Elucidation of the diversity of target genes in GATA1
| Project/Area Number |
24890015
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
General medical chemistry
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| Research Institution | Tohoku University |
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Principal Investigator |
KANEKO Hiroshi 東北大学, 医学(系)研究科(研究院), 助教 (80635558)
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| Project Period (FY) |
2012-08-31 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 遺伝子発現制御 / GATA因子 / 転写活性化部位 / 転写因子 / GATA転写因子 / 細胞分化 / マイクロアレイ解析 / トランスジェニックマウス / ノックアウトマウス |
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| Research Abstract |
Transcription factor GATA1 has two distinct transactivation domains (N-TAD and C-TAD). It remains to be uncovered what these multiple TADs systems confers on GATA1 function in vivo. In this study, I revealed that GATA1 target genes were classified into three groups with their dependency to TAD. In addition to this GST-pull down assay showed that GATA1 and Rb interaction was dependent to N-TAD. Because, GATA1 mutations which causes the deletion of N-TAD are found in Down's related acute megakaryoblastic leukemia(DS-AMkL) and transient myeoproliferative disorder(TMD), this result suggests that GATA1 transcriptional regulatory mechanism based on multiple TAD system is involvement to the pathology of DS-AMkL and TMD.
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Report
(3 results)
Research Products
(3 results)
