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| 1 | Structural insights into the TRIM family of ubiquitin E3 ligases显示文摘 | Yang Li Han Wu Wei Wu Wei Zhuo Weixiao Liu Yixiao Zhang Minzhang Cheng Ye-Guang Chen Ning Gao Hongtao Yu Linfang Wang Wei Li Maojun Yang | 2014 | Cell Research2014，24，6： | 12 |
| 2 | Rational development of a human antibody cocktail that deploys multiple functions to confer Pan-SARS-CoVs protection显示文摘Structural principles underlying the composition and synergistic mechanisms of protective monoclonal antibody cocktails are poorly defined.Here,we exploited antibody cooperativity to develop a therapeutic antibody cocktail against SARS-CoV-2.On the basis of our previously identified humanized cross-neutralizing antibody H014,we systematically an a lyzed a fully human n aive antibody library and rationally identified a potent neutralizing antibody partner,P17,which confers effective protection in animal model.Cryo-EM studies dissected the nature of the P17 epitope,which is SARS-CoV-2 specific and distinctly different from that of HOI4.High-resolution structure of the SARS-CoV-2 spike in complex with HOM and P17,together with functional investigations revealed that in a two-antibody cocktail,synergistic neutralization was achieved by S1 shielding and conformational locking,thereby blocking receptor attachment and viral membrane fusion,conferring high potency as well as robustness against viral mutation escape.Furthermore,cluster analysis identified a hypothetical 3rd antibody partner for further reinforcing the cocktail as pan-SARS-CoVs therapeutics. | Hangping Yao Yao Sun Yong-Qiang Deng Nan Wang Yongcong Tan Na-Na Zhang Xiao-Feng Li Chao Kong Yan-Peng Xuc Qi Chen Tian-Shu Cao Hui Zhao Xintian Yan Lei Cao Zhe Lv Dandan Zhu Rui Feng Nanping Wu Wenhai Zhang Yuhao Hu Keda Chen Rong-Rong Zhang Qingyu Lv Shihui Sun Yunhua Zhou Run Yan Guan Yang Xinglu Chanjuan Liu Xiangyun Lu Linfang Cheng Hongying Qiu Xing-Yao Huang Tianhao Weng Danrong Shi Weidong Jiang Junbin Shao Lei Wang Jie Zhang Tao Jiang Guojun Lang Cheng-Feng Qinc Lanjuan Li Xiangxi Wang | 2021 | Cell Research2021，31，1： | 5 |
| 3 | Parthenolide inhibits LPS-induced inflammatory cytokines through the toll-like receptor 4 signal pathway in THP-1 cells显示文摘Parthenolide (PTL ) 显示出反煽动性的有势力和反癌症活动。在现在的学习, PTL 的活动的分子的机制在导致的 lipopolysaccharide (LPS ) 被探索人的白血病 monocytic THP-1 房间和人的主要单核白血球。3-(4,5-dimethylthiazol-2-yl )-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium 盐(山) 试金被用来在 THP-1 房间生存能力上分析 PTL 的效果。连接酶的 immunosorbent 试金被用来在导致 LPS 的煽动性的 cytokine 分泌物上决定 PTL 的效果。流动 cytometry 和量的即时聚合酶链反应被用来在导致 LPS 的像使用费的受体上估计 PTL 的效果 4 (TLR4 ) 表示。表明分子的 Phosphorylation 层次被西方的污点分析决定。结果显示出那 PTL < 12.5 M 显著地没影响 THP-1 房间生存能力。LPS 治疗导致了 interleukin (IL ) 的一条显著起来规定 -6, IL-1, IL-8, IL-12p40,肿瘤坏死因素 -- , IL-18,并且没有在里面 THP-1 房间。然而, PTL 以一种剂量依赖者方式禁止了这些 cytokines 的表示,与 1.0912.620 M 的 IC 50 价值。PTL 与由流动 cytometry 分析决定了的 1.373 M 的 IC 50 值堵住了 TLR4 表示,并且这堵住的效果在蛋白质和 mRNA 层次被验证。另外的分子的表情的细胞外的调整信号的 kinase 1/2 ,6月N终端 kinase , p38 ,原子因素 B ( NF-B ) p65 ,和 IB 和起来规定的 phosphorylation 层次的起来规定(可诱导的氮的氧化物 synthase , TLR4 ,并且 TNF 联系受体的因素 6 )由 LPS 导致了被 PTL 以一种剂量依赖者方式废除。PTL 的反煽动性的机制通过表明小径的调停 TLR4 的激活 mitogen 的蛋白质 kinase 和 NF-B 部分操作。因此, TLR4 可以是为反发炎治疗的一个新目标。 | Shuangshuang Li Xiangli Gao Xiaoxin Wu Zhigang Wu Linfang Cheng Lifen Zhu Dan Shen Xiangmin Tong | 2015 | Acta Biochimica et Biophysica Sinica2015，47，5： | 5 |
| 4 | Atorvastatin protects cardiomyocytes from oxidative stress by inhibiting LOX-1 expression and cardiomyocyte apoptosis显示文摘冠的动脉疾病(CAD ) 是世界范围的一个主要健康问题。CAD 的最严重的形式是急性冠的症候群(交流) 。最近的研究在交流表明了 atorvastatin 的有益的角色;然而,位于这效果下面的机制充分没被澄清。成长证据显示氧化低密度的脂蛋白 receptor-1 (LOX-1 ) 玩的象 lectin 一样的那激活在氧化导致压力的 cardiomyocyte apoptosis 的一个重要角色在交流期间。在这研究,我们检验了 atorvastatin 是否禁止 H 2 O 2-induced LOX-1 表示和 H9c2 cardiomyocyte apoptosis,并且调查了内在的发信号小径。有 H 2 O 2 导致了 LOX-1 mRNA 和蛋白质的提高的表示,以及增加了 caspase-3 和 -9 蛋白质表示和房间 apoptosis。H 2 O 2-induced LOX-1 表示, caspase 蛋白质表示,和 cardiomyocyte apoptosis 被预告的处理与 atorvastatin 稀释。Atorvastatin 激活 H 2 以一种集中依赖者方式的 Akt 的 O 2-inhibited phosphorylation。Akt 禁止者, LY294002,在导致 Akt phosphorylation 上并且在压制 H 2 O 2-mediated caspase 起来规定和房间 apoptosis。这些调查结果显示 atorvastatin 经由 LOX-1 的抑制保护 cardiomyocyte 免受氧化应力的伤害表示和 apoptosis,和 H 2 Akt 的 O 2-inhibited phosphorylation 可以在 atorvastatin 的保护的功能起一个重要作用。 | Lei Zhang Linfang Cheng Qiqi Wang Dongchen Zhou Zhigang Wu Ling Shen Li Zhang Jianhua Zhu | 2015 | Acta Biochimica et Biophysica Sinica2015，47，3： | 4 |
| 5 | Interspecific hybrids between Dendranthema morifolium (Ramat.) Kitamura and D. nankingense (Nakai) Tzvel. achieved using ovary rescue and their cold tolerance characteristics显示文摘 | Xi Cheng Sumei Chen Fadi Chen Weimin Fang Yanming Deng Linfang She | 2010 | Euphytica2010，，1： | 1 |
| 6 | RING finger 138 deregulation distorts NF-κB signaling and facilities colitis switch to aggressive malignancy显示文摘Prolonged activation of nuclear factor(NF)-кB signaling significantly contributes to the development of colorectal cancer(CRC).New therapeutic opportunities are emerging from targeting this distorted cell signaling transduction.Here,we discovered the critical role of RING finger 138(RNF138)in CRC tumorigenesis through regulating the NF-кB signaling,which is independent of its Ubiquitin-E3 ligase activity involved in DNA damage response.RNF138^(−/−) mice were hyper-susceptible to the switch from colitis to aggressive malignancy,which coincided with sustained aberrant NF-кB signaling in the colonic cells.Furthermore,RNF138 suppresses the activation of NF-кB signaling pathway through preventing the translocation of NIK and IKK-Beta Binding Protein(NIBP)to the cytoplasm,which requires the ubiquitin interaction motif(UIM)domain.More importantly,we uncovered a significant correlation between poor prognosis and the downregulation of RNF138 associated with reinforced NF-кB signaling in clinical settings,raising the possibility of RNF138 dysregulation as an indicator for the therapeutic intervention targeting NF-кB signaling.Using the xenograft models built upon either RNF138-dificient CRC cells or the cells derived from the RNF138-dysregulated CRC patients,we demonstrated that the inhibition of NF-кB signaling effectively hampered tumor growth.Overall,our work defined the pathogenic role of aberrant NF-кB signaling due to RNF138 downregulation in the cascade events from the colitis switch to colonic neoplastic transformation and progression,and also highlights the possibility of targeting the NF-кB signaling in treating specific subtypes of CRC indicated by RNF138-ablation. | Yalan Lu Rong Huang Jianming Ying Xingchen Li Tao Jiao Lei Guo Haitao Zhou Han Wang Amannisa Tuersuntuoheti Jianmei Liu Qichen Chen Yanhong Wang Luying Su Changyuan Guo Fu Xu Ziyi Wang Yan Lu Kai Li Junbo Liang Zhen Huang Xiao Chen Jinjie Yao Hanjie Hu Xiaowen Cheng Yufeng Wan Xinyan Chen Ning Zhang Shiying Miao Jianqiang Cai Linfang Wang Changzheng Liu Wei Song Hong Zhao | 2022 | Signal Transduction and Targeted Therapy2022，7，7： | 0 |
| 7 | Retinoblastoma binding protein 4 represses HIV-1 long terminal repeat–mediated transcription by recruiting NR2F1 and histone deacetylase显示文摘Human immunodeficiency virus (HIV) transcription is closely associated with chromatin remodeling. Retinoblastoma binding protein 4 (RBBP4) is a histone chaperone implicated in chromatin remodeling. However, the role of RBBP4 in HIV-1 infection and the underlying mechanism remain elusive. In the present study, we showed that RBBP4 plays a negative regulatory role during HIV-1 infection. RBBP4 expression was significantly increased in HIV-1–infected T cells. RBBP4 binds to the HIV-1 long terminal repeat (LTR), represses HIV-1 LTR-mediated transcription through recruiting nuclear receptor subfamily 2 group F member 1(NR2F1) and histone deacetylase 1 and 2 (HDAC1/2) to HIV-1 LTR, and further controls local histone 3 (H3) deacetylation and chromatin compaction. Furthermore, the occupancy of RBBP4, HDAC1/2, and NR2F1 on LTR in HIV-latent J-lat cells was significantly higher than that in HIV-1–activated cells. In conclusion, our results establish RBBP4 as a new potent antiretroviral factor, which may provide theoretical basis for the treatment of HIV in the future. | Juan Wang Zongxing Yang Linfang Cheng Lingna Lu Kenv Pan Jin Yang Nanping Wu | 2019 | Acta Biochimica et Biophysica Sinica2019，51，9： | 0 |
| 8 | Gp120 binding with DC-SIGN induces reactivation of HIV-1 provirus via the NF-κB signaling pathway显示文摘潜伏的人的 immunodeciency 病毒类型 1 的复活机制(HIV-1 ) 感染是不清楚的,特别在树枝状的房间(DC ) 。DC 特定的细胞间的粘附 molecule-3-grabbing non-integrin (DC 签名) 与 HIV-1 和另外的病原体绑激活细胞外的调整蛋白质 kinase (英皇家空军之阶级最低之兵) 和原子 factor-kappa B (NF-B ) 小径并且调整 cytokine 表示。我们假设了表明小径的那 DC-SIGN-induced 可以激活 HIV-1 provirus。调查这个假设,我们与 DC 签名表示 plasmid 和 HIV-1 5 长终端重复(LTR ) 记者 plasmid 由 transfecting 293T 房间产生了一个模型,然后与 HIV-1 gp120 蛋白质,野类型的 HIV-1 或 VSV-G-pNL4.3 pseudotype 病毒刺激了 293T 房间(没有 gp120 蛋白质) 。HIV-1 5LTR 被 HIV-1 gp120 在 DC-SIGN-expressing 293T 房间重新激活,这被发现。然后, HIV-1 长期地感染了 CEM-Bru 房间是有 DC 签名表示 plasmid 的 transfected 并且由 HIV-1 gp120 蛋白质刺激了。早、迟了的 HIV-1 provirus 复制被 HIV-1 gp120/DC-SIGN 刺激重新激活,这被发现。我们然后调查了 ERK,的参与 p38 由明确地禁止小径在 HIV-1 provirus 的 HIV-1 gp120/DC-SIGN-induced 激活表明小径的激活 mitogen 的蛋白质 kinases 和 NF-B。我们的结果显示 HIV-1 gp120/DC-SIGN 刺激经由 NF-B 信号小径重新激活潜伏的 HIV-1 provirus。 | Changzhong Jin Jie Li Linfang Cheng Fumin Liu Nanping Wu | 2016 | Acta Biochimica et Biophysica Sinica2016，48，3： | 0 |
| 9 | Recombinant human interferon-α1b inhibits SARS-CoV-2 better than interferon-α2b in vitro显示文摘Dear Editor,The coronavirus disease 2019(COVID-19)outbreak,has spread across the world(Wu et al.,2020).The causative agent of COVID-19,severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),is highly pathogenic and infectious,which become a major public health hazard that has had a devastating social and economic impact worldwide(Li Q.Q.et al.,2020).Variants of the virus have emerged that behave differently(CDC2021;Gobeil et al.,2020;Leung et al.,2021).Some of them show increased infectivity(Li Q.et al.,2020;Zhang et al.,2020)and may escape from neutralizing antibodies(Weisblum et al.,2020). | Danrong Shi Keda Chen Xiangyun Lu Linfang Cheng Tianhao Weng Fumin Liu Nanping Wu Lanjuan Li Hangping Yao | 2022 | Virologica Sinica2022，37，2： | 0 |
| 10 | Lrrc34 Is Highly Expressed in SSCs and Is Necessary for SSC Expansi on In Vitro显示文摘Objective To discover critical genes contributing to the sternness and maintenance of spermatogonial stem cells(SSCs)and provide new insights into the function of the leucine-rich repeat(LRR)family member Lrrc34(leudne-rich repeat-containing 34)in SSCs from mice.Methods Bioinformatic methods,including differentially expressed gene(DEG),gene ontology(GO)enrichment and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analyses,were used to uncover latent pluripotency-related genes.Reverse transcription-polymerase chain reaction(RT-PCR)and immunofluorescence analyses were utilized to verify the mRNA and protein expression levels,respectively.RNA interference of Lrrc34 using siRNA was performed to detect its transient impact on SSCs.Results Eight DEGs between ID4-EGFP+(G)and ID4-EGFP+/TSPAN8Hig11(TH),eight DEGs between G and ID4-EGFP+/TSPAN8Uw(TL)and eleven DEGs between TH and TL were discovered,and eleven proteinprotein interaction(PPI)modules were found to be significant in the PPI network of DEGs.One of the DEGs,Lrrc34,was selected as a potential pluripotency?related gene due to its differential expression among ID4-EGFP+spermatogonia subsets and its interaction with fibroblast growth factor 2 in the fifth module.Immunofluorescence experiments exhibited specific expression of Lrrc34 in a subpopulation of undifferentiated spermatogonia marked by LIN28A,and RT-PCR experiments confirmed the high expression of Lrrc34 in SSCs from P7 and adult mice.The transient knockdown of Lrrc34 in SSCs resulted in reduced colony sizes and significant changes in the transcriptome and apoptotic pathways.Conclusion Lrrc34 is highly expressed in mouse SSCs and is required for SSC proliferation in vitro through effects on transcriptome and signaling transduction pathways. | Jinhuan Ou Yiran Li Zhipeng Wang Cheng Jin Kai Li Yan Lu Dingfeng Zou Pengyu Li Mengzhen Li Shiying Miao Linfang Wang Wei Song | 2020 | Chinese Medical Sciences Journal2020，35，1： | 0 |
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