| Project/Area Number |
62570223
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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 | The Institute of Physical and Chemical Research |
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Principal Investigator |
YOKOYAMA Kazushige RIKEN (The Institute of physical and chemical Research), ジーンバンク室, 研究員 (80182707)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1988: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Adenoviruse Type 12 E1A / mouse class I MHC gene / 転写制御 / アデノウイルスEIA型遺伝子 / マウスクラスエ抗原 / アデノウィルスE1A / 遺伝子 |
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| Research Abstract |
The mechanism of transcriptional regulation of the H-2K@>D2bml@>D1 major histocompatibility complex class I gene by adenovirus type 12 ElA (Ad12-ElA) was studied in transfected rat embryonal fibroblasts. Results of long-term expression of the chloramphenicol acetyl transferase (CAT) gene placed under the control of the 5'-flanking region of the mouse MHC class I gene, H-2K^<bm1>, and the results of nuclear run-on transcription assays, yield evidence for both positive and negative regulation of H-2K^<bml> by ElA gene product. Deletion studies in the H-2K^<bm1> promoter region revealed that a proximal 58 bp upstream sequence (-194 to -136) and a distal 316 bp sequence (-1837 to -1521), relative to the cap site respectively contribute to positive and negative regulations mediated by ElA gene product. Both regulatory elements of NHC class I gene promoter region are responsiblefor the differential expression of the H-2K^<bm1> gene in Ad12 transformed cells.
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