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© 2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

OTUD6A is a deubiquitinase that plays crucial roles in various human diseases. However, the precise regulatory mechanism of OTUD6A remains unclear. In this study, we found that OTUD6A significantly inhibited the production of type I interferon. Consistently, peritoneal macrophages and bone marrow-derived macrophages from Otud6a−/− mice produced more type I interferon after virus infection compared to cells from WT mice. Otud6a−/− mice also exhibited increased resistance to lethal HSV-1 and VSV infections, as well as LPS attacks due to decreased inflammatory responses. Mechanistically, mass spectrometry results revealed that UBC13 was an OTUD6A-interacting protein, and the interaction was significantly enhanced after HSV-1 stimulation. Taken together, our findings suggest that OTUD6A plays a crucial role in the innate immune response and may serve as a potential therapeutic target for infectious disease.

Details

Title
Deubiquitinase OTUD6A Regulates Innate Immune Response via Targeting UBC13
Author
Li, Zhiwei 1 ; Li, Guanwen 2 ; Li, Yunfei 3 ; Luo, Yujie 3 ; Jiang, Yuhan 1 ; Zhang, Ziyu 1 ; Zhou, Ziyi 1 ; Liu, Shengde 4 ; Wu, Chen 1 ; You, Fuping 3   VIAFID ORCID Logo 

 College of Life Sciences, Hebei University, Baoding 071002, China; [email protected] (Z.L.); [email protected] (Y.J.); [email protected] (Z.Z.); [email protected] (Z.Z.) 
 College of Life Sciences, South China Agricultural University, Guangzhou 510642, China; [email protected] 
 Department of Systems Biomedicine, Institute of Systems Biomedicine, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China; [email protected] (Y.L.); [email protected] (Y.L.) 
 Department of Gastrointestinal Oncology, Key Laboratory of Carcinogenesis and Translational Research, Peking University Cancer Hospital and Institute, Beijing 100142, China 
First page
1761
Publication year
2023
Publication date
2023
Publisher
MDPI AG
e-ISSN
19994915
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2857443441
Copyright
© 2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.