Identification of ATLL-associated genes in Rapid ATLL model mouse
Project/Area Number |
15K14388
|
Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
Allocation Type | Multi-year Fund |
Research Field |
Tumor biology
|
Research Institution | National Institute of Infectious Diseases |
Principal Investigator |
Saito Masumichi 国立感染症研究所, 血液・安全性研究部, 主任研究官 (20571045)
|
Co-Investigator(Kenkyū-buntansha) |
日吉 真照 国立感染症研究所, 血液・安全性研究部, 主任研究官 (40448519)
|
Co-Investigator(Renkei-kenkyūsha) |
HIDEKATSU Iha 大分大学, 医学部, 准教授 (50242631)
HIROO Hasegawa 長崎大学, 医学部, 准教授 (00398166)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
Keywords | 実験動物モデル / 実験動物 / ATL発症原因遺伝子 / HTLV-1 / ATLL / マウスモデル |
Outline of Final Research Achievements |
In ATLL model mouse, we found that point mutations and 5’deletions of HTLV-1 induce HBZ activation. Furthermore, the HBZ activation mechanism on HTLV-1 carrying the deletion was due to disruption of mir-324-3P mediated HBZ repression. Interestingly, we also found that mir-324-3P was deleted in about 40% of ATLL cases. This result strongly suggests that mir-324-3P might function as a tumor suppressor gene in the process of ATLL development
|
Report
(4 results)
Research Products
(8 results)
-
-
-
-
[Journal Article] Proviral features of human T cell leukemia virus type 1 in carriers with indeterminate western blot analysis results.2017
Author(s)
Kuramitsu M, Sekizuka T, Yamochi T, Firouzi S, Sato T, Umeki K, Sasaki D, Hasegawa H, Kubota R, Sobata R, Matsumoto C, Kaneko N, Momose H, Araki K, Saito M, Nosaka K, Utsunomiya A, Koh K, Ogata M, Uchimaru K, Iwanaga M, Sagara Y, Yamano Y, et al.
-
Journal Title
J Clin Microbiol.
Volume: 55(9)
Issue: 9
Pages: 2838-2849
DOI
Related Report
Peer Reviewed / Open Access
-
-
-
-