The regulation of Paneth cells gene expression by Hath1
The regulation of Paneth cells gene expression by Hath1
批准号:
21790653
负责人:
TSUCHIYA Kiichirou
金额:
$2.75万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Young Scientists (B)
财政年份:
2009
资助国家:
日本
项目状态:
已结题
起止时间:
2009 至 2010
中文摘要
已有研究表明Hath 1参与了潘氏细胞的分化过程,但Hath 1如何调控潘氏细胞基因表达尚不清楚。本研究揭示了Hath 1在人肠道Paneth细胞表型表达的机制。本研究提示Hath 1和β-catenin通过与HD 6基因5'端启动子区的E-box序列结合,对潘氏细胞表型的形成起重要作用。
英文摘要
Previous studies have indicated that Hath1 contributes to the differentiation program of Paneth cells, however it remains unknown how Hath1 regulates the Paneth cell gene expression. This study shows the mechanism of phenotypic expression for Paneth cells by Hath1 in human intestine. The present study suggests that Hath1 and beta-catenin are essential for HD6 gene expression by binding to E-box sequence in 5' promoter region of HD6 resulting in the contribution to Paneth cell phenotype.
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Silencing of Atoh1 gene expression by Hes1 via Notch signaling results in the goblet cell depletion of Ulcerative Colitis.
Hes1 通过 Notch 信号传导沉默 Atoh1 基因表达,导致溃疡性结肠炎的杯状细胞耗竭。
DOI:
--
发表时间:
2010
期刊:
影响因子:
--
作者:
[Tsuchiya K, Okamoto R, Watanabe M]
通讯作者:
Watanabe M
The suppression of Hath1 gene expression directly regulated by Hes1 via Notch signaling is associated with goblet cell depletion in ulcerative colitis.
Hes1 通过 Notch 信号传导直接调节 Hath1 基因表达的抑制与溃疡性结肠炎中的杯状细胞耗竭有关。
DOI:
--
发表时间:
2011
期刊:
Inflamm Bowel Dis. in press
影响因子:
--
作者:
[Zheng X, Tsuchiya K, Okamoto R, Iwasaki M, Kano Y, Sakamoto N, Nakamura T, Watanabe M]
通讯作者:
Watanabe M
DOI:
10.1016/j.virol.2010.07.041
发表时间:
2010-11
期刊:
Virology
影响因子:
3.7
作者:
[G. Suda;N. Sakamoto;Yasuhiro Itsui;M. Nakagawa;Megumi Tasaka-Fujita;Yusuke Funaoka;Takako Watanabe;S. Nitta;Kei Kiyohashi;Seishin Azuma;S. Kakinuma;K. Tsuchiya;M. Imamura;N. Hiraga;K. Chayama;Mamoru Watanabe]
通讯作者:
G. Suda;N. Sakamoto;Yasuhiro Itsui;M. Nakagawa;Megumi Tasaka-Fujita;Yusuke Funaoka;Takako Watanabe;S. Nitta;Kei Kiyohashi;Seishin Azuma;S. Kakinuma;K. Tsuchiya;M. Imamura;N. Hiraga;K. Chayama;Mamoru Watanabe
Colon carcinogenesis is divided in the undifferentiation and proliferation regulated by Atoh1 and beta-catenin on Wnt signaling, respectively.
结肠癌发生分为未分化和增殖,分别受Wnt信号传导上的Atoh1和β-catenin调节。
DOI:
--
发表时间:
2009
期刊:
影响因子:
--
作者:
[Tsuchiya K, Okamoto R, Watanabe M]
通讯作者:
Watanabe M
GSK3 inhibitor induces the intestinal differentiation by the protein stabilization of Atoh1
GSK3 抑制剂通过 Atoh1 的蛋白质稳定作用诱导肠分化
DOI:
--
发表时间:
2009
期刊:
影响因子:
--
作者:
[Tsuchiya K, et al.]
通讯作者:
et al.
共 23 条
The analysis of the regulation in intestinal differentiation by thecomprehensive search of Hath1 target genes
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批准号:19590717
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.91万
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财政年份:2007
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负责人:TSUCHIYA Kiichirou
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依托单位:
海外基金