Functional analysis of Kinesin superfamily protein in kidney development

驱动蛋白超家族蛋白在肾脏发育中的功能分析

• 批准号: 21770232
• 负责人: TERABAYASHI Takeshi
• 金额: $ 2.91万
• 依托单位: Kumamoto 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-21770232/
• 关键词: 腎臓発生; キネシンスーパーファミリー蛋白質; 細胞骨格; 微小管; 細胞接着; キネシン; 細胞極性

In this study, we performed the functional analysis of Kif26b, a member of kinesin super family proteins. Kif26b is expressed in the metanephric mesenchymes, a population of multipotent kidney progenitors. Disruption of Kif26b causes kidney agenesis because of impaired ureteric bud attraction. In the Kif26b-null metanephros, compact adhesion between mesenchymal cells adjacent to the ureteric buds and the polarized distribution of integrin alpha 8 were impaired, resulting in failed maintenance of Gdnf, a critical ureteric bud attractant. Overexpression of Kif26b in vitro caused increased cell adhesion through interactions with nonmuscle myosin. Thus, Kif26b is essential for kidney development because it regulates the adhesion of mesenchymal cells in contact with ureteric buds.

本研究对驱动蛋白超家族成员Kif 26 b进行了功能分析。Kif 26 b在后肾间充质中表达，后肾间充质是多能肾祖细胞的群体。Kif 26 b的破坏会导致肾发育不全，因为输尿管芽吸引力受损。在Kif 26 b-null后肾中，邻近输尿管芽的间充质细胞之间的紧密粘附和整合素α 8的极化分布受损，导致关键的输尿管芽引诱剂GDNF的维持失败。Kif 26 b在体外过表达通过与非肌肉肌球蛋白的相互作用引起细胞粘附增加。因此，Kif 26 b对于肾脏发育至关重要，因为它调节与输尿管芽接触的间充质细胞的粘附。

项目成果

Par1b/MARK2 Phosphorylates Kinesin-Like Motor Protein GAKIN/KIF13B To Regulate Axon Formation

• DOI: 10.1128/mcb.01181-09
• 发表时间: 2010-03
• 期刊: Molecular and Cellular Biology
• 影响因子: 5.3
• 作者: Yuta Yoshimura;T. Terabayashi;H. Miki

Sall1 is essential for maintenance of nephron progenitors.

Sall1 对于维持肾单位祖细胞至关重要。

• 发表时间: 2009
• 作者: Terabayashi T.;Shuji Inoue;Nishinakamura R.
• 通讯作者: Nishinakamura R.

A Coated Vesicle-associated Kinase of 104 kDa (CVAK104) Induces Lysosomal Degradation of Frizzled 5 (Fzd5)*

• DOI: 10.1074/jbc.m109.039313
• 发表时间: 2009-07
• 期刊: The Journal of Biological Chemistry
• 作者: T. Terabayashi;Y. Funato;M. Fukuda;H. Miki

Nucleoredoxin negatively regulates Toll-like receptor 4 signaling via recruitment of Flightless-I to Myeloid differentiation prinlary response gelle (88).

核氧还蛋白通过将 Flightless-I 招募到骨髓分化主要反应凝胶中，负向调节 Toll 样受体 4 信号传导 (88)。

• 发表时间: 2010
• 期刊: Journal of Biological Chemistry
• 影响因子: 4.8
• 作者: Takashi Okumura;Shunya Hozumi;Kiichiro Taniguchi;Reo Maeda;Kenji Matsuno;林達也
• 通讯作者: 林達也

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