| Project/Area Number |
01570279
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Immunology
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| Research Institution | RIKEN (The Institute of Physical and Chemical Research) |
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Principal Investigator |
YOKOYAMA Kazushige RIKEN, Gene Bank, Research Scientist., ジーンバンク室, 研究員 (80182707)
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| Project Period (FY) |
1989 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1991: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1990: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1989: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | MHC Class I gene / Transcriptional Regulation / Adenovirus E1A / Nuclear Factor / CAA repeat / TFIID / Domain analysis / Rb protein / ヒ-トショックエレメント / プリンボックス / マウスクラスI抗原 / アデノウィルスーEIA / 転写制御 |
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| Research Abstract |
We have investigated the transcriptional regulation of MHC Class I gene to identify the controlled elements in the MHC Class I gene promoter. To understand this molecular regulation is the first step to know the immunological regulation of "Self-Nonself" discrimination. We focus upon the controlled regulation of Class I MHC gene expression by adenovirus type 12 EIA. First, we determined the nucleotide sequence of the promoter region of MHC Class I H-2K^<bml> gene to compare the parent H-2K^b gene promoter. To identify the cis-element in H-2K^b gene, a seubs of deletion CAT mutants of the promoter region were constructed and used for the analysis of the CAT activity. Thus, we have identified the positive and negative elements in the H-2K^b promoter which were corresponded with the ElA-mediated response. By using a gel-shift and the footprint studies, we have characterized the nuclear proteins to bind Co this sequence. We also obtained the gene corresponding to bind to these elements, CAA repeated. motif, of the H-2K^b gene. These gene products including TFIID were responsible to the cooperative interaction with the EIA and Rb proteins to perform the negative regulation of H-2 Class I gene by ElA.
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