| Project/Area Number |
13670153
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Tohoku University (2003)
Tokyo Medical and Dental University (2001-2002) |
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Principal Investigator |
MIYAKE Satoshi Tohoku University, Graduate School of Medicine, Lecture, 大学院・医学系研究科, 講師 (00332346)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2003: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | EID-1 / EID-2 / histone acetyltransferase / histone deacetylase / differentiation / pRB |
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| Research Abstract |
We recently identified E1A-like inhibitor of differentiation-1 (EID-1) as a pRB-binding protein. EID-1 inhibited differentiation via blocking histone acetyltransferase (HAT) activity of p300, a transcriptional coactivator which promotes differentiation. In addition to p300, EID-1 bound to core histones and this binding inhibited histone acetylation (histone masking). pRB promoted differentiation when it bound and helped degradation of EID-1.
We also identified EID-2 and EID-3 as family proteins of EID-1. When overexpressed in the cells, EID-2 and -3 inhibited differentiation like ED-1. Surprisingly, EID-1 did not block HAT activity of p300 rather it bound to histone deacetylases (HDAC). EID-2 also interacted with Smads and inhibited transcription.
These results shows that EIDs belong to a new protein family which functions as repressors of transcription involved in differentiation. We are now generating knock out mice of EID family genes and investigating their involvement to human diseases.
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