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10.1016j.celrep.2017.05.009.pdf5.65 MBAdobe PDF見る/開く
タイトル: Regnase-1 Maintains Iron Homeostasis via the Degradation of Transferrin Receptor 1 and Prolyl-Hydroxylase-Domain-Containing Protein 3 mRNAs
著者: Yoshinaga, Masanori  kyouindb  KAKEN_id
Nakatsuka, Yoshinari
Vandenbon, Alexis  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0003-2180-5732 (unconfirmed)
Ori, Daisuke
Uehata, Takuya  kyouindb  KAKEN_id
Tsujimura, Tohru
Suzuki, Yutaka
Mino, Takashi  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0002-9562-008X (unconfirmed)
Takeuchi, Osamu  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0002-1260-6232 (unconfirmed)
著者名の別形: 吉永, 正憲
竹内, 理
発行日: 23-May-2017
出版者: Elsevier BV
誌名: Cell Reports
巻: 19
号: 8
開始ページ: 1614
終了ページ: 1630
抄録: Iron metabolism is regulated by transcriptional and post-transcriptional mechanisms. The mRNA of the iron-controlling gene, transferrin receptor 1 (TfR1), has long been believed to be negatively regulated by a yet-unidentified endonuclease. Here, we show that the endonuclease Regnase-1 is critical for the degradation of mRNAs involved in iron metabolism in vivo. First, we demonstrate that Regnase-1 promotes TfR1 mRNA decay. Next, we show that Regnase-1−/− mice suffer from severe iron deficiency anemia, although hepcidin expression is downregulated. The iron deficiency anemia is induced by a defect in duodenal iron uptake. We reveal that duodenal Regnase-1 controls the expression of PHD3, which impairs duodenal iron uptake via HIF2α suppression. Finally, we show that Regnase-1 is a HIF2α-inducible gene and thus provides a positive feedback loop for HIF2α activation via PHD3. Collectively, these results demonstrate that Regnase-1-mediated regulation of iron-related transcripts is essential for the maintenance of iron homeostasis.
記述: 腸で鉄の吸収を調節するメカニズムの一端を解明 -- 貧血時に鉄吸収を促進するフィードバック機構を発見--. 京都大学プレスリリース. 2017-05-24.
著作権等: © 2017 The Authors. This is an open access article under the CC BY 4.0 license (https://creativecommons.org/licenses/by/4.0/).
URI: http://hdl.handle.net/2433/224949
DOI(出版社版): 10.1016/j.celrep.2017.05.009
PubMed ID: 28538180
関連リンク: http://www.kyoto-u.ac.jp/ja/research/research_results/2017/170524_1.html
出現コレクション:学術雑誌掲載論文等

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