| アイテムタイプ |
itemtype_ver1(1) |
| 公開日 |
2024-12-11 |
| タイトル |
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タイトル |
Identification of APBB1 as a substrate for anaplastic lymphoma kinase |
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言語 |
en |
| 著者 |
Suzuki, Yuji
Tsubota, Shoma
Kadomatsu, Kenji
Sakamoto, Kazuma
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| アクセス権 |
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アクセス権 |
open access |
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アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
| 権利 |
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|
権利情報 |
This is a pre-copyedited, author-produced version of an article accepted for publication in [The Journal of Biochemistry] following peer review. The version of record [Yuji Suzuki, Shoma Tsubota, Kenji Kadomatsu, Kazuma Sakamoto, Identification of APBB1 as a substrate for anaplastic lymphoma kinase, The Journal of Biochemistry, Volume 176, Issue 5, November 2024, Pages 395–403, https://doi.org/10.1093/jb/mvae055] is available online at: https://doi.org/10.1093/jb/mvae055. |
|
言語 |
en |
| 内容記述 |
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|
内容記述タイプ |
Abstract |
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内容記述 |
Anaplastic lymphoma kinase (ALK) is a well-known oncogene involved in various malignancies such as anaplastic large cell lymphoma, lung cancer and neuroblastoma. Several substrates for fused ALK have been identified and their biological functions have been described. However, the lack of a comprehensive identification of ALK substrates limits our understanding of the biological roles of receptor ALK. Thus, this study aimed to identify novel ALK substrates and characterize their biological functions. We screened the interactors of the kinase domain of receptor ALK using proximity-dependent biotin identification and identified 43 interactors. We narrowed down the candidates by evaluating whether these interactors were downstream of ALK in a neuroblastoma cell line, NB-1. Amongst these, we identified amyloid beta precursor protein-binding family B member 1 (APBB1) as an ALK downstream molecule involved in NB-1 cell viability. Finally, we assessed the kinase-substrate relationship between ALK and APBB1 and found that ALK phosphorylated multiple tyrosine residues in APBB1 both in-cell and in-tube assays, with tyrosine 269 as a major target. In conclusion, we successfully identified a new substrate for receptor ALK. Our results may help further elucidate the molecular mechanism of ALK downstream signalling in neuroblastoma. |
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言語 |
en |
| 出版者 |
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出版者 |
Oxford University Press |
|
言語 |
en |
| 言語 |
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|
言語 |
eng |
| 資源タイプ |
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資源タイプresource |
http://purl.org/coar/resource_type/c_6501 |
|
タイプ |
journal article |
| 出版タイプ |
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出版タイプ |
AM |
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出版タイプResource |
http://purl.org/coar/version/c_ab4af688f83e57aa |
| 関連情報 |
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|
関連タイプ |
isVersionOf |
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|
識別子タイプ |
DOI |
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|
関連識別子 |
https://doi.org/10.1093/jb/mvae055 |
| 収録物識別子 |
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収録物識別子タイプ |
PISSN |
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収録物識別子 |
0021-924X |
| 書誌情報 |
en : The Journal of Biochemistry
巻 176,
号 5,
p. 395-403,
発行日 2024-11
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| ファイル公開日 |
|
|
日付 |
2025-11-01 |
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日付タイプ |
Available |
acceptedManuscript_20240711.pdf (348 KB)
