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MafB protein stability is regulated by the JNK and ubiquitin-proteasome pathways
http://hdl.handle.net/10091/3580
http://hdl.handle.net/10091/3580ba89b1f3-4dd6-4969-bc49-d94328e94f89
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
Tanahashi R2.pdf (398.9 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||||||||||
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| 公開日 | 2009-11-26 | |||||||||||||
| タイトル | ||||||||||||||
| タイトル | MafB protein stability is regulated by the JNK and ubiquitin-proteasome pathways | |||||||||||||
| 言語 | ||||||||||||||
| 言語 | eng | |||||||||||||
| DOI | ||||||||||||||
| 関連識別子 | https://doi.org/10.1016/j.abb.2009.11.018 | |||||||||||||
| 関連名称 | 10.1016/j.abb.2009.11.018 | |||||||||||||
| キーワード | ||||||||||||||
| 主題 | JNK, MafB, phosphorylation, proteasome, stability, ubiquitin | |||||||||||||
| 資源タイプ | ||||||||||||||
| 資源 | http://purl.org/coar/resource_type/c_6501 | |||||||||||||
| タイプ | journal article | |||||||||||||
| 著者 |
Tanahashi, Hiroshi
× Tanahashi, Hiroshi
× Kito, Keiji
× Ito, Takashi
× Yoshioka, Katsuji
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| 出版者 | ||||||||||||||
| 出版者 | ELSEVIER SCIENCE INC | |||||||||||||
| 引用 | ||||||||||||||
| 内容記述 | ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS. 494(1):94-100 (2010) | |||||||||||||
| 書誌情報 |
Archives of Biochemistry and Biophysics 巻 494, 号 1, p. 94-100, 発行日 2010-02-01 |
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| 抄録 | ||||||||||||||
| 内容記述 | MafB is a basic leucine zipper transcription factor that plays important roles in development and differentiation processes. During osteoclastogenesis, its expression is downregulated at the transcriptional level via the JNK and p38 MAP kinase pathways. In the present study, we demonstrated that MafB protein stability is regulated by JNK and identified a phosphorylation site, Thr62. The expression of a constitutively active form of JNK (a fusion protein MKK7α1-JNK1β1) promoted the degradation of MafB in COS7 cells, and a T62A substitution significantly reduced the instability of MafB. The introduction of a four-fold (T58A/T62A/S70A/S74A) substitution in an acidic transcription-activating domain almost protected the instability resulting from the activation of JNK. Furthermore, treatment with proteasome inhibitors increased the MafB level, and a high-molecular-weight smear, characteristic of polyubiquitination, was observed in lysates from cells in which MafB, ubiquitin, and MKK7α1-JNK1β1 were co-expressed. These results suggest that phosphorylation of MafB by JNK confers susceptibility to proteasomal degradation. | |||||||||||||
| 資源タイプ（コンテンツの種類） | ||||||||||||||
| ISSN | ||||||||||||||
| 収録物識別子タイプ | PISSN | |||||||||||||
| 収録物識別子 | 0003-9861 | |||||||||||||
| 書誌レコードID | ||||||||||||||
| 収録物識別子タイプ | NCID | |||||||||||||
| 収録物識別子 | AA11539811 | |||||||||||||
| PubMed | ||||||||||||||
| 識別子タイプ | PMID | |||||||||||||
| 関連識別子 | https://pubmed.ncbi.nlm.nih.gov/19932079 | |||||||||||||
| 関連名称 | 19932079 | |||||||||||||
| 出版タイプ | ||||||||||||||
| 出版タイプ | AM | |||||||||||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||||||||||
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| URL | http://gateway.isiknowledge.com/gateway/Gateway.cgi?&GWVersion=2&SrcAuth=ShinshuUniv&SrcApp=ShinshuUniv&DestLinkType=FullRecord&DestApp=WOS&KeyUT=000274745700013 | |||||||||||||
