| Project/Area Number |
03670257
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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(RIKEN) |
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Principal Investigator |
MAEKAWA Toshio RIKEN, Biodesign group, バイオデザイン研究グループ, 研究員 (90201764)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1992: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1991: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | transcriptional regulators / lymphocyte / signal transduction / HIVー1 / エンハンサ-結合蛋白質 / HIVーTF1 / HIVーEP2 |
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| Research Abstract |
The cAMP response element was originally identified as an inducible enhancer element in the transcriptional regulatory region of the gene which can be transcribed in response to increased cAMP level. On the other hand, CRE can also act as a constitutive enhancer. So far,many CRE-binding proteins have been identified by cDNA cloning. All of them have the DNA-binding domain consisting of a basic amino acid cluster and a leucine zipper(so called B-ZIP structure), and bind to CRE as a homodimer or a heterodimer. Our analyses have indicated that these CRE-binding proteins can be classified into two groups based on their functions. One group involves CREB that was identified by Montiminy's group, and the transactivating capacity of CRE-binding proteins belonging to this group is stimulated by PKA-dependent phosphorylation. The typical member of the second group is CRE-BP1 that was identified by our group, and the transactivating capacity of CRE-BP1 is not stimulated by PKA. The striking feature of CRE-BP1 is that CRE-BP1 forms a heterodimer with c-Jun and that a CRE-BP1/c-Jun heterodimer can bind to CRE. A c-Jun/c-Fos heterodimer(Ap-1)is well known to bind to the TPA response element(TRE). Therefore CRE-BP1 plays an important role for a cross-talk between the cAMP pathway and TPA pathway for intracellular signal transduction.
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