Analysis of function of PP2C delta/ILKAP that is a novel substrate of caspase3

Caspase3新型底物PP2C delta/ILKAP的功能分析

• 批准号: 24890023
• 负责人: KANTOH YUSUKE
• 金额: $ 1.91万
• 依托单位: Tohoku University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Research Activity Start-up
• 财政年份: 2012
• 资助国家: 日本
• 起止时间: 2012-08-31 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-24890023/
• 关键词: アポトーシス; プロテインホスファターゼ

PP2C delta/ILKAP, a PP2C family member, has been shown to be a pro-apoptotic factor. However, mechanisms of regulation of PP2C delta/ILKAP function has not been known. We reported that PP2C delta/ILKAP was cleaved by caspase3 at Asp39, previously. In this study, we demonstrate that cleavage of PP2C delta/ILKAP suppresses apoptosis in a negative-feedback loop manner in cells.

PP 2C delta/ILKAP是PP 2C家族成员，已被证明是促凋亡因子。然而，PP 2C δ/ILKAP功能的调节机制尚不清楚。我们以前报道过，PP 2C delta/ILKAP在Asp 39被caspase 3切割。在这项研究中，我们证明了PP 2C δ/ILKAP的裂解以负反馈回路的方式抑制细胞凋亡。