Clarification of reguratory mechanism of cell proliferation by HTLV-1.
| Project/Area Number |
10470077
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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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 |
SHIMOTOHNO Kunitada Kyoto University, Institute for Virus Research, Professor, ウイルス研究所, 教授 (10000259)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥11,800,000 (Direct Cost: ¥11,800,000)
Fiscal Year 1999: ¥5,800,000 (Direct Cost: ¥5,800,000)
Fiscal Year 1998: ¥6,000,000 (Direct Cost: ¥6,000,000)
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| Keywords | human T-cell leukemia virus / suppressor oncogene / p53 / p53 gene family / co-activator / immortalization / trans-activation / HTLV-1 / Tax / 転写抑制 |
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| Research Abstract |
Human T-cell leukemia virus type 1 (HTLV-1) is a causative agent for the development of adult T-cell leukemia (ATL). Tax encoded by HTLV-1 plays important role in immortalization of primary human lymphocytes. This capacity of Tax is conducted by modulation of cellular genes regulated by CREB, NFkB. We previously reported that p53, a suppresser oncogene, is also regulated its transacting function by Tax. Purpose in this work is to clarify molecular mechanism of Tax to suppress p53 trans-acting function. We observed that p53 accumulates in cells expressing Tax. Tax mutant which lacks to bind CBP/p300 failed to suppress p53 trans-acting function, suggested that Tax regulates p53 function through interaction with CBP/p300. From binding analysis of CBP/p300 with p53 or Tax, we concluded that suppressive effect of Tax for p53 function is occurred by competitive association with CBP/p300. Suppressive effect of Tax to p53 family gene products other than p53 was also occurred by the similar mechanism seen in p53.
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Report
(3 results)
Research Products
(14 results)
