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TRiM25 inhibits HBV replication by promoting HBx degradation and the rig-i-mediated pgRNA recognition

Chinese Medical Journal 2023年第7期136卷 799-806页

作者： Hongxiao Song Qingfei Xiao Fengchao Xu Qi Wei Fei Wang Guangyun Tan Department of Hepatology Center for Pathogen Biology and Infectious DiseasesInstitute of Translational MedicineThe First Hospital of Jilin UniversityChangchunJilin 130000China Department of Nephrology The First Hospital of Jilin UniversityChangchunJilin 130000China Department of Anesthesiology The First Hospital of Jilin UniversityChangchunJilin 130000China

Background:The hepatitis B virus(HBV)vaccine has been efficiently used for ***,hepatocellular carcinoma caused by HBV is still prevalent *** previously reported that interferon(iFN)-induced tripartite motif-containing 25(TRiM25)inhibited HBV replication by increasing the iFN expression,and this study aimed to further clarify the anti-HBV mechanism of ***:The TRiM25-mediated degradation of hepatitis B virus X(HBx)protein was determined by detecting the expression of HBx in TRiM25-overexpressed or knocked-out HepG2 or HepG2-NTCP cells via Western ***-immunoprecipitation was performed to confirm the interaction between TRiM25 and HBx,and colocalization of TRiM25 and HBx was identified via immunofluorescence;HBV e-antigen and HBV surface antigen were qualified by using an enzyme-linked immunosorbent assay(ELiSA)kit from Kehua ***25 mRNA,pregenomic RNA(pgRNA),and HBV DNA were detected by quantitative real-time polymerase chain *** retinoic acid-inducible gene i(rig-i)and pgRNA interaction was verified by RNA-binding protein immunoprecipitation ***:We found that TRiM25 promoted HBx degradation,and confirmed that TRiM25 could enhance the K90-site ubiquitination of HBx as well as promote HBx degradation by the proteasome ***,apart from the Really interesting New Gene(RiNG)domain,the SPRY domain of TRiM25 was also indispensable for HBx *** addition,we found that the expression of TRiM25 increased the recognition of HBV pgRNA by interacting with rig-i,which further increased the iFN production,and SPRY,but not the RiNG domain is critical in this ***:The study found that TRiM25 interacted with HBx and promoted HBx-K90-site ubiquitination,which led to HBx *** the other hand,TRiM25 may function as an adaptor,which enhanced the recognition of pgRNA by rig-i,thereby further promoting iFN *** study can contribute to a better understanding of host-vir

关键词： HBx Hepatitis B virus pgRNA rig-i TRiM25

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Viral suppression of type i interferon signaling by NSs of DBV,SFSV and UUKV via NSs-mediated rig-i degradation

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Biosafety and Health 2022年第4期4卷 244-252页

作者： Leling Xu Xueping Li Xiaoning Gao Sihua Liu Zheng Pang Zhiyun Wang School of Life Sciences Tianjin UniversityTianjin 300072China The Key Laboratory of Molecular Microbiology and Technology Ministry of EducationNankai UniversityTianjin 300071China Tianjin international Joint Academy of Biomedicine Tianjin 300457China School of Environmental Science and Engineering Tianjin UniversityTianjin 300072China

Phenuiviridae,a member of the Bunyavirales order,can lead to significant human morbidity and *** phenuiviruses target specific cellular proteins and have strategies to counteract the effects of type i interferon(iFN).Previous studies have shown that phenuiviruses infection inhibits the synthesis of type i iFNs,and viral nonstructural proteins(NSs)had been further identified as an iFN *** study found that the NSs proteins of Dabie bandavirus(DBV),Sandfly fever Sicilian virus(SFSV),and Uukuniemi virus(UUKV)can inhibit Sendai virus-induced activation of iFN-βpromoter and phosphorylation of iFN regulatory factor 3(iRF3).Moreover,detailed analysis revealed that the phenuivirus NSs protein could directly interact with retinoic acid inducible gene-i(rig-i)and degrade it via a proteasome-dependent *** short,this study demonstrate a novel mechanism of phenuiviruses to resist host antiviral immunity,which may help understand these pathogens and suggest novel therapeutic approaches.

关键词： Phenuiviridae innate immunity iFN signaling NSs rig-i

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rig-i： a multifunctional protein beyond a pattern recognition receptor

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Protein & Cell 2018年第3期9卷 246-253页

作者： Xiao-xiao Xu Han Wan Li Nie Tong Shao Li-xin Xiang Jian-zhong Shao Key Laboratory for Cell and Gene Engineering of Zhejiang Province College of Life Sciences Zhejiang University Hangzhou 310058 China Laboratory for Marine Biology and Biotechnology Qingdao National Laboratory for Marine Science and Technology Qingdao 266235 China

it was widely known that retinoic acid inducible gene i （rig-i） functions as a cytosolic pattern recognition receptor that initiates innate antiviral immunity by detecting exogenous viral RNAs. However, recent stud- ies showed that rig-i participates in other various cellular activities by sensing endogenous RNAs under different circumstances. For example, rig-i facilitates the therapy resistance and expansion of breast cancer cells and promotes T cell-independent B cell activation through interferon signaling activation by recognizing non-coding RNAs and endogenous retroviruses in certain situations. While in hepatocellular carcinoma and acute myeloid leukemia, rig-i acts as a tumor suppressor through either augmenting STAT1 activation by competitively binding STAT1 against its negative regulator SliP1 or inhibiting AKT-mTOR signaling pathway by directly interacting with Src respectively. These new findings suggest that rig-i plays more diverse roles in various cellular life activities, such as cell proliferation and differentiation, than previously known. Taken together, the function of rig-i exceeds far beyond that of a pattern recognition receptor.

关键词： rig-i viral RNA endogenous RNA immunity cancer

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rig-i immunotherapy overcomes radioresistance in p53-positive malignant melanoma

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分子细胞生物学报:英文版 2023年第1期15卷 13-26页

作者： Silke Lambing Yu Pan Tan Paraskevi Vasileiadou Stefan Holdenrieder Patrick Müller Christian Hagen Stephan Garbe Rayk Behrendt Martin Schlee Jasper G.van den Boorn Eva Bartok Marcel Renn Gunther Hartmann institute of Clinical Chemistry and Clinical Pharmacology University Hospital BonnBonn 53127Germany institute of Laboratory Medicine German Heart CentreMunich 80636Germany Department of Radiation Oncology University Hospital BonnBonn 53127Germany Unit of Experimental immunology Department of Biomedical SciencesInstitute of Tropical MedicineAntwerp 2000Belgium institute of Experimental Haematology and Transfusion Medicine University Hospital BonnBonn 53127Germany Mildred Scheel School of Oncology BonnUniversity Hospital BonnMedical FacultyBonn 53127Germany

Radiotherapy induces DNA damage,resulting in cell cycle arrest and activation of cell-intrinsic death ***,the radioresistance of some tumour entities such as malignant melanoma limits its clinical *** innate immune sensing receptor retinoic acid-inducible gene i(rig-i)is ubiquitously expressed and upon activation triggers an immunogenic form of cell death in a variety of tumour cell types including *** date,the potential of rig-i ligands to overcome radioresistance of tumour cells has not been ***,we demonstrate that rig-i activation enhanced the extent and immunogenicity of irradiation-induced tumour cell death in human and murine melanoma cells in vitro and improved survival in the murine B16 melanoma model in *** analysis pointed to a central role for p53,which was confirmed using p53^(-/-)B16 *** vivo,the additional effect of rig-i in combination with irradiation on tumour growth was absent in mice carrying p53^(-/-)B16 tumours,while the antitumoural response to rig-i stimulation alone was *** results identify p53 as a pivotal checkpoint that is triggered by rig-i resulting in enhanced irradiation-induced tumour cell ***,the combined administration of rig-i ligands and radiotherapy is a promising approach to treating radioresistant tumours with a functional p53 pathway,such as melanoma.

关键词： rig-i p53 melanoma immunotherapy irradiation radiotherapy radioresistance

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Unanchored ubiquitin chain sustains rig-i-induced interferon-i activation and controls selective gene expression

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Science Bulletin 2021年第8期66卷 794-802,M0004页

作者： Huifang Xian Wanming Huang Tingzhe Sun Shuai Yang Chuanxia Zhang Jun Wang Yuxia Zhang Jun Cui MOE Key Laboratory of Gene Function and Regulation State Key Laboratory of BiocontrolSchool of Life SciencesSun Yat-sen UniversityGuangzhou 510275China Department of Gastroenterology Guangzhou Institute of PediatricsGuangzhou Women and Children’s Medical CenterGuangzhou Medical UniversityGuangzhou 510623China School of Life Sciences Anqing Normal UniversityAnqing 246133China

Ubiquitination plays a crucial role in retinoic acid-inducible gene i(rig-i)-induced antiviral ***, the precise regulatory mechanisms of rig-i activity mediated by conjugated and unanchored ubiquitin chains remain to be determined. in this study, we discovered that T55 of rig-i was required for its binding ability for the unanchored ubiquitin chains. Experimental and mathematical analysis showed that unanchored ubiquitin chains associated with rig-i were essential for sustained activation of type i interferon(iFN) signaling. Transcriptomics study revealed that the binding of rig-i with unanchored ubiquitin chains additionally regulated the expression of a subset of metabolic and cell fate decision genes. Moreover, we found that ubiquitin-specific peptidase 21(USP21) and USP3 deubiquitinate conjugated and unanchored ubiquitin chains on rig-i respectively. Taken together, characterization of the regulation mode and functions of conjugated ubiquitination and the unconjugated ubiquitin chainbinding of rig-i may provide means to fine-tune rig-i-mediated type i iFN signaling.

关键词： Antiviral immunity Type i interferon Ubiquitination rig-i Unanchored ubiquitin chains Cellular homeostasis

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Ectopic Expression of TRiM25 Restores rig-i Expression and iFN Production Reduced by Multiple Enteroviruses 3Cpro

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Virologica Sinica 2021年第6期36卷 1363-1374页

作者： Huimin Xiao Jingliang Li Xu Yang Zhaolong Li Ying Wang Yajuan Rui Bin Liu Wenyan Zhang institute of Virology and AiDS Research Key Laboratory of Organ Regeneration and Transplantation of The Ministry of EducationThe First Hospital of Jilin UniversityChangchun130021China Cancer institute(Key Laboratory of Cancer Prevention and intervention Ministry of Education)Second Affiliated HospitalSchool of MedicineZhejiang UniversityHangzhou310058China Department of Hand Surgery First Hospital of Jilin UniversityChangchun130021China Changchun institute of Biological Products Co. LtdChangchun130012China

Enteroviruses(EVs) 3C proteins suppress type i interferon(iFN) responses mediated by retinoid acid-inducible gene i(rig-i), while an E3 ubiquitin ligase, tripartite motif protein 25(TRiM25)-mediated rig-i ubiquitination is essential for rig-i antiviral activity. Therefore, whether the effect of EVs 3C on rig-i is associated with TRiM25 expression is worth to be further investigated. Here, we demonstrate that 3C proteins of EV71 and coxsackievirus B3(CVB3) reduced not only rig-i expression but also TRiM25 expression through protease cleavage activity, while overexpression of TRiM25 restored rig-i expression and iFN-b production reduced by 3C proteins. Further investigation confirmed that the two amino acids and functional domains in TRiM25 required for rig-i ubiquitination and TRiM25 structural conformation were essential for the recovery of rig-i expression. Moreover, we also observed that TRiM25 could rescue rig-i expression reduced by 3C proteins of CVA6 and EV-D68 but not CVA16. Our findings provide an insightful interpretation of 3C-mediated host innate immune suppression and support TRiM25 as an attractive target against multiple EVs infection.

关键词： 3C proteins rig-i TRiM25 innate immunity Enteroviruses(EVs)

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TRiM4 modulates type i interferon induction and cellular antiviral response by targeting rig-i for K63-1inked ubiquitination

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Journal of Molecular Cell Biology 2014年第2期8卷 154-163页

作者： Jie Yan Qi Li Ai-Ping Mao Hong-Bing Shu College of Life Sciences Wuhan University Wuhan 430072 China

rig-i is a pivotal cytoplasmic sensor that recognizes different species of viral RNAs. This recognition leads to activation of the transcription factors NF-κB and iRF3, which collaborate to induce type i interferons （iFNs） and innate antiviral response. in this study, we identified the TRiM family protein TRiM4 as a positive regulator of rig-i-mediated iFN induction. Overexpression of TRiM4 potentiated virus-triggered activation of iRF3 and NF-κB, as well as iFN-13 induction, whereas knockdown of TRiM4 had opposite effects. Mechanistically, TRiM4 associates with rig-i and targets it for K63-linked poiyubiquitination. Our findings demonstrate that TRiM4 is an important regulator of the virus-induced iFN induction pathways by mediating rig-i for K63-Unked ubiquitination.

关键词： TRiM4 rig-i ubiquitination type i interferon antiviral response

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SUMOylation of rig-i positively regulates the type i interferon signaling

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Protein & Cell 2010年第3期1卷 275-283页

作者： Zhiqiang Mi Jihuan Fu Yanbao Xiong Hong Tang Center for Molecular immunology Institute of MicrobiologyChinese Academy of SciencesBeijing 100101China Key Laboratory of infection and immunity of Chinese Academy of Sciences Institute of BiophysicsBeijing 100101China

Retinoic acid-inducible gene-i(rig-i)functions as an intracellular pattern recognition receptor(PRR)that recognizes the 5'-triphosphate moiety of single-stranded RNA viruses to initiate the innate immune *** studies have shown that Lys63-linked ubiquitylation is required for rig-i activation and the downstream anti-viral type i interferon(iFN-i)*** we reported that,rig-i was also modified by small ubiquitin-like modifier-1(SUMO-1).Functional analysis showed that rig-i SUMOylation enhanced iFN-i production through increased ubiquitylation and the interaction with its downstream adaptor molecule *** results therefore suggested that SUMOylation might serve as an additional regulatory tier for rig-i activation and iFN-i signaling.

关键词： rig-i SUMOylation type i interferon innate immunity

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Emerging complexity and new roles for the rig-i-like receptors in innate antiviral immunity

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Virologica Sinica 2015年第3期30卷 163-173页

作者： John S.Errett Michael Gale Jr. Center for innate immunity and immune Disease Department of Immunology School of Medicine University of Washington

innate immunity is critical for the control of virus infection and operates to restrict viral susceptibility and direct antiviral immunity for protection from acute or chronic viral-associated diseases including cancer. rig-i like receptors(RLRs) are cytosolic RNA helicases that function as pathogen recognition receptors to detect RNA pathogen associated molecular patterns(PAMPs) of virus infection. The RLRs include rig-i, MDA5, and LGP2. They function to recognize and bind to PAMP motifs within viral RNA in a process that directs the RLR to trigger downstream signaling cascades that induce innate immunity that controls viral replication and spread. Products of RLR signaling also serve to modulate the adaptive immune response to infection. Recent studies have additionally connected RLRs to signaling cascades that impart inflammatory and apoptotic responses to virus infection. Viral evasion of RLR signaling supports viral outgrowth and pathogenesis, including the onset of viral-associated cancer.

关键词： rig-i MDA5 pattern recognition receptor pathogen associated molecular pattern innate immunity virus infection

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Structural and biochemical studies of rig-i antiviral signaling

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Protein & Cell 2013年第2期4卷 142-154页

作者： Miao Feng Zhanyu Ding Liang Xu Liangliang Kong Wenjia Wang Shi Jiao Zhubing Shi Mark iGreene Yao Cong Zhaocai Zhou State Key Laboratory of Cell Biology Institute of Biochemistry and Cell BiologyShanghai Institutes for Biological SciencesChinese Academy of SciencesShanghai 200031China State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell BiologyShanghai Institutes for Biological SciencesChinese Academy of SciencesShanghai 200031China Department of Pathology and Laboratory Medicine University of PennsylvaniaPA 19104USA

Retinoic acid-inducible gene i(rig-i)is an important pattern recognition receptor that detects viral RNA and triggers the production of type-i interferons through the downstream adaptor MAVS(also called iPS-1,CARDiF,or ViSA).A series of structural studies have elaborated some of the mechanisms of dsRNA recognition and activation of *** studies have proposed that K63-linked ubiquitination of,or unanchored K63-linked polyubiquitin binding to rig-i positively regulates MAVS-mediated antiviral *** phos-phorylation of rig-i appears to play an inhibitory role in controlling rig-i antiviral signal *** we performed a combined structural and biochemical study to further define the regulatory features of rig-i *** and dsRNA binding triggered dimeriza-tion of rig-i with conformational rearrangements of the tandem CARD *** length rig-i appeared to form a complex with dsRNA in a 2:2 molar ***-pared with the previously reported crystal structures of rig-i in inactive state,our electron microscopic struc-ture of full length rig-i in complex with blunt-ended dsRNA,for the first time,revealed an exposed active conformation of the CARD ***,we found that purified recombinant rig-i proteins could bind to the CARD domain of MAVS independently of dsRNA,while S8E and T170E phosphorylation-mimick-ing mutants of rig-i were defective in binding E3 ligase TRiM25,unanchored K63-linked polyubiquitin,and MAVS regardless of *** findings suggested that phosphorylation of rig inhibited downstream signaling by impairing rig-i binding with polyubiquitin and its interaction with MAVS.

关键词： rig-i MAVS antiviral signaling polyubiq-uitin phosphorylation

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