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TIPE1 induces apoptosis by negatively regulating Rac1 activation in hepatocellular carcinoma cells

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TIPE1 induces apoptosis by negatively regulating Rac1 activa...

第十届全国免疫学学术大会

作者： xiaohong liang Shandong University

TIPE1(tumor necrosis factor-alpha induced protein 8-like 1 or TNFAIP8L1)is a newly identified member of the TIPE(TNFAIP8)family,which play roles in regulating cell ***,the biological functions of TIPE1 in physiological and pathological conditions are largely ***,we report the roles of TIPE1 in hepatocelluar carcinoma(HCC).Evaluated by immunohistochemical staining,HCC tissues showed significantly downregulated TIPE1 expression compared to adjacent nontumor tissues,which positively correlated with tumor pathological grades and patient *** a homograft tumor model in Balb/c mice,we discovered that TIPE1 significantly diminished the growth and tumor weight of murine liver cancer ***,TIPE1 inhibited both cell growth and colony formation ability of cultured HCC cell lines,which was further identified to be due to TIPE1 inducing apoptosis in a caspase-independent,Nec-1-insensitive ***,mechanistic investigations revealed that TIPE1 interacted with Rac1,and inhibited the activation of Rac1 and its downstream p65 and JNK ***,overexpression of constitutively active Rac1partially rescued the apoptosis induced by TIPE1,and Rac1 knockdown significantly restored the deregulated cell growth induced by TIPE1 si *** finding revealed that TIPE1 induced apoptosis in HCC cells by negatively regulating Rac1 pathway,and loss of TIPE1 might be a new prognostic indicator for HCC patients.

关键词： TIPE1 HCC apoptosis Rac1

Palmitoylation of SARS-CoV-2 S protein is essential for viral infectivity

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Signal Transduction and Targeted Therapy 2021年第7期6卷 1989-1992页

作者： Zhuanchang Wu Zhaoying Zhang Xin Wang Jing Zhang Caiyue Ren Yuming Li Lifen Gao xiaohong liang Peihui Wang Chunhong Ma Key Laboratory for Experimental Teratology of Ministry of Education and Dept.Immunology School of Basic Medical SciencesCheeloo Medical CollegeShandong UniversityJinanShandongChina College of Agriculture and Forestry Linyi UniversityLinyiShandongChina Advanced Medical Research Institute Shandong UniversityJinanShandongChina State Key Laboratory of Respiratory Disease National Clinical Research Center for Respiratory DiseaseGuangzhou Institute of Respiratory HealthThe First Affiliated Hospital of Guangzhou Medical UniversityGuangzhouChina Key Laboratory of Infection and Immunity of Shandong Province Shandong UniversityJinanShandongChina Collaborative Innovation Center of Technology and Equipment for Biological Diagnosis and Therapy in Universities of Shandong JinanShandongChina

Dear Editor,Severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)is the causative agent of the unprecedented coronavirus disease 2019(COVID-19).SARS-CoV-2 entry into host cells is mediated by the viral transmemb... 详细信息

关键词： acute respiratory glycoprotein

Peptide targeting the interaction of S protein cysteine-rich domain with Ezrin restricts pan-coronavirus infection

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Signal Transduction and Targeted Therapy 2023年第2期8卷 361-364页

作者： Zhuanchang Wu Xiaobo Lei Xin Wang Zhaoying Zhang Yuming Li Lifen Gao xiaohong liang Peihui Wang Jianwei Wang Chunhong Ma Key Laboratory for Experimental Teratology of Ministry of Education Key Laboratory of Infection and Immunity of Shandong Province and Dept.ImmunologySchool of Basic Medical SciencesCheeloo Medical CollegeShandong University250012JinanShandongChina NHC Key Laboratory of Systems Biology of Pathogens Institute of Pathogen BiologyChinese Academy of Medical Sciences and Peking Union Medical College100730BeijingChina College of Agriculture and Forestry Linyi UniversityLinyiShandongChina School of Public Health Shandong First Medical University&Shandong Academy of Medical Sciences271016Tai’anChina Key Laboratory for Experimental Teratology of Ministry of Education and Advanced Medical Research Institute Shandong University250012JinanShandongChina

Dear Editor,To date,seven human coronaviruses(HCoVs)have been identified,among which the highly pathogenic severe acute respiratory syndrome-associated coronavirus(SARS-CoV),Middle East respiratory syndrome coronavirus(MERS-CoV),and severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)have caused public health disasters worldwide.

关键词： respiratory acute Ezrin

Increased Tim-3 expression alleviates liver injury by regulating macrophage activation in MCD-induced NASH mice

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Cellular & Molecular Immunology 2019年第11期16卷 878-886页

作者： Xianhong Du Zhuanchang Wu Yong Xu Yuan Liu Wen Liu Tixiao Wang Chunyang Li Cuijuan Zhang Fan Yi Lifen Gao xiaohong liang Chunhong Ma Key Laboratory for Experimental Teratology of Ministry of Education Department of ImmunologyShandong University School of Basic Medical ScienceJinanShandong 250012PR China Department of Radiation Oncology Qilu Hospital of Shandong UniversityJinanShandongPR China Key Laboratory for Experimental Teratology of Ministry of Education Department of Histology and EmbryologyShandong University School of Basic Medical ScienceJinanShandongPR China Institute of Pathology and Pathophysiology Shandong University School of MedicineJinanPR China Key Laboratory of Infection and Immunity of Shandong Province School of Basic Medical SciencesShandong UniversityJinanChina

As an immune checkpoint,Tim-3 plays roles in the regulation of both adaptive and innate immune cells including macrophages and is greatly involved in chronic liver ***,the precise roles of Tim-3 in nonalcoholic steatohepatitis(NASH)remain *** the current study,we analyzed Tim-3 expression on different subpopulations of liver macrophages and further investigated the potential roles of Tim-3 on hepatic macrophages in methionine and choline-deficient diet(MCD)-induced NASH *** results of flow cytometry demonstrated the significantly increased expression of Tim-3 on all detected liver macrophage subsets in MCD mice,including F4/80^(+)CD11b^(+),F4/80^(+)CD68^(+),and F4/80^(+)CD169^(+)***,Tim-3 knockout(KO)significantly accelerated MCD-induced liver steatosis,displaying higher serum ALT,larger hepatic vacuolation,more liver lipid deposition,and more severe liver ***,compared with wild-type C57BL/6 mice,Tim-3 KO MCD mice demonstrated an enhanced expression of NOX2,NLRP3,and caspase-1 p20 together with increased generation of IL-1βand IL-18 in *** vitro studies demonstrated that Tim-3 negatively regulated the production of reactive oxygen species(ROS)and related downstream pro-inflammatory cytokine secretion of IL-1βand IL-18 in *** administration of N-Acetyl-L-cysteine(NAC),a small molecular inhibitor of ROS,remarkably suppressed caspase-1 p20 expression and IL-1βand IL-18 production in livers of Tim-3 KO mice,thus significantly reducing the severity of steatohepatitis induced by *** conclusion,Tim-3 is a promising protector in MCD-induced steatohepatitis by controlling ROS and the associated pro-inflammatory cytokine production in macrophages.

关键词： macrophage NASH ROS Tim-3

Ribosomal protein S26 serves as a checkpoint of T-cell survival and homeostasis in a p53-dependent manner

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Cellular & Molecular Immunology 2021年第7期18卷 1844-1846页

作者： Chaojia Chen Jiali Peng Shuaiya Ma Yuming Ding Tao Huang Shigang Zhao Lifen Gao xiaohong liang Chunyang Li Chunhong Ma Key Laboratory for Experimental Teratology of the Ministry of Education and Department of Immunology School of Basic Medical ScienceShandong UniversityJinanShandongPR China School of Medicine Shandong UniversityJinanShandongPR China Center for Reproductive Medicine School of MedicineCheeloo College of MedicineShandong UniversityNational Research Center for Assisted Reproductive Technology and Reproductive GeneticsKey Laboratory of Reproductive Endocrinology of the Ministry of EducationShandong Provincial Clinical Medicine Research Center for Reproductive HealthJinanShandongPR China Key Laboratory for Experimental Teratology of the Ministry of Education and Department of Histology and Embryology School of Basic Medical ScienceShandong UniversityJinanShandongPR China Key Laboratory of Infection and Immunity of Shandong Province School of Basic Medical ScienceShandong UniversityJinanShandongPR China

Ribosomal proteins(RPs),which play critical roles in ribosome assembly and protein translation,have been proven to be associated with important physiological and pathological processes,including the regulation of T-cell development and immune-related diseases.1,2,3 A recent study reported that ribosomal protein S26(Rps26),which is a Diamond–Blackfan anemia-associated RP located in the 40S subunit that controls oocyte growth,4,5 may influence multiple different immune phenotypes.6 Moreover,a SNP in the 5′UTR of the Rps26 gene in CD4^(+)and CD8+T cells was implicated in several autoimmune diseases.7 However,the function of Rps26 in T lymphocytes remains ***,we found that Rps26 was highly expressed in T *** examined a T-cell-specific Rps26 knockout mouse model and reported for the first time that ablation of Rps26 in T cells not only impairs peripheral T-cell homeostasis but also leads to T-cell developmental arrest in the ***,Rps26 critically regulates T-cell survival in a p53-dependent *** findings reveal the indispensable role of the Rps26-p53 axis in T-cell development and homeostasis.

关键词： homeostasis p53 finding

NAD+ salvage governs the mitochondrial homeostasis and functional response of NK cells

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NAD+ salvage governs the mitochondrial homeostasis and funct...

第十四届全国免疫学学术大会

作者： Xiaowei Guo xiaohong liang Shandong University

Natural killer(NK) cells are important effector lymphocytes that are poised to eliminate virus-infected or transformed cells. Recent advances highlight a pivotal role for cellular metabolism in programming immune responses of NK cells. The nicotinamide adenine dinucleotide(NAD) has emerged as a vital cofactor that carry high energy electrons to support OxPhos by reversibly oxidizing or reducing NAD and sustain cellular redox *** the present study, we found that NAD level was elevated in cytokine or activating receptor-mediated NK cell activation. We identified the salvage pathway as the main source of NAD in activated NK cells, which was critical for mitochondria homeostasis and effector function of NK cells. And we uncovered the impaired NAD salvage in tumor-infiltrating NK cells(TINKs), while the supplementation of NAD precursor NMN significantly promoted anti-tumor activity of NK *** findings show that NAD homeostasis is prerequisite for NK cell activation and optimal function and identify NAD supplementation as a promising strategy for enhancing NK cell-based immunotherapy.

关键词： NK cell NAD+ mitochondria OxPhos

CUL4B facilitates HBV replication by promoting HBx stabilization

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Cancer Biology & Medicine 2022年第1期19卷 120-131页

作者： Haixia Shan Bo Wang Xiaodong Zhang Hui Song Xi Li Yongxin Zou Baichun Jiang Huili Hu Hao Dou Changshun Shao Lifen Gao Chunhong Ma Xiaoyun Yang xiaohong liang Yaoqin Gong Key Laboratory for Experimental Teratology of the Ministry of Education Key Laboratory of Infection and Immunity of Shandong Province and Department of ImmunologySchool of Basic Medical SciencesShandong UniversityJinan 250012China Department of Laboratory Diagnosis Cangzhou Combination of Traditional Chinese and Western Medicine Hospital of Hebei ProvinceCangzhou 061000China Division of Gastroenterology and Hepatology Renji HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghai Institute of Digestive DiseaseShanghai 200120China Ministry of Education Key Laboratory of Experimental Teratology and Institute of Molecular Medicine and Genetics School of Basic Medical SciencesShandong UniversityJinan 250012China Collaborative Innovation Center of Technology and Equipment for Biological Diagnosis and Therapy in Universities of Shandong Jinan 250012China Department of Gastroenterology Qilu HospitalShandong UniversityJinan 250012China

Objective:Hepatitis B virus(HBV)infection is a major public health problem ***,the regulatory mechanisms underlying HBV replication remain *** 4 B-RING ubiquitin E3 ligase(CRL4 B)is involved in regulating diverse physiological and pathophysiological *** our study,we aimed to explain the role of CUL4 B in HBV ***:Cul4 b transgenic mice or conditional knockout mice,as well as liver cell lines with CUL4 B overexpression or knockdown,were used to assess the role of CUL4 B in HBV *** assays and immunofluorescence staining were performed to study the interaction between CUL4 B and *** chase assays and in vivo ubiquitination assays were performed to evaluate the half-life and the ubiquitination status of ***:The hydrodynamics-based hepatitis B model in Cul4 b transgenic or conditional knockout mice indicated that CUL4 B promoted HBV replication(P<0.05).Moreover,the overexpression or knockdown system in human liver cell lines validated that CUL4 B increased HBV replication in an HBx-dependent ***,immunoprecipitation assays and immunofluorescence staining showed an interaction between CUL4 B and ***,CUL4 B upregulated HBx protein levels by inhibiting HBx ubiquitination and proteasomal degradation(P<0.05).Finally,a positive correlation between CUL4 B expression and HBV pg RNA level was observed in liver tissues from HBV-positive patients and HBV transgenic ***:CUL4 B enhances HBV replication by interacting with HBx and disrupting its ubiquitin-dependent proteasomal ***4 B may therefore be a potential target for anti-HBV therapy.

关键词： CUL4B HBV ubiquitination HBx HCC

Hepatitis B virus evades immune recognition via RNA adenosine deaminase ADAR1-mediated viral RNA editing in hepatocytes

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Cellular & Molecular Immunology 2021年第8期18卷 1871-1882页

作者： Liyuan Wang Yang Sun Xiaojia Song Zehua Wang Yankun Zhang Ying Zhao Xueqi Peng Xiaodong Zhang Chunyang Li Chengjiang Gao Nailin Li Lifen Gao xiaohong liang Zhuanchang Wu Chunhong Ma Key Laboratory for Experimental Teratology Ministry of EducationSchool of Basic Medical SciencesCheeloo Medical CollegeShandong UniversityJinanShandongChina Department of Immunology School of Basic Medical SciencesCheeloo Medical CollegeShandong UniversityJinanShandongChina Key Laboratory of Infection and Immunity of Shandong Province Shandong UniversityJinanChina Advanced Medical Research Institute Shandong UniversityJinanChina Clinical Pharmacology Group Department of MedicineSolnaKarolinska InstituteStockholmSweden

HBV is considered as a“stealth”virus that does not invoke interferon(IFN)responses;however,the mechanisms by which HBV bypasses innate immune recognition are poorly *** this study,we identified adenosine deaminases acting on RNA 1(ADAR1),which is a key factor in HBV evasion from IFN responses in ***,ADAR1 interacted with HBV RNAs and deaminated adenosine(A)to generate inosine(I),which disrupted host immune recognition and thus promoted HBV *** of ADAR1 or its deficient deaminase activity promoted IFN responses and inhibited HBV replication in hepatocytes,and blocking the IFN signaling pathways released the inhibition of HBV replication caused by ADAR1 ***,the HBV X protein(HBx)transcriptionally promoted ADAR1 expression to increase the threshold required to trigger intrinsic immune activation,which in turn enhanced HBV escape from immune recognition,leading to persistent *** with 8-azaadenosine,an ADAR1 inhibitor,efficiently enhanced liver immune activation to promote HBV clearance in vivo and in *** together,our results delineate a molecular mechanism by which HBx promotes ADAR1-derived HBV immune escape and suggest a targeted therapeutic intervention for HBV infection.

关键词： ADAR1 RNA editing IFN response HBV replication HBx

CUL4B facilitates HBV replication by disrupting the ubiquitination and proteasomal degradation of HBx

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CUL4B facilitates HBV replication by disrupting the ubiquiti...

第十届全国免疫学学术大会

作者： xiaohong liang Haixia Shan Bo Wang Shandong University

Background&Aims:Cullin 4B-RING ubiquitin E3 ligase(CRL4B)is involved in regulating diverse physiological and pathophysiological ***,the role of CUL4B in hepatitis B virus(HBV)infection remains completely ***:The correlation of CUL4B expression with HBV pg RNA or ccc DNA level was statistically analyzed in HBVpositive human or mouse liver ***4b transgenic mice or conditional knockout mice,as well as liver cell lines with CUL4B overexpression or knockdown,were used for estimating the role of CUL4B in HBV *** associations between CUL4B and HBx were examined by immunoprecipitation assay and immunofluorescence ***(CHX)chase experiment was performed to evaluate the half-life of HBx *** in vivo ubiquitination assay was used for determining the ubiquitination status of ***:Positive correlations between CUL4B expression and HBV pg RNA or ccc DNA level were found in HBVpositive human liver tissues or HBV transgenic mice liver *** hydrodynamics-based hepatits B model in Cul4b transgenic or conditional knockout mice indicated the promotion of CUL4B on HBV ***,the overexpression or knockdown system in human liver cell lines validated that CUL4B improved HBV replication in an HBx-dependent ***,the immunoprecipitation assay and the immunofluorescence staining showed the association between CUL4B and ***,CUL4B upregulated HBx protein level and increased the half-life of HBx by inhibiting the ubiquitination and proteasomal degradation of ***:CUL4B enhances HBV replication by interacting with HBx and disrupting its ubiquitin-dependent proteasomal *** of CUL4B represents a potential target for anti-HBV therapy.

关键词： DDB1 Hijack MG132