Project/Area Number |
16K19580
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Hematology
|
Research Institution | Kumamoto University |
Principal Investigator |
Katsuya Hiroo 熊本大学, エイズ学研究センター, 特任助教 (80632041)
|
Co-Investigator(Renkei-kenkyūsha) |
SATOU Yorifumi 熊本大学, エイズ学研究センター, 教授 (70402807)
|
Research Collaborator |
MIYAZATO Paola 熊本大学, 国際先端医学研究機構, 特任助教 (90573105)
|
Project Period (FY) |
2016-04-01 – 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 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | HTLV-1 / 成人T細胞白血病-リンパ腫 / エンハンサー / ChIP-seq / 転写因子 / 内科 / ウイルス |
Outline of Final Research Achievements |
The nucleosome-free region (NFR) was found near the 3’LTR of HTV-1 provirus by MNase-sequence in both an ATL cell line and PBMCs from the ATL patients. Chromatin immunoprecipitation sequencing (ChIP-seq) showed the histone modification pattern of enhancer regions in the NFR, such as H3K4me1, H3K4me2, and H3K27Ac. The enhancer function of the NFR was also confirmed by Luciferase Reporter Assay. Furthermore, the binding of transcriptional factors, SRF and ELK-1, was detectable in the NFR by ChIP-seq and electrophoretic mobility shift assay. These data suggests that the NFR in HTLV-1 provirus plays a role of enhancer for HBZ expression, which is reverse-transcribed from 3’LTR, and might contribute to persistent infection in infected individuals.
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