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通过其C2域,自抑制HECT类型的泛素化酶Smurf2的自抑制

Silke Wiesner¹, Abiodun A Ogunjimi, Hong-Rui Wang

¹Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada. silke@pound.med.utoronto.ca

|August 28, 2007

概括

蛋白质无化调节细胞过程. 史默夫2 E3 的结合酶.

科学领域:

分子生物学分子生物学
生物化学生物化学
细胞生物学细胞生物学

背景情况:

蛋白质ubiquitination是一个关键的翻译后修改控制多样化的细胞功能.
乌比基因酶 (E3s) 调解基质的乌比基因化,通常针对自身和基质进行降解.
控制E3结合酶催化活性的机制在很大程度上仍未被阐明.

研究的目的:

研究C2-WW-HECT-域E3连接酶的调节机制,重点是Smurf2.
阐明Smurf2的催化活性是如何控制的,以防止基质和自身不受控制的降解.

主要方法:

生物化学测定用于研究Smurf2活动和相互作用.
核磁共振 (NMR) 谱学用于分析域相互作用.
细胞研究以评估Smurf2在体内稳定性和功能.

主要成果:

Smurf2 的 C2 和 HECT 域之间的分子内相互作用抑制了它的结合酶活性.
这种C2-HECT相互作用稳定了细胞内的Smurf2蛋白水平.
核磁共振分析显示,C2域与催化氨酸附近结合,阻碍了全方位氨酸 thioester 的形成.
Smad7结合对抗抑制的C2-HECT相互作用,激活了Smurf2.2.

结论:

通过C2-HECT域相互作用自抑制是一种调节HECT型E3酶子集的机制.
这种自身抑制机制保护E3链酶及其基质免受过早或徒劳的降解.
了解这种调节可以了解控制TGF-β信号传递和其他由Smurf2.2调解的途径.

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