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Science China(Life Sciences) 2010年第2期53卷 159-168页

作者： WANG YaYa1,ZHANG Peng2.LIU YingFang2.& cheng genhong1 1 {2. of microbiology,immunology & molecular genetics,university of california los angeles,609 Charles E.Young Drive East,los angeles,california 90095,usa 2.National Laboratory of Biomacromolecules,Institute of Biophysics,Chinese Academy of Sciences,Beijing 100101,China 1. department of microbiology Immunology & Molecular Genetics University of California Los Angeles 609 Charles E. Young Drive East Los Angeles California 90095 USA2. National Laboratory of Biomacromolecules Institute of Biophysics Chinese Academy of Sciences Beijing 100101 China

The tumor necrosis factor (TNF) receptor-associated factor (TRAF) family consists of six mammalian members,and is shown to participate in signal transduction of a large number of receptor families including TNF receptor family (TNFR) and Toll-like receptors-interleukin-1 receptors (TLR-IL-1R) *** receptor activation,TRAFs are directly or indirectly recruited to the intracellular domains of these *** subsequently engage other signaling proteins to activate inhibitor of κB kinase (IKK) complex,TRAF family member-associated NF-κB activator (TANK)-binding kinase 1 (TBK1) and inducible I κB kinase (IKK-i) (also known as IKKε),ultimately leading to activation of transcription factors such as NF-κB and interferon-regulatory factor (IRF) to induce immune and inflammatory responses.

关键词： TRAF NF-κB type 1 interferon innate immunity

Ubiquitination and deubiquitination:tussling of viral and host innate gene programs

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Ubiquitination and deubiquitination:tussling of viral and ho...

第六届全国免疫学学术大会

作者： Dahai Zheng~1 Gang Chen~1 Beichu Guo~1 Ganhong cheng~(1,2. Hong Tang~1 1 Center for Infection and Immunity and National Laboratory of Biomacromolecules,Institute of Biophysics,Chinese Academy of Sciences,15 Da Tun Road,Beijing 100101,China 2.department of {2.,immunology and molecular genetics,university of california los angeles,los angeles,ca,90095,usa

The antiviral innate signaling pathways involve activation of TLR/RLR to recruit downstream adaptors for initiation of phosphorylation cascade,which transcribe numerous anti-viral genes, most prominently among these,t...

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Editorial

Science China(Life Sciences) 2010年第2期53卷 157-158页

作者： genhong cheng (1) YongJun Liu (2. Hong Tang (3) 1. department of microbiology Immunology & Molecular Genetics University of California Los Angeles 609 Charles E. Young Drive East Los Angeles California 90095 USA2. Department of Immunology and Center for Cancer Immunology Research University of Texas M.D. Anderson Cancer Center Houston Texas 77030 USA3. Key Laboratory of Infection and Immunity Institute of Biophysics Chinese Academy of Sciences Beijing 100101 China

SM (spatial multiplexing) can effectively increase the information rate in multiple input multiple output system. BLAST is the typical representation of SM, especially VBLAST, which has some simple de- tection algorithms such as ML, ZF-DFE and ML-DFE, etc. However, the existing algorithms cannot approach ML performance. This paper discusses the effect for detection performance by the correlation of channel ma- trix, proposes a new algorithm—HPML detection algorithm, which can approach ML performance with low complexity. In the new algorithm, we travel the first d layers, and use the DFE procedure for the remaining layers, then perform ML detection for all obtained signals. Simulation results show that HPML can approach ML performance when the traveling numbers are not less than half of the number of transmitting antennas, and the algorithm complexity is smaller than ML.

关键词： BLAST correlation of channel matrix ML detecting algorithm HPML detecting algorithm

SARS-CoV-2.virus NSP14 Impairs NRF2.HMOX1 activation by targeting Sirtuin 1

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Cellular & molecular immunology 2022年第8期19卷 872-882页

作者： Shilei Zhang Jingfeng Wang Lulan Wang Saba Aliyari genhong cheng department of microbiology Immunologyand Molecular GeneticsUniversity of CaliforniaLos AngelesLos Angeles90095CAUSA

Most deaths from the COVID-19 pandemic are due to acute respiratory distress syndrome(ARDS)-related respiratory *** storms and oxidative stress are the major players in ARDS development during respiratory virus ***,it is still unknown how oxidative stress is regulated by viral and host factors in response to SARS-CoV-2.***,we found that activation of NRF2.HMOX1 significantly suppressed SARS-CoV-2.replication in multiple cell types by producing the metabolite biliverdin,whereas SARS-CoV-2.impaired the NRF2.HMOX1 axis through the action of the nonstructural viral protein ***,NSP14 interacts with the catalytic domain of the NAD-dependent deacetylase Sirtuin 1(SIRT1)and inhibits its ability to activate the NRF2.HMOX1 ***,both genetic and pharmaceutical evidence corroborated the novel antiviral activity of SIRT1 against ***,our findings reveal a novel mechanism by which SARS-CoV-2.dysregulates the host antioxidant defense system and emphasize the vital role played by the SIRT1/NRF2.axis in host defense against SARS-CoV-2.

关键词： SARS-CoV-2 NRF2 HMOX1 NSP14 SIRT1 Oxidative stress

New targets for controlling Ebola virus disease

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National Science Review 2015年第3期2卷 266-267页

作者： F.Xiao-Feng Qin cheng-Yu Jiang Taijiao Jiang genhong cheng Center for Systems Medicine Institute of Basic Medical Sciences Chinese Academy of Medical Sciences and Peking Union Medical College State Key Laboratory of Medical molecular Biology Institute of Basic Medical SciencesChinese Academy of Medical Sciences department of Biochemistry and molecular Biology Peking Union Medical College Tsinghua University Key Laboratory of Protein and Peptide Pharmaceuticals Institute of Biophysics Chinese Academy of Sciences department of microbiology Immunology and Molecular Genetics University of California

EBOV infects multiple diferent cell types and replicates rapidly in vivo[1].Due to its long ilamentous structure,EBOV is internalized by macropinocytosis ater cell surface receptor binding by the viral glycoprotein(GP).Unlike many other enveloped viruses,EBOV entry process involves multiple steps of traversing of the virion through endosomal vesicle route before its nuclear core is released into cell cytoplasm for replication[2..

关键词： New targets for controlling Ebola virus disease GP TPC

Crystal structure of the ubiquitin-like domain of human TBK1

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Protein & Cell 2012年第5期3卷 383-391页

作者： Jian Li Jun Li Andrea Miyahira Jian Sun Yingfang Liu genhong cheng Huanhuan Liang State Key Laboratory of Biomacromolecules Institute of BiophysicsChinese Academy of SciencesBeijing 100101China department of microbiology Immunology&Molecular GeneticsUniversity of CaliforniaLos AngelesCA 90095USA Graduate School of the Chinese Academy of Sciences Beijing 100101China

TANK-binding kinase 1(TBK1)is an important enzyme in the regulation of cellular antiviral ***1 regulates the activity of the interferon regulatory factors IRF3 and IRF7,thereby playing a key role in type I interferon(IFN)signaling *** structure of TBK1 consists of an N-terminal kinase domain,a middle ubiquitin-like domain(ULD),and a C-terminal elongated helical *** has been reported that the ULD of TBK1 regulates kinase activity,playing an important role in signaling and mediating interactions with other molecules in the IFN *** this study,we present the crystal structure of the ULD of human TBK1 and identify several con-served residues by multiple sequence *** found that a hydrophobic patch in TBK1,containing residues Leu316,Ile353,and Val382.corresponding to the“Ile44 hydrophobic patch”observed in ubiquitin,was conserved in TBK1,IκB kinase epsilon(IKKε/IKKi),IκB kinase alpha(IKKα),and IκB kinase beta(IKKβ).In com-parison with the structure of the IKKβULD domain of Xenopus laevis,we speculate that the Ile44 hydrophobic patch of TBK1 is present in an intramolecular binding surface between ULD and the C-terminal elongated *** varying surface charge distributions in the ULD domains of IKK and IKK-related kinases may be relevant to their specificity for specific partners.

关键词： TBK1 ubiquitin-like domain crystal struc-ture hydrophobic patch

Type III interferon-induced CBFβinhibits HBV replication by hijacking HBx

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Cellular & molecular immunology 2019年第4期16卷 357-366页

作者： Fengchao Xu Hongxiao Song Qingfei Xiao Na Li Hong Zhang genhong cheng Guangyun Tan department of immunology Institute of Translational MedicineThe First Hospital of Jilin UniversityChangchunJilin 130061China department of Nephrology The First HospitalJilin UniversityChangchunJilin 130021China department of Obstetrics The First Hospital of Jilin UniversityChangchunJilin 130021China Phase I Clinical Research Center The First Hospital of Jilin UniversityJilin 130021China department of microbiology Immunology and Molecular GeneticsUniversity of CaliforniaLos AngelesCA 90095USA Center of Systems Medicine Institute of Basic Medical SciencesChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100005 Suzhou Institute of Systems Medicine SuzhouJiangsu 215123China

Hepatitis B virus(HBV)and its associated chronic infection remain serious health threats ***,there is still no impactful approach for clinical treatment of hepatitis B ***,developing a better understanding of the interactions between HBV and its host is particularly *** infection has been reported to induce type-III but not type-I or type-II interferon(IFN).In this study,we identified CBFβ,an HIV enhancer,as an HBV restriction factor that is specifically induced by type-III IFN in the early stages of HBV ***-III IFN-induced IL-10 played an important role in the production of CBFβ.Interestingly,the interaction between CBFβ-and HBV-encoded regulatory protein X(HBx)enhanced the stability of CBFβ,but notably blocked HBx-mediated promotion of HBV ***βexpression was lower in HBV patients than in healthy persons,and the addition of serum from HBV patients inhibited CBFβexpression in HepG2.*** the contrary,HBV via HBsAg inhibited type-III IFN-induced CBFβexpression and decreased the anti-HBV activity of type-III IFN,suggesting that HBV inhibits antiviral interferon-stimulated gene(ISG)expression and induces IFN ***,our results demonstrate that type-III IFN-triggered and IL-10-induced CBFβare crucial factors for inhibiting HBV replication,and the HBx–CBFβ–HBsAg axis reveals a new molecular mechanism of interaction between HBV and its hosts.

关键词： inhibited interferon CBF

Structural and functional analyses of human DDX41 DEAD domain

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Protein & Cell 2017年第1期8卷 72-76页

作者： Yan Jiang Yanping Zhu Weicheng Qiu Yong-Jun Liu genhong cheng Zhi-Jie Liu Songying Ouyang National Laboratory of Biomacromolecules Institute of BiophysicsChinese Academy of Sciences Beijing 100101 China Baylor Research Institute Baylor Scott and White Health DallasTX 75246 USA department of microbiology Immunology and Molecular GeneticsUniversity of California Los Angeles Los Angeles CA 90095 USA Institute of molecular and Clinical Medicine Kunming MedicalUniversity Kunming 650500 China

Dear Editor, DEAD-box proteins, which are named after the strictly con- served amino acid sequence Asp-Glu-Ala-Asp, were first identified as a distinct family in the late 1980s when alignments based on eight homologue... 详细信息

关键词： Acute Myeloid Leukemia Isothermal Titration calorimetry Mutate Amino Acid Helicase Domain Thermal Shift Assay

Homeoprotein SIX1 compromises antitumor immunity through TGF-β-mediated regulation of collagens

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Cellular & molecular immunology 2021年第12期18卷 2660-2672页

作者： Wancheng Liu Meiling Gao Lili Li Yu Chen Huimin Fan Qiaomei cai Yueyue Shi Chaohu Pan Junxiao Liu Lucy S.cheng Heng Yang {2. cheng Institute of Systems Medicine Chinese Academy of Medical Sciences&Peking Union Medical CollegeBeijing100005China Suzhou Institute of Systems Medicine Suzhou215123China department of Dermatology University of Pittsburgh Medical Center3708 Fifth AvenueSuite 500.68PittsburghPA15213USA department of microbiology Immunology&Molecular GeneticsUniversity of CaliforniaLos AngelesCAUSA

The tumor microenvironment(TME),including infiltrated immune cells,is known to play an important role in tumor growth;however,the mechanisms underlying tumor immunogenicity have not been fully ***,we discovered an unexpected role for the transcription factor SIX1 in regulating the tumor immune *** on analyses of patient datasets,we found that SIX1 was upregulated in human tumor tissues and that its expression levels were negatively correlated with immune cell infiltration in the TME and the overall survival rates of cancer *** of Six1 in cancer cells significantly reduced tumor growth in an immune-dependent manner with enhanced antitumor immunity in the ***,SIX1 was required for the expression of multiple collagen genes via the TGFBR2.dependent Smad2.3 activation pathway,and collagen deposition in the TME hampered immune cell infiltration and ***,our study uncovers a crucial role for SIX1 in modulating tumor immunogenicity and provides proof-of-concept evidence for targeting SIX1 in cancer immunotherapy.

关键词： Homeoprotein SIX1 anti-tumor immunity collagens.