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RNA export factor RAE1 contributes to NUP98-HOXA9-mediated leukemogenesis
https://doi.org/10.24517/00039997
https://doi.org/10.24517/00039997abbe13e0-89ea-4e13-a8a1-7bc5a5b87c3d
| 名前 / ファイル | ライセンス | アクション |
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FR-PR-FUNASAKA-T-1456.pdf (701.1 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||||||
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| 公開日 | 2017-10-06 | |||||||||
| タイトル | ||||||||||
| タイトル | RNA export factor RAE1 contributes to NUP98-HOXA9-mediated leukemogenesis | |||||||||
| 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 | 10.24517/00039997 | |||||||||
| ID登録タイプ | JaLC | |||||||||
| 著者 |
Funasaka, Tatsuyoshi
× Funasaka, Tatsuyoshi× Nakano, Hiroshi× Wu, Yu× Hashizume, Chieko× Gu, Ling× Nakamura, Takuro× Wang, Wei× Zhou, Pengbo× Moore, Malcolm AS× Sato, Hiroshi× Wong, Richard W. |
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| 著者別表示 |
船坂, 龍善
× 船坂, 龍善
× 佐藤, 博
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| 提供者所属 | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | 金沢大学フロンティアサイエンス機構 | |||||||||
| 書誌情報 |
Cell Cycle 巻 10, 号 9, p. 1456-1467, 発行日 2011-05-01 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | ISSN | |||||||||
| 収録物識別子 | 1538-4101 | |||||||||
| NCID | ||||||||||
| 収録物識別子タイプ | NCID | |||||||||
| 収録物識別子 | AA11638609 | |||||||||
| DOI | ||||||||||
| 関連タイプ | isVersionOf | |||||||||
| 識別子タイプ | DOI | |||||||||
| 関連識別子 | 10.4161/cc.10.9.15494 | |||||||||
| 出版者 | ||||||||||
| 出版者 | Landes Bioscience | |||||||||
| 抄録 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | Chromosomal translocations involving chimeric fusions of the nucleoporin NUP98 protein have often been described in acute myelogenous leukemia (AML). All the fusion proteins have an identical NUP98 N terminus, which contains the GLEBS motif for interaction with the mRNA export factor RAE1 and FG repeats that associate with the transcription factors HDAC1 and p300. It is virtually unknown whether these interaction partners affect leukemogenesis. We previously showed that RAE1 depletion caused aneuploidy, which enhanced tumorigenesis. We speculated that RAE1 may also be directly involved in NUP98 fusion-mediated leukemogenesis. We show here that RNA interference (RNAi)-mediated knockdown of NUP98 caused severe chromosome segregation defects and disrupted RAE1 but not HDAC1 expression and localization. Next, we performed rescue experiments to confirm that the RAE1-NUP98 complex orchestrates proper chromosome segregation. Interestingly, we found diverse behaviors of NUP98 and the leukemogenic fusion protein NUP98-HOXA9 throughout the cell cycle. Strikingly, in NUP98-HOXA9-transfected cells, RAE1 protein were reduced and mis-localized. Our cellular interpretations were further confirmed by NUP98-HOXA9 transgenic mice and the NUP98-HOXA9 AML patient. These data suggest that RAE1 orchestrates NUP98-mediated leukemogenesis and raise the possibility that targeting this negative feedback loop may provide a new strategy for the therapy of aggressive leukemias. © 2011 Landes Bioscience. | |||||||||
| 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 | |||||||||
