute of Health Biosciences, the University of Tokushima Graduate School
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- Hagita Hiroko
- Department of Molecular Biology, Institute of Health Biosciences, the University of Tokushima Graduate School
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- Noma Takafumi
- Department of Molecular Biology, Institute of Health Biosciences, the University of Tokushima Graduate School
書誌事項
- タイトル別名
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- Sp6 regulation of <i>Rock1 </i>promoter activity in dental epithelial cells
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抄録
Sp6 is a transcription factor of the SP/KLF family and an indispensable regulator of the morphological dynamics of ameloblast differentiation during tooth development. However, the underlying molecular mechanisms remain unclear. We have previously identified one of the Sp6 downstream genes, Rock1, which is involved in ameloblast polarization. In this study, we investigated the transcriptional regulatory mechanisms of Rock1 by Sp6. First, we identified the transcription start sites (TSS) and cloned the 5'-flanking region of Rock1. Serial deletion analyses identified a critical region for Rock1 promoter activity within the 249-bp upstream region of TSS, and chromatin immunoprecipitation assays revealed Sp6-binding to this region. Subsequent transient transfection experiments showed that Rock1 promoter activity is enhanced by Sp6, but reduced by Sp1. Treatment of dental epithelial cells with the GC-selective DNA binding inhibitor, mithramycin A, affected Rock1 promoter activity in loss of enhancement by Sp6, but not repression by Sp1. Further site-directed mutagenesis indicated that the region from -206 to -150 contains responsive elements for Sp6. Taken together, we conclude that Sp6 positively regulates Rock1 transcription by direct binding to the Rock1 promoter region from -206 to -150, which functionally distinct from Sp1. J. Med. Invest. 61: 306-317, August, 2014
収録刊行物
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- The Journal of Medical Investigation
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The Journal of Medical Investigation 61 (3.4), 306-317, 2014
国立大学法人 徳島大学医学部
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詳細情報 詳細情報について
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- CRID
- 1390001204243134976
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- NII論文ID
- 130004822736
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- NII書誌ID
- AA11166929
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- ISSN
- 13496867
- 13431420
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- PubMed
- 25264049
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- PubMed
- CiNii Articles
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