USP53

Last update 08 May 2025

Basic Info

Synonyms

Inactive ubiquitin carboxyl-terminal hydrolase 53, Inactive ubiquitin-specific peptidase 53, KIAA1350

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Introduction

Tight junction-associated protein that is involved in the survival of auditory hair cells and hearing. Maybe by modulating the barrier properties and mechanical stability of tight junctions. Has no peptidase activity (PubMed:14715245).

100 Clinical Results associated with USP53

100 Translational Medicine associated with USP53

0 Patents (Medical) associated with USP53

Literatures (Medical) associated with USP53

01 Mar 2025·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Loss of hepatocyte Usp53 protects mice from a form of xenobiotic-induced liver injury

Review

Author: She, Hui-Yu ; Xing, Qing-He ; Zhang, Jing ; Yang, Jing ; Chi, Hao ; Wang, Ren-Xue ; Ding, Jian ; Wang, Jian-She ; Ling, Victor ; Qiu, Yi-Ling

BACKGROUNDUbiquitin-specific protease 53 (USP53) deficiency is associated with familial intrahepatic cholestasis in which serum gamma-glutamyl transferase (GGT) activity is relatively low. However, how USP53 deficiency contributes to cholestasis is obscure. No animal model has been reported.METHODSUsp53 liver-specific knockout (Usp53 cKO) mice generated by crossing Usp53^fl/fl mice with albumin-cre (Alb-cre) recombinase transgenic mice were challenged with dietary cholic acid (CA) or 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC). General well-being, hepatobiliary-injury biomarker values, histopathologic and ultrastructural appearances, and expression of key genes were compared with those in wild-type (WT) littermates. Interactions of USP53 and TJP2 were investigated by immunofluorescence and co-immunoprecipitation.RESULTSUsp53 cKO mice exhibited no obvious differences from WT mice when fed with either normal-chow or CA-added diet. However, after 4 weeks of DDC feeding, Usp53 cKO mice lost less weight, were less icteric, had more nearly normal biomarker values, and accumulated less intrahepatic pigment than WT mice. On normal chow, mRNA expression of critical hepatic transporters Abcb11, Ntcp, and Abcc2 was lower in Usp53 cKO liver than in WT liver; after DDC feeding, mRNA expression of Tjp2 was higher, while detoxification enzymes Cyp3a11, Cyp2b10, and Sult2a1 was lower in Usp53 cKO liver than in WT liver, and hepatocellular tight junctions were significantly longer. USP53 interacts with TJP2.CONCLUSIONSUsp53 deficiency can protect mice from DDC-induced liver injury. Liver Usp53 cKO causes upregulation of hepatobiliary Tjp2, with biochemical and histologic features that largely mimic those of liver Tjp2 cKO, implying that USP53 deficiency may share similar mechanism to TJP2 deficiency.

01 Mar 2025·International Journal of Biological Macromolecules

Protein molecular structures of USP53, NPY2R, and DCTN1-AS1 and impact on tumors: Analysis of prognostic biomarkers for diffuse large B-cell lymphoma

Article

Author: Shi, Runze ; Jia, Fan ; Gao, Shiqi ; Zhang, Han ; Ma, Jianli ; Zhao, Wenhui ; Zhao, Shu

In the past few years, three protein molecules-USP53, NPY2R, and DCTN1-AS1-have garnered significant attention in scientific research due to their potential implications in tumor development. Mass spectrometry and proteomics techniques were used to analyze the three-dimensional structure of these protein molecules and predict their active sites and functional domains. The effects of USP53, NPY2R and DCTN1-AS1 on biological behavior of tumor cells were studied by constructing gene knockout and overexpression cell models. The data showed that when USP53 was overexpressed, there was a notable enhancement in both the proliferation and invasion capabilities of tumor cells, indicating its potential role in promoting cancer aggressiveness. Conversely, the knockout of USP53 resulted in a significant reduction of these capabilities, highlighting its importance in tumor cell behavior. Similarly, the overexpression of NPY2R correlated with an increased apoptosis rate among tumor cells, suggesting that this protein may play a role in regulating cell survival. On the other hand, the knockout of DCTN1-AS1 markedly diminished the metastatic ability of the tumor cells, emphasizing its potential involvement in cancer spread. Furthermore, the analysis of clinical data provided compelling evidence that high levels of USP53 and NPY2R expression are closely linked to a poor prognosis for patients, suggesting that these proteins could serve as negative prognostic indicators. In contrast, low levels of DCTN1-AS1 expression were found to predict a poor response to treatment, further underscoring its importance in the context of therapy outcomes.

06 Dec 2024·Journal of Molecular Endocrinology

ATF3 suppresses 3T3-L1 adipocyte adipogenesis by transcriptionally repressing USP53

Article

Author: Li, Jun ; Li, Haoyue ; Xu, Yuling ; Hu, Huimin ; Ye, Man

Obesity is a widespread nutritional disorder, leading to a strong predisposition toward adverse health consequences. Activating transcription factor 3 (ATF3), a stress-induced transcription factor, has been documented as a therapeutic target for obesity. The intent of this project was to characterize the detailed role of ATF3 in adipogenesis in the context of obesity and its obscure downstream mechanism. After adipogenic differentiation, RT-qPCR and western blot examined ATF3 and ubiquitin-specific peptidase 53 (USP53) mRNA levels and protein levels. Adipogenesis was identified by Oil Red O staining, triglyceride (TG) levels, and western blot analysis. JASPAR database, ChIP and luciferase reporter assays predicted and validated the transcriptional regulation of USP53 by ATF3. Western blot also examined the protein levels of Ras homolog family member A (RhoA)/Rho-associated coiled-coil kinase (ROCK) pathway-involved proteins. ATF3 mRNA and protein levels were depleted in the differentiated 3T3-L1 adipocytes, and ATF3 elevation hindered the adipogenesis of 3T3-L1 adipocytes. ATF3 suppressed the transcription of USP53 as a transcription factor and lowered USP53 expression. Eventually, USP53 upregulation partially blunted the inhibitory role of ATF3 overexpression in adipogenesis and the RhoA/ROCK pathway. Consequently, ATF3 might transcriptionally inactivate USP53 to repress adipocyte adipogenesis and downregulate the RhoA/ROCK pathway.

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USP53

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