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USP2 可变剪接的调控分子机制及其产物的意义。

The Molecular Mechanisms of Regulation on USP2's Alternative Splicing and the Significance of Its Products.

机构信息

Department of Oncology, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhi Zao Ju Rd, Shanghai, China.

出版信息

Int J Biol Sci. 2017 Nov 2;13(12):1489-1496. doi: 10.7150/ijbs.21637. eCollection 2017.

DOI:10.7150/ijbs.21637
PMID:29230097
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5723915/
Abstract

Ubiquitin-specific protease 2 (USP2) has a regulatory function in cell growth or death and is involved in the pathogenesis of various diseases. USP2 gene can generate 7 splicing variants through alternative splicing, and 5 variants respectively as USP2-201, USP2-202, USP2-204, USP2-205, USP2-206 can encode proteins. The influence of circadian rhythm, nutrition and androgen on specific signaling molecules or cytokines can regulate the alternative splicing of USP2. Specifically, PKC activator, IL-1β, TNF-α, PDGF-BB, TGF-β1 are all regulatory factors for USP2's alternative splicing. USP2-201 plays a crucial role in cell cycle progression, and is also of great significance in EGFR recycling. USP2-202 can activate apoptosis signaling pathway to participate in cell apoptosis, and USP2-204 can induce cell anti-virus reaction to decrease. In general, we collect and summarize the factors involved in the alternative splicing of USP2 in this review to further understand the mechanism behind the USP2's alternative splicing.

摘要

泛素特异性蛋白酶 2(USP2)在细胞生长或死亡中具有调节功能,并且参与各种疾病的发病机制。USP2 基因可以通过选择性剪接产生 7 种剪接变体,其中 5 种变体分别为 USP2-201、USP2-202、USP2-204、USP2-205、USP2-206,可以编码蛋白质。昼夜节律、营养和雄激素对特定信号分子或细胞因子的影响可以调节 USP2 的选择性剪接。具体而言,PKC 激活剂、IL-1β、TNF-α、PDGF-BB、TGF-β1 都是 USP2 选择性剪接的调节因子。USP2-201 在细胞周期进展中起着至关重要的作用,在 EGFR 回收中也具有重要意义。USP2-202 可以激活凋亡信号通路参与细胞凋亡,USP2-204 可以诱导细胞抗病毒反应减少。总的来说,我们在这篇综述中收集并总结了参与 USP2 选择性剪接的因素,以进一步了解 USP2 选择性剪接的机制。

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High dietary Fructose Drives Metabolic Dysfunction-Associated Steatotic Liver Disease via Activating ubiquitin-specific peptidase 2/11β-hydroxysteroid dehydrogenase type 1 Pathway in Mice.高膳食果糖通过激活泛素特异性肽酶 2/11β-羟类固醇脱氢酶 1 途径导致代谢功能障碍相关脂肪性肝病。
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