Involvement of SUMOylation in pathogenesis of neural diseases

SUMO化参与神经疾病的发病机制

• 批准号: 23790224
• 负责人: MATSUZAKI Shinsuke
• 金额: $ 2.75万
• 依托单位: Osaka University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23790224/
• 关键词: SUMO 化; アルツハイマー病; 小胞体ストレス; 細胞死; 神経変性疾患; SUMO化; 国際研究者交流; カナダ; トロント; 国際情報交流; スモ化

In this project, effects of SUMOylation on neural system has been investigated to elucidate the involvement of it in the pathogenesis of neural and neurodegenerative diseases. As results, SUMOylation should play important roles to maintain synaptic functions and protective function against the neural death pathway observed in neurodegenerative diseases, especially ER stress pathway. The data show that SUMOylation regulates CHOP expression, one of inducers of apoptosis. These results suggest that neural SUMOylation should work protectively against ER stress and regulates the synapse function in neural and neurodegenerative disease.

在该项目中，研究了 SUMOylation 对神经系统的影响，以阐明它在神经和神经退行性疾病发病机制中的作用。因此，SUMO化在维持突触功能和针对神经退行性疾病中观察到的神经死亡途径（尤其是内质网应激途径）的保护功能方面发挥着重要作用。数据显示SUMO化调节CHOP表达，CHOP表达是细胞凋亡的诱导剂之一。这些结果表明，神经 SUMO 化应该对 ER 应激起到保护作用，并调节神经和神经退行性疾病中的突触功能。

项目成果

Ubiquitin, UBL Proteins: Implications for Human Diseases, Neuronal SUMOylation and Its Contributions to Form, Function and Neurodegenerative Diseases

泛素、UBL 蛋白：对人类疾病的影响、神经元 SUMO 化及其对形式、功能和神经退行性疾病的贡献

• 发表时间: 2012
• 作者: Shinsuke Matsuzaki; Kohei Yamada; Nicola St George;Paul Fraser
• 通讯作者: Paul Fraser

KIAA2022 is expressed transiently and regulates neurite outgrowth．

KIAA2022 短暂表达并调节神经突生长。

• 发表时间: 2012
• 作者: Toshiko Ishikawa; Shingo Miyata; Yoshihisa Koyama; Shinsuke Matsuzaki; Kouhei Yamada; Hironori Takamura; Takuya Magome; Taiichi Katayama; Masaya Tohyama
• 通讯作者: Masaya Tohyama

Involvement of SUMOylation in Plaque and Tangle Pathology.

SUMOylation 参与斑块和缠结病理学。

• 发表时间: 2012
• 作者: Shinsuke Matsuzaki; Kohei Yamada;Nicola St George
• 通讯作者: Nicola St George

NGF-p75 and neuropsin/KLK8 pathways stimulate each other to cause hyperkeratosis and acanthosis in inflamed skin.

NGF-p75 和神经蛋白酶/KLK8 通路相互刺激，导致发炎皮肤角化过度和棘皮症。

• 发表时间: 2012
• 作者: Shingaki K; Taniguchi M; Kanazawa S; Matsuzaki S; Maeda T; Miyata S; Kubo T; Torii K; Shiosaka S; Tohyama M.
• 通讯作者: Tohyama M.

KIAA2022 is expressed transiently and regulates neurite outgrowth

KIAA2022 短暂表达并调节神经突生长

• 发表时间: 2012
• 作者: Toshiko Ishikawa; Shingo Miyata; Yoshihisa Koyama; Shinsuke Matsuzaki; Kouhei Yamada; Hironori Takamura; Takuya Magome; Taiichi Katayama; Masaya Tohyama
• 通讯作者: Masaya Tohyama