杜比基酶Leon/USP5与Atg1/ULK1相互作用并对抗自
Yueh-Ling Pai1, Yuchieh Jay Lin2,3, Wen-Hsin Peng1
1Institute of Biological Chemistry, Academia Sinica, Taipei, 115, Taiwan.
Cell death & disease
|August 22, 2023
概括
莱昂/USP5,一个二基化酶 (DUB),负面调节自. 削减Leon/USP5通过与Atg1/ULK1.1相互作用,增加了自细胞形成和自流量.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 细胞蛋白质稳定依赖于蛋白质质量控制,涉及到全方位蛋白质酶体系统 (UPS) 和自-溶酶体通路.
- 脱化酶 (DUB) 是UPS的关键调节者,但它们在自中的作用尚不清楚.
研究的目的:
- 为了研究duebiquitinating酶 (DUBs) 在自调节中的功能.
- 阐明Leon/USP5在自过程中的作用.
主要方法:
- 在细胞和Drosophila模型中,Leon/USP5的淘汰和过度表达.
- 自细胞形成和自流量测试.
- 基因分析和免疫阻塞检测与自相关蛋白的相互作用.
主要成果:
- 击败Leon/USP5显著增加了自细胞形成和自流量.
- 过度表达Leon抑制了Drosophila中的Atg1诱导的细胞死亡.
- 莱昂/USP5直接与自启动激酶Atg1/ULK1.1相互作用.
- 莱昂/USP5的耗尽导致Atg1/ULK1水平升高.
结论:
- 莱昂/USP5作为自的DUB功能.
- 莱昂/USP5通过与Atg1/ULK1.1的相互作用来负面调节自.
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