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  1. H-2. ナノ生命科学研究所
  2. h-2 10.学術雑誌掲載論文
  3. 1. 査読済論文

Retinoid X receptor α in human liver is regulated by miR-34a

https://doi.org/10.24517/00015094
https://doi.org/10.24517/00015094
cd7f8cef-b3a4-4a71-9d72-cd4d89cb099a
名前 / ファイル ライセンス アクション
PH-PR-NAKAJIMA-M-179.pdf PH-PR-NAKAJIMA-M-179.pdf (367.2 kB)
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Item type 学術雑誌論文 / Journal Article(1)
公開日 2017-10-04
タイトル
タイトル Retinoid X receptor α in human liver is regulated by miR-34a
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
ID登録
ID登録 10.24517/00015094
ID登録タイプ JaLC
著者 Oda, Yuki

× Oda, Yuki

WEKO 27228

Oda, Yuki

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Nakajima, Miki

× Nakajima, Miki

WEKO 196
e-Rad 70266162
金沢大学研究者情報 70266162
研究者番号 70266162

Nakajima, Miki

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Tsuneyama, Koichi

× Tsuneyama, Koichi

WEKO 25217
研究者番号 10293341

Tsuneyama, Koichi

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Takamiya, Masataka

× Takamiya, Masataka

WEKO 27229

Takamiya, Masataka

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Aoki, Yasuhiro

× Aoki, Yasuhiro

WEKO 27230

Aoki, Yasuhiro

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Fukami, Tatsuki

× Fukami, Tatsuki

WEKO 26716
e-Rad 00532300
金沢大学研究者情報 00532300
研究者番号 00532300

Fukami, Tatsuki

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Yokoi, Tsuyoshi

× Yokoi, Tsuyoshi

WEKO 63
研究者番号 70135226

Yokoi, Tsuyoshi

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著者別表示 中嶋, 美紀

× 中嶋, 美紀

中嶋, 美紀

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深見, 達基

× 深見, 達基

深見, 達基

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横井, 毅

× 横井, 毅

横井, 毅

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提供者所属
内容記述タイプ Other
内容記述 金沢大学ナノ生命科学研究所 / 金沢大学医薬保健研究域薬学系
書誌情報 Biochemical Pharmacology

巻 90, 号 2, p. 179-187, 発行日 2014-07-15
ISSN
収録物識別子タイプ ISSN
収録物識別子 0006-2952
NCID
収録物識別子タイプ NCID
収録物識別子 AA00564486
DOI
関連タイプ isVersionOf
識別子タイプ DOI
関連識別子 10.1016/j.bcp.2014.05.002
出版者
出版者 Elsevier
抄録
内容記述タイプ Abstract
内容記述 Retinoid X receptor α (RXRα) forms a heterodimer with numerous nuclear receptors to regulate drug- or lipid-metabolizing enzymes. In this study, we investigated whether human RXRα is regulated by microRNAs. Two potential recognition elements of miR-34a were identified in the RXRα mRNA: one in the coding region and the other in the 3′-untranslated region (3′-UTR). Luciferase assays revealed that miR-34a recognizes the element in the coding region. The overexpression of miR-34a in HepG2 cells significantly decreased the endogenous RXRα protein and mRNA levels. The stability of RXRα mRNA was decreased by the overexpression of miR-34a, indicating that miR-34a negatively regulates RXRα expression by facilitating mRNA degradation. We found that the miR-34a-dependent down-regulation of RXRα decreases the induction of CYP26 and the transactivity of CYP3A4. miR-34a has been reported to be up-regulated by p53, which has an ability to promote liver fibrosis. The p53 activation resulted in an increase of the miR-34a level and a decrease of the RXRα protein level. In addition, the miR-34a levels in eight fibrotic livers were higher than those in six normal livers, and the reverse trend was found for the RXRα protein levels. An inverse correlation was observed between the miR-34a and the RXRα protein levels in the 14 samples. Taken together, the data show that miR-34a negatively regulates RXRα expression in human liver, and affects the expression of its downstream genes. This miR-34a-dependent regulation might be the underlying mechanism responsible for the decreased expression of the RXRα protein in fibrotic livers. © 2014 Elsevier Inc.
著者版フラグ
出版タイプ AM
出版タイプResource http://purl.org/coar/version/c_ab4af688f83e57aa
関連URI
識別子タイプ URI
関連識別子 http://www.elsevier.com/locate/issn/00062952
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