| Item type |
☆紀要論文 / Departmental Bulletin Paper(1) |
| 公開日 |
2014-08-17 |
| タイトル |
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タイトル |
<Originals> Trib1 and Trib2 inhibit granulocytic differentiation by suppressing Akt pathway |
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言語 |
en |
| 著者 |
Kanai, Yoshitaka
Shimada, Takahiro
Taniguchi, Yasuhiro
Rai, Shinya
Hirase, Chikara
Hanamoto, Hitoshi
Morita, Yasuyoshi
Tanaka, Hirokazu
Tatsumi, Yoichi
Ashida, Takashi
Matsumura, Itaru
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| 言語 |
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言語 |
eng |
| キーワード |
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主題 |
Trib1, Trib2, C/EBPα, Akt, AML, differentiation |
| 資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
departmental bulletin paper |
| 著者 所属 |
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値 |
Division of Hematology and Rheumatology, Department of Internal Medicine, Kinki University Faculty of Medicine |
| 著者 所属 |
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値 |
Division of Hematology and Rheumatology, Department of Internal Medicine, Kinki University Faculty of Medicine |
| 著者 所属 |
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値 |
Division of Hematology and Rheumatology, Department of Internal Medicine, Kinki University Faculty of Medicine |
| 著者 所属 |
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値 |
Division of Hematology and Rheumatology, Department of Internal Medicine, Kinki University Faculty of Medicine |
| 著者 所属 |
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値 |
Division of Hematology and Rheumatology, Department of Internal Medicine, Kinki University Faculty of Medicine |
| 著者 所属 |
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値 |
Department of Hematology, Nara Hospital, Kinki University Faculty of Medicine |
| 著者 所属 |
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値 |
Division of Hematology and Rheumatology, Department of Internal Medicine, Kinki University Faculty of Medicine |
| 著者 所属 |
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値 |
Division of Hematology and Rheumatology, Department of Internal Medicine, Kinki University Faculty of Medicine |
| 著者 所属 |
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値 |
Division of Hematology and Rheumatology, Department of Internal Medicine, Kinki University Faculty of Medicine |
| 著者 所属 |
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値 |
Division of Hematology and Rheumatology, Department of Internal Medicine, Kinki University Faculty of Medicine |
| 著者 所属 |
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値 |
Division of Hematology and Rheumatology, Department of Internal Medicine, Kinki University Faculty of Medicine |
| 著者所属(翻訳) |
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値 |
Kinki University |
| 著者所属(翻訳) |
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値 |
Kinki University |
| 著者所属(翻訳) |
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値 |
Kinki University |
| 著者所属(翻訳) |
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値 |
Kinki University |
| 著者所属(翻訳) |
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値 |
Kinki University |
| 著者所属(翻訳) |
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値 |
Kinki University |
| 著者所属(翻訳) |
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値 |
Kinki University |
| 著者所属(翻訳) |
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値 |
Kinki University |
| 著者所属(翻訳) |
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値 |
Kinki University |
| 著者所属(翻訳) |
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値 |
Kinki University |
| 著者所属(翻訳) |
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値 |
Kinki University |
| 版 |
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出版タイプ |
VoR |
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出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| 出版者 名前 |
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出版者 |
Kinki University Medical Association |
| 書誌情報 |
en : ACTA MEDICA KINKI UNIVERSITY
巻 39,
号 1,
p. 29-37,
発行日 2014-06-01
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| ISSN |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
03866092 |
| 抄録 |
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内容記述タイプ |
Abstract |
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内容記述 |
[Abstract] Background :Overexpression of Tribbles homolog 1 (Tribl) and Tribbles homolog 2 (Trib2) in hematopoietic stem/progenitor cells evokes acute myeloid leukemia (AML) in murine transplantation models. Degradation of CCAAT-enhancer-binding-protein α (C/EBPα) plays a crucial role in Trib1 or Trib2-induced AML. However, because C/EBPα knockout mice do not develop AML, it is likely that Trib1 and Trib2 influence other signaling pathways besides C/EBPα. Elevated Akt phosphorylation is considered to contribute to the development of AML. In contrast, two groups recently reported that reduced Akt activity is involved in the pathogenesis of leukemia. We performed this study to reveal the role of Akt signaling in Trib family-induced AML.Methods : G-CSF-induced granulocytic differentiation of 32D cells was assessed morphologically and phenotypically. G-CSF-induced signaling wasassessed by Westernblotting. Results : Overexpression of Trib1 or Trib2 inhibited GCSF-induced granulocytic differentiation of 32D cells, which was accompanied by reduced Akt phosphorylation. Also, an Akt inhibitor API-2 blocked G-CSF-induced granulocytic differentiation independently of C/EBPα degradation. Furthermore, retroviral C/EBPα restoration did not completely abolish the differentiation block caused by Trib1 and Trib2. Conclusion :Trib1 and Trib2 block granulocytic differentiation, at least partially, by suppressing Akt phosphorylation. |
| フォーマット |
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内容記述タイプ |
Other |
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内容記述 |
application/pdf |
AA0050842X-20140600-0029.pdf (8.2 MB)
