Molecular mechanism of transcriptional regulation by NFATc in tumor endothelial cells
| Project/Area Number |
24700969
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
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| Research Institution | Kyorin University (2013)
The University of Tokyo (2012) |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 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 | 血管内皮細胞 / 腫瘍血管新生 / ＶＥＧＦ / ＮＦＡＴｃ / NFATc / タンパク質相互作用 / in vivo発現解析 / ＣｈＩＰ－ｓｅｑ |
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| Research Abstract |
To elucidate molecular mechanism of transcriptional activation by NFATc, I performed global analysis of target genes using microarray and ChIP-seq and examined beta-galactosidase activities in hprt locus-target in EGR3 promoter-lacZ transgenic mice. CXCR7 and RND1 were first identified as NFATc targets and contributed to VEGF-mediated angiogenesis. NFAT-mediated EGR3 promoter activities in vivo were upregulated by inflammatory stimuli in various types of endothelial cells.
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Report
(3 results)
Research Products
(26 results)
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[Journal Article] Inhibition of histone demethylase JMJD1A improves anti-angiogenic therapy and reduces tumor associated macrophages2013
Author(s)
Shimamura T, Wang F, Suehiro J, Kanki Y, Wada Y, Yuasa Y, Aburatani H, Miyano S, Minami T, Kodama T, Shibuya M
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Journal Title
Cancer Res
Volume: 73
Issue: 10
Pages: 3019-3028
DOI
Related Report
Peer Reviewed
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