2017 Fiscal Year Final Research Report
Counteractive functions of Tax and HBZ in pathogenesis of HTLV-1
| Project/Area Number |
26460554
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Virology
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Keywords | HTLV-1 |
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| Outline of Final Research Achievements |
It was found that HTLV-1 bZIP factor (HBZ) and Tax competitively bind to a tumor suppressor Rb, and dysregulate transcription of E2F-1 target genes in HTLV-1-infected cells. It was also found that Tax is transiently expressed in ATL cells and expression level of HBZ is negatively correlated with that of Tax. According to the results of single-cell qRT-PCR, it was suggested that Tax has anti-apoptotic function and HBZ accelerates cell proliferation.
It was shown that HBZ induces immune-related molecules such as T-cell immunoreceptor with Ig and ITIM domains (TIGIT), C-C motif chemokine receptor 4 (CCR4), IFN-gamma, and has important roles to fix the immunophenotypes of HTLV-1-infected cells.
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| Free Research Field |
血液腫瘍学
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