The cell transplant system using improved TRECK mice

使用改进的 TRECK 小鼠的细胞移植系统

• 批准号: 23500496
• 负责人: SAITO Michiko
• 金额: $ 3.33万
• 依托单位: Nara Institute of Science and Technology
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23500496/
• 关键词: 再生医療; 糖尿病; 毒素受容体; 再生移植

The TRECK method is very useful for generating model mice and obtaining useful donor cells. However, it has been difficult to make DTR expressed in whole bodies of mice because DTR is a growth factor and overexpression of it induces a slightly abnormal phenotype. In this study, to solve these problems, we generated improved TRECK mice using a modified DT receptor with reduced growth factor activity. The improved TRECK mice showed a normal phenotype and the DTR could be expressed in whole mice bodies. This improvement is expected to extend the applicable range of the TRECK method. Furthermore, we could demonstrate that transplanted and accepted donor cells from this mouse could be removed again from the recipient mouse by DT administration to examine the effect of the transplantation.

TRECK方法对于生成模型小鼠和获得有用的供体细胞是非常有用的。然而，由于DTR是一种生长因子，过表达会引起轻微的表型异常，因此很难使DTR在小鼠全身表达。在本研究中，为了解决这些问题，我们使用了一种改良的DT受体，降低了生长因子活性，从而产生了改良的trek小鼠。改良后的trek小鼠表型正常，DTR可在小鼠全体中表达。这一改进有望扩大trek方法的适用范围。此外，我们可以证明从该小鼠移植和接受的供体细胞可以通过DT给药再次从受体小鼠中移除，以检查移植的效果。

项目成果

Fetal exposure to 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin transactivates aryl hydrocarbon receptor‐responsive element III in the tyrosine hydroxylase immunoreactive neurons of the mouse midbrain

• DOI: 10.1002/jat.2839
• 发表时间: 2014-02
• 期刊: Journal of Applied Toxicology
• 影响因子: 3.3
• 作者: Takashi Tanida;K. Tasaka;Eiichi Akahoshi;M. Ishihara-Sugano;M. Saito;Shigehisa Kawata;Megumi Danjo;Junko Tokumoto;Y. Mantani;D. Nagahara;Y. Tabuchi;T. Yokoyama;H. Kitagawa;M. Kawata;N. Hoshi

Generation of mouse models for type 1 diabetes by selective depletion of pancreatic beta cells using toxin receptor-mediated cell knockout

• DOI: 10.1016/j.bbrc.2013.05.114
• 发表时间: 2013-07-05
• 期刊: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
• 影响因子: 3.1
• 作者: Matsuoka, Kunie;Saito, Michiko;Yonekawa, Hiromichi
• 通讯作者: Yonekawa, Hiromichi

細胞系譜の異なる細胞から膵 ・ 細胞へのダイレクトリプログラミング

从不同细胞谱系的细胞直接重编程为胰腺细胞

• 发表时间: 2014
• 作者: 森田この美;斉藤美知子;河野憲二
• 通讯作者: 河野憲二

Mechanism of diabetes development due to dysfunction of unfolded protein response

未折叠蛋白反应功能障碍导致糖尿病发生的机制

• 发表时间: 2012
• 作者: 斉藤美知子;土屋雄一;岩脇隆夫;森和俊;河野憲二
• 通讯作者: 河野憲二

The Role of the Unfolded Protein Response in Pancreatic β cells

未折叠蛋白反应在胰腺 β 细胞中的作用

• 发表时间: 2012
• 作者: Yuichi Tsuchiya;Michiko Saito;Takao Iwawaki;Jun-ichi Miyazaki;Kazutoshi Mori;Kenji Kohno
• 通讯作者: Kenji Kohno