USP47

更新于：2024-11-01

基本信息

别名

Deubiquitinating enzyme 47、Ubiquitin carboxyl-terminal hydrolase 47、ubiquitin specific peptidase 47

+ [3]

简介

Ubiquitin-specific protease that specifically deubiquitinates monoubiquitinated DNA polymerase beta (POLB), stabilizing POLB thereby playing a role in base-excision repair (BER). Acts as a regulator of cell growth and genome integrity. May also indirectly regulate CDC25A expression at a transcriptional level.

关联

项与 USP47 相关的药物

P22077

靶点

USP47 x USP7

作用机制

USP47 inhibitors [+1]

在研机构

上海交通大学医学院 [+1]

原研机构

Progenra, Inc.

在研适应症

慢性粒细胞性白血病 [+1]

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 USP47 相关的临床结果

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100 项与 USP47 相关的转化医学

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0 项与 USP47 相关的专利（医药）

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项与 USP47 相关的文献（医药）

2024-07-01·International Immunopharmacology

Role of deubiquitinase USP47 in cardiac function alleviation and anti-inflammatory immunity after myocardial infarction by regulating NLRP3 inflammasome-mediated pyroptotic signal pathways

Article

作者: Li, Wenzheng ; Wu, Zheng ; Zheng, Ze ; Wang, Shaoping

Myocardial infarction (MI) is an event of heart attack due to the formation of plaques in the interior walls of the arteries. This study is conducted to explore the role of ubiquitin-specific peptidase 47 (USP47) in cardiac function and inflammatory immunity. MI mouse models were established, followed by an appraisal of cardiac functions, infarct size, pathological changes, and USP47 and NLRP3 levels. MI cell models were established in HL-1 cells using anoxia. Levels of cardiac function-associated proteins, USP7, interferon regulatory factor 1 (IRF1), platelet factor-4 (CXCL4), pyroptotic factors, and neutrophil extracellular traps (NETs) were determined. The bindings of IRF1 to USP47 and the CXCL4 promoter and the ubiquitination of IRF1 were analyzed. USP47 was upregulated in myocardial tissues of MI mice. USP47 inhibition alleviated cardiac functions, and decreased infarct size, pro-inflammatory cytokines, NETs, NLRP3, and pyroptosis. The ubiquitination and expression levels of IRF1 were increased by silencing USP47, and IRF1 bound to the CXCL4 promoter to promote CXCL4. Overexpression of IRF1 or CXCL4 in vitro and injection of Nigericin in vivo reversed the effect of silencing USP47 on alleviating pyroptosis and cardiac functions. Collectively, USP47 stabilized IRF1 and promoted CXCL4, further promoting pyroptosis, impairing cardiac functions, and aggravating immune inflammation through NLRP3 pathways.

2024-02-09·Oncogene

USP47 stabilizes YBX1 to promote the progression of acute myeloid leukemia

Letter

作者: Lei, Hu ; Zhang, Youping ; Xu, Hanzhang ; Yang, Li ; Wu, Yingli ; Wang, Yingying

2024-02-01·Chemical Biology & Drug Design

Icariin promotes osteogenic differentiation of human bone marrow mesenchymal stem cells by regulating USP47/SIRT1/Wnt/β‐catenin

Article

作者: Zhang, Hongyue ; Wang, Panfeng ; Wang, Hongrui ; Zhang, Yuntong

AbstractIcariin has been shown to promote osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). However, the underlying molecular mechanism by which Icariin regulates osteogenic differentiation needs to be further revealed. The viability of BMSCs was assessed by cell counting kit 8 assay. BMSC osteogenic differentiation ability was evaluated by detecting alkaline phosphatase activity and performing alizarin red S staining. The protein levels of osteogenic differentiation‐related markers, sirtuin 1 (SIRT1), ubiquitin‐specific protease 47 (USP47), and Wnt/β‐catenin‐related markers were determined using western blot. SIRT1 mRNA level was measured using quantitative real‐time PCR. The regulation of USP47 on SIRT1 was confirmed by ubiquitination detection and co‐immunoprecipitation analysis. Icariin could promote BMSC osteogenic differentiation. SIRT1 expression was enhanced by Icariin, and its knockdown suppressed Icariin‐induced BMSC osteogenic differentiation. Moreover, deubiquitinating enzyme USP47 could stabilize SIRT1 protein expression. Besides, SIRT1 overexpression reversed the inhibiting effect of USP47 knockdown on BMSC osteogenic differentiation, and USP47 knockdown also restrained Icariin‐induced BMSC osteogenic differentiation. Additionally, Icariin enhanced the activity of the Wnt/β‐catenin pathway by upregulating SIRT1. Icariin facilitated BMSC osteogenic differentiation via the USP47/SIRT1/Wnt/β‐catenin pathway.