The regulation of Paneth cells gene expression by Hath1

Hath1对潘氏细胞基因表达的调控

• 批准号: 21790653
• 负责人: TSUCHIYA Kiichirou
• 金额: $ 2.75万
• 依托单位: Tokyo Medical and Dental University
• 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
• 起止时间: 2009 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21790653/
• 关键词: Atoh1; Hath1; 小腸; パネート細胞; 抗菌物質; FGFシグナル; TCF4; HD6; クローン病; 小腸上皮細胞; 炎症性腸疾患

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.

以往的研究表明，Hath1参与了Paneth细胞的分化过程，但目前尚不清楚Hath1如何调控Paneth细胞的基因表达。本研究揭示了Hath1在人肠道中表达Paneth细胞表型的机制。本研究提示Hath1和β-catenin通过与HD6基因5‘端启动子区域的E-box序列结合，对Paneth细胞表型的影响，对HD6基因的表达起重要作用。

项目成果

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。

• 发表时间: 2010
• 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。

• 发表时间: 2011
• 期刊: Inflamm Bowel Dis. in press
• 作者: Zheng X;Tsuchiya K;Okamoto R;Iwasaki M;Kano Y;Sakamoto N;Nakamura T;Watanabe M
• 通讯作者: Watanabe M

IL-6-mediated intersubgenotypic variation of interferon sensitivity in hepatitis C virus genotype 2a/2b chimeric clones.

• 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

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。

• 发表时间: 2009
• 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

• 发表时间: 2009
• 作者: Tsuchiya K;et al.
• 通讯作者: et al.