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Heme Positively Regulates the Expression of β-Globin at the Locus Control Region via the Transcriptional Factor Bach1 in Erythroid Cells

https://hiroshima.repo.nii.ac.jp/records/2006368
https://hiroshima.repo.nii.ac.jp/records/2006368
06c06399-440b-4288-916b-eeb40fb52e83
名前 / ファイル ライセンス アクション
BBRC_324_77.pdf BBRC_324_77.pdf (1.4 MB)
Item type デフォルトアイテムタイプ_(フル)(1)
公開日 2023-03-18
タイトル
タイトル Heme Positively Regulates the Expression of β-Globin at the Locus Control Region via the Transcriptional Factor Bach1 in Erythroid Cells
言語 en
作成者 Tahara, Tsuyoshi

× Tahara, Tsuyoshi

en Tahara, Tsuyoshi

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Sun, Jiying

× Sun, Jiying

en Sun, Jiying

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Nakanishi, Katsuyuki

× Nakanishi, Katsuyuki

en Nakanishi, Katsuyuki

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Yamamoto, Masafumi

× Yamamoto, Masafumi

en Yamamoto, Masafumi

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Mori, Hajime

× Mori, Hajime

en Mori, Hajime

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Fujita, Hiroyoshi

× Fujita, Hiroyoshi

en Fujita, Hiroyoshi

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Igarashi, Kazuhiko

× Igarashi, Kazuhiko

en Igarashi, Kazuhiko

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Taketani, Shigeru

× Taketani, Shigeru

en Taketani, Shigeru

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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
権利情報
権利情報 Copyright (c) 2004 Elsevier Inc.
主題
主題Scheme NDC
主題 490
内容記述
内容記述 The transcription factor Bach1 hetero-dimerizes with small Maf proteins, to repress Maf recognition element (MARE) -dependent gene expression. The repressor activity of Bach1 is inhibited by the direct binding of heme. To the investigate involvement of Bach1 in the heme-dependent regulation of the expression of the β-globin gene, mouse erythroleukemia (MEL) cells were cultured with succinylacetone (SA), a specific inhibitor of heme biosynthesis, and the level of β-globin mRNA was examined. A marked decrease of β-globin mRNAin SA-treated cells was observed, and was reversed by the addition of hemin. An iron chelator, desferrioxamine, also lowered the level of β-globin mRNA. The heme-dependent expression of β-globin is a transcriptional event since the expression of the human β-globin gene promoter-reporter gene containing the micro-locus control region (μLCR) was inhibited when human erythroleukemia K562 cells and MEL cells were cultured with SA. Hemin treatment restored the decrease in promoter activity caused by SA. The control of the μLCR-β-globin promoter reporter gene by heme was dependent on DNase I-hypersensitive site 2 which contains MARE. Transient expression of Bach1 suppressed the μLCR activity, and this repressor activity was cancelled by treatment with hemin. The expression of a mutated Bach1 lacking heme-binding sites led to a loss in the heme-responsiveness of the μLCR. The MARE-binding activity of Bach1 in K562 and MEL cells increased upon SA-treatment, and the increase was diminished by the treatment with hemin. Furthermore, during erythroid differentiation of MEL cells, the MARE-binding activity of Bach1 decreased while simultaneously, the NF-E2 activity increased. Wepropose that heme positively regulates the β-globin gene expression by blocking the interaction of Bach1 with the MAREin the LCR in erythoid cells.
言語 en
出版者
出版者 Elsevier
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
出版タイプ
出版タイプ AO
出版タイプResource http://purl.org/coar/version/c_b1a7d7d4d402bcce
関連情報
識別子タイプ DOI
関連識別子 10.1016/j.bbrc.2004.09.022
関連情報
識別子タイプ DOI
関連識別子 http://dx.doi.org/10.1016/j.bbrc.2004.09.022
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 0006-291X
収録物識別子
収録物識別子タイプ NCID
収録物識別子 AA00564395
開始ページ
開始ページ 77
書誌情報 Biochemical and Biophysical Research Communications
Biochemical and Biophysical Research Communications

巻 324, 号 1, p. 77-85, 発行日 2004-11-05
旧ID 21534
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