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  1. 原著論文

ADAR1 Forms a Complex with Dicer to Promote MicroRNA Processing and RNA-Induced Gene Silencing

https://repo.qst.go.jp/records/46932
https://repo.qst.go.jp/records/46932
6ef75912-da0d-4201-819a-502eba50c922
Item type 学術雑誌論文 / Journal Article(1)
公開日 2014-11-13
タイトル
タイトル ADAR1 Forms a Complex with Dicer to Promote MicroRNA Processing and RNA-Induced Gene Silencing
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
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Ota, Hiromitsu

× Ota, Hiromitsu

WEKO 468366

Ota, Hiromitsu

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Sakurai, Masayuki

× Sakurai, Masayuki

WEKO 468367

Sakurai, Masayuki

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Gupta, Ravi

× Gupta, Ravi

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Gupta, Ravi

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Valente, Louis

× Valente, Louis

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Valente, Louis

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Wulff, Bjorn-Erik

× Wulff, Bjorn-Erik

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Wulff, Bjorn-Erik

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Ariyoshi, Kentaro

× Ariyoshi, Kentaro

WEKO 468371

Ariyoshi, Kentaro

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Iizasa, Hisashi

× Iizasa, Hisashi

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Iizasa, Hisashi

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V, Davuluri Ramana

× V, Davuluri Ramana

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V, Davuluri Ramana

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Nishikura, Kazuko

× Nishikura, Kazuko

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Nishikura, Kazuko

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et.al

× et.al

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et.al

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有吉 健太郎

× 有吉 健太郎

WEKO 468376

en 有吉 健太郎

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抄録
内容記述タイプ Abstract
内容記述 Adenosine deaminases acting on RNA (ADARs) are involved in RNA editing that converts adenosine residues to inosine specifically in double-stranded RNAs. In this study, we investigated the interaction of the RNA editing mechanism with the RNA interference (RNAi) machinery and found that ADAR1 forms a complex with Dicer through direct protein-protein interaction. Most importantly, ADAR1 increases the maximum rate (Vmax) of pre-microRNA (miRNA) cleavage by Dicer and facilitates loading of miRNA onto RNA-induced silencing complexes, identifying a new role of ADAR1 in miRNA processing and RNAi mechanisms. ADAR1 differentiates its functions in RNA editing and RNAi by the formation of either ADAR1/ADAR1 homodimer or Dicer/ADAR1 heterodimer complexes, respectively. As expected, the expression of miRNAs is globally inhibited in ADAR1-/- mouse embryos, which, in turn, alters the expression of their target genes and might contribute to their embryonic lethal phenotype.
書誌情報 Cell

巻 153, 号 3, p. 575-589, 発行日 2013-04
ISSN
収録物識別子タイプ ISSN
収録物識別子 0092-8674
関連サイト
識別子タイプ URI
関連識別子 http://www.sciencedirect.com/science/article/pii/S0092867413003462
関連名称 http://www.sciencedirect.com/science/article/pii/S0092867413003462
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