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| 1 | CRISPR/Cas9-mediated gene editing in human tripronuclear zygotes显示文摘染色体编辑工具例如定期聚类短 palindromic 重复(CRISPR ) 联系了的 interspaced 系统(Cas ) 广泛地被用来包括动物接合子和人的房间在模型系统修改基因,并且为基本研究和临床的应用保持巨大的诺言。迄今为止,严肃的知识差距在人的早胚胎,并且在效率和在人的培植前胚胎使用象 CRISPR/Cas9 那样的技术的潜在的离开目标效果留在我们 DNA 修理机制的理解。在这份报告,我们使用了推进的接合子调查 CRISPR/Cas9-mediated 基因在人的房间编辑的 tripronuclear (3PN ) 。我们发现 CRISPR/Cas9 能有效地劈开内长的 -globin 基因(HBB ) 。然而,相应再结合的效率指导了 HBB 的修理(HDR ) 是低的,编辑胚胎是马赛克。离开目标劈开在由 T7E1 试金并且 whole-exome 定序揭示了的这些 3PN 接合子也是明显的。而且,内长的 delta-globin 基因(HBD ) 对 HBB 相应,与外长的施主 oligos 竞争了充当修理模板,导致倔强的变化。我们的数据也显示在这些胚胎的 HBB 地点的修理通过非转线路 HDR 小径优先地发生了。一起拿,我们的工作加亮紧迫的需要进一步改进 CRISPR/Cas9 平台的忠实和特性,为编辑的 CRSIPR/Cas9-mediated 的任何临床的应用程序的一个前提。 | Puping Liang Yanwen Xu Xiya Zhang Chenhui Ding Rui Huang Zhen Zhang Jie Lv Xiaowei Xie Yuxi Chen Yujing Li Ying Sun Yaofu Bai Zhou Songyang Wenbin Ma Canquan Zhou Junjiu Huang | 2015 | Protein & Cell2015，6，5： | 149 |
| 2 | Correction of β-thalassemia mutant by base editor in human embryos显示文摘 | Puping Liang Chenhui Ding Hongwei Sun Xiaowei Xie Yanwen Xu Xiya Zhang Ying Sun Yuanyan Xiong Wenbin Ma Yongxiang Liu Yali Wang Jianpei Fang Dan Liu Zhou Songyang Canquan Zhou Junjiu Huang | 2017 | Protein & Cell2017，8，11： | 34 |
| 3 | Effective gene editing by high-fidelity base editor 2 in mouse zygotes显示文摘通过相应再结合的指向的点 mutagenesis 广泛地在基因研究被使用了并且为在病人修理引起疾病的变化保持可观的诺言。然而,象 mosaicism 那样的问题和低 mutagenesis 效率继续提出挑战到如此的途径的临床的申请。最近,一个基础编辑器() 在 cytidine (C) 脱氨基酶上造的系统和 CRISPR/Cas9 技术在植物,酵母,和人的房间为指向的点 mutagenesis 作为一个其他的方法被开发。然而,基础编辑器高效地在 deamination 窗口中把 C 变换成 thymidine (T) 是否指向了在鼠标胚胎的基础编辑,仍然保持不清楚是可行的。在这份报告,我们产生了基础编辑的一个修改高保真版本 2 (HF2-BE2 ) ,并且调查了它在老鼠胚胎编辑功效的底。我们发现 HF2-BE2 能高效地把 C 变换成 T,与直到在老鼠胚胎的 100% biallelic 变化效率。不同于 BE3, HF2-BE2 能在目标和非目标海滨上把 C 变换成 T,扩展基础编辑器的编辑范围。令人惊讶地,我们发现 HF2-BE2 能也使脱去氨基对 gRNA 有约束力的区域近似的 C。一起拿,我们的工作表明由基础编辑,和下划线在鼠标产生点变化的可行性小心地优化编辑系统以便消除近似地点的 deamination 的底的需要。 | Puping Liang Hongwei Sun Ying Sun Xiya Zhang Xiaowei Xie Jinran Zhang zhen Zhang Yuxi Chen Chenhui Ding Yuanyan Xiong Wenbin Ma Dan Liu Junjiu Huang Zhou Songyang | 2017 | Protein & Cell2017，8，8： | 17 |
| 4 | USP19 suppresses inflammation and promotes M2-like macrophage polarization by manipulating NLRP3 function via autophagy显示文摘Macrophage polarization to proinflammatory M1-like or anti-inflammatory M2-like cells is critical to mount a host defense or repair tissue.The exact molecular mechanisms controlling this process are still elusive.Here,we report that ubiquitin-specific protease 19(USP19)acts as an anti-inflammatory switch that inhibits inflammatory responses and promotes M2-like macrophage polarization.USP19 inhibited NLRP3 inflammasome activation by increasing autophagy flux and decreasing the generation of mitochondrial reactive oxygen species.In addition,USP19 inhibited the proteasomal degradation of inflammasome-independent NLRP3 by cleaving its polyubiquitin chains.USP19-stabilized NLRP3 promoted M2-like macrophage polarization by direct association with interferon regulatory factor 4,thereby preventing its p62-mediated selective autophagic degradation.Consistent with these observations,compared to wild-type mice,Usp19−/−mice had decreased M2-like macrophage polarization and increased interleukin-1βsecretion,in response to alum and chitin injections.Thus,we have uncovered an unexpected mechanism by which USP19 switches the proinflammatory function of NLRP3 into an anti-inflammatory function,and suggest that USP19 is a potential therapeutic target for inflammatory interventions. | Tao Liu Liqiu Wang Puping Liang Xiaojuan Wang Yukun Liu Jing Cai Yuanchu She Dan Wang Zhi Wang Zhiyong Guo Samuel Bates Xiaojun Xia Junjiu Huang Jun Cui | 2021 | Cellular & Molecular Immunology2021，18，10： | 15 |
| 5 | m6A RNA modification controls autophagy through upregulating ULK1 protein abundance显示文摘 | Shouheng Jin Xiya Zhang Yanyan Miao Puping Liang Kaiyu Zhu Yuanchu She Yaoxing Wu Di-Ao Liu Junjiu Huang Jian Ren Jun Cui | 2018 | Cell Research2018，28，9： | 12 |
| 6 | Questions about NgAgo显示文摘 | Shawn Burgess Linzhao Cheng Feng Gu Zhiwei Huang Shuo Lin Jinsong Li Wei Li Wei Qin Yujie Sun Zhou Songyang Wensheng Wei Qiang Wu Haoyi Wang Xiaoqun Wang Jing-Wei Xiong Jianzhong Xi Hui Yang Bin Zhou Bo Zhang Junjiu Huang | 2016 | Protein & Cell2016，7，12： | 5 |
| 7 | Effective and precise adenine base editing n mouse zygotes显示文摘 | Puping Liang Hongwei Sun Xiya Zhang Xiaowei Xie Jinran Zhang Yaofu Bai Xueling Ouyang Shengyao Zhi Yuanyan Xiong Wenbin Ma Dan Liu Junjiu Huang Zhou Songyang | 2018 | Protein & Cell2018，9，9： | 4 |
| 8 | HBB-deficient Macaca fascicularis monkey presents with human β-thalassemia显示文摘Dear Editor,β-Thalassemia is a common severe genetic disease caused by mutations in HBB and affects approximately 1.5% of the global population (Origa, 2017). In southern China, the carrier rate of β-thalassemia is as high as 6.43%, creating a high socio-economic burden (Xiong et al., 2010). In adult humans, there are three types of hemoglobin: HbA1 (~97%), HbA2 (~2%) and HbF (~1%). HbA1 (α2β2) is composed of two a-globin and two β-globi n sub units en coded by HBA and HBB, respectively;HbF (α2β2)is made up of two α-globin subunits and two β-globin sub units en coded by HBG. Mutations in the coding region or regulatory region of HBB are involved in β-thalassemia pathogenesis. Except for some rare dominant mutations, most HBB mutations are recessive (Origa, 2017). Depending on the mutation type, the β-globin level will either be reduced or completely depleted, resulting in α-globin accumulation and precipitation. These α-globin precipitates lead to red blood cell death, resulting in anemia and tissue damage, and even death in thalassemia major patients. Blood transfusions can help slow disease progression but lead to iron overload, ultimately resulting in iron toxicity. Bone marrow transfer is the only cure in the clinic and is available only to a small percentage of patients with human leukocyte antigervmatched donors. Recently, gene therapy and gene editing therapy have shown great promise in curing β-thalassemia (Glaser et al., 2015;Thompson et al., 2018). However, no appropriate animal models are available for evaluating the safety and efficacy of such advanced therapeutic strategies in vivo.β-thalassemia mice are the sole animal model available for research. However, substantial differences have been reported between the types and expressi on patter ns of human and mouse globins (McColl and Vadolas, 2016). Moreover, mice contain no fetal globin gene equivalent, and homozygous mutations of HBB in mouse for early models of β-thalassemia major or Cooley anemia are all embryonic lethal (Huo et al., 2009). Recently, significant phenotype and physiology differences have been reported between SIRT6- null mice and the non-human primate model (Zhang et al., 2018). Thus, an appropriate non-human primate model is needed for human β-thalassemia studies and treatments. | Yan Huang Chenhui Ding Puping Liang Duanduan Li Yu Tang Wei Meng Hongwei Sun Hongyu Lu Yu Chen Xueying Chen Qunshan Huang Jianpei Fang Canquan Zhou Shihua Yang Junjiu Huang | 2019 | Protein & Cell2019，10，7： | 4 |
| 9 | Telomere regulation in pluripotent stem cells显示文摘Pluripotent 干细胞(PSC ) 有潜力从所有三基本细菌层和能力生产房间的任何类型到自我更新并且在 vitro 无止境地增殖。PSC,胚胎的干细胞(转换字符) 和导致的 pluripotent 干细胞(iPSCs ) 的二种主要类型,分享象殖民地形态学, Oct4 和 Nanog 的高表示,和强壮的碱的磷酸酶活动那样的普通特征。在最近的年里,增加证据建议那 telomere 长度在维持干细胞 pluripotency 代表另一个重要内部因素。Telomere 长度动态平衡和它的结构的正直帮助保护染色体结束免受再结合,结束熔化,和 DNA 的伤害损坏回答,保证哺乳动物的房间的师的能力。PSC 通常展出高 telomerase 活动坚持说他们的极其长、稳定的 telomeres,和新兴的数据显示小径可以玩的 telomeres (中高音) 的其他的变长在 telomere 的一个重要角色也工作。如此的特征对他们在 vivo 区分进多样的房间类型的能力多半关键。在这评论,我们将在转换字符和 iPSCs 集中于 telomeres 的功能和规定,从而使 telomere 长度的重要性清楚些到在 PSC 调整 telomeres 的 pluripotency 和机制。 | Yan Huang Puping Liang Dan Liu Junjiu Huang Zhou Songyang | 2014 | Protein & Cell2014，5，3： | 3 |
| 10 | Association of telomere length with authentic pluripotency of ES/iPS cells显示文摘Telomerase 和 telomeres 为干细胞的不定的复制是重要的。最近,体的房间的 telomeres 被发现是 reprogrammed 在导致的 pluripotent 干细胞(iPSCs ) 伸长。然而,在在胚胎的干细胞(转换字符) 或 iPSCs 的 vivo 的发展 pluripotency 的 telomeres 的角色直接没被探讨。我们证明有长 telomeres 的转换字符展出真发展 pluripotency,由完全的转换字符小狗以及 germline 能干的怪物的产生证实了在啮齿类动物可得到的最紧的测试。有短 telomeres 的转换字符显示出减少的 teratoma 形成和怪物生产,并且没能产生完全的转换字符小狗。Telomere 长度高度被相关(r > 0.8 ) 与转换字符的发展 pluripotency。短 telomeres 减少 proliferative 率或转换字符的能力,改变与 telomere epigenetics 有关的基因的表示,为 embryogenesis 重要的下面调整基因并且破坏细菌房间区别。而且,有更长的 telomeres 的 iPSCs 与短 telomeres 比那些与更高的效率产生怪物。我们功能的 telomeres 为 ESCs/iPSCs 的发展 pluripotency 是必要的并且建议那 telomere 长度可以提供一个珍贵标记评估干细胞 pluripotency 的数据表演,特别地当紧测试不是可行的时。 | Junjiu Huang Fang Wang Maja Okuka Na Liu Guangzhen Ji Xiaoying Ye Bingfeng Zuo Minshu Li Ping Liang William W Ge John CM Tsibris David L Keefe Lin Liu | 2011 | Cell Research2011，21，5： | 3 |
| 11 | Homology-based repair induced by CRISPR-Cas nucleases in mammalian embryo genome editing显示文摘Recent advances in genome editing,especially CRISPR-Cas nucleases,have revolutionized both laboratory research and clinical therapeutics.CRISPR-Cas nucleases,together with the DNA damage repair pathway in cells,enable both genetic diversification by classical non-homologous end joining(c-NHEJ)and precise genome modification by homology-based repair(HBR).Genome editing in zygotes is a convenient way to edit the germline,paving the way for animal disease model generation,as well as human embryo genome editing therapy for some life-threatening and incurable diseases.HBR efficiency is highly dependent on the DNA donor that is utilized as a repair template.Here,we review recent progress in improving CRISPR-Cas nuclease-induced HBR in mammalian embryos by designing a suitable DNA donor.Moreover,we want to provide a guide for producing animal disease models and correcting genetic mutations through CRISPR-Cas nuclease-induced HBR in mammalian embryos.Finally,we discuss recent developments in precise genome-modification technology based on the CRISPR-Cas system. | Xiya Zhang Tao Li Jianping Ou Junjiu Huang Puping Liang | 2022 | Protein & Cell2022，13，5： | 3 |
| 12 | Inhibition of p53 and/or AKT as a new therapeutic approach specifically targeting ALT cancers显示文摘While the majority of all human cancers court teract telomere shortening by expressing telomerase,-15%of all cancers maintain telomere length by a telomerase?independent mechanism known as alternative lengthening of telomeres(ALT).Here,we show that high load of intrinsic DNA damage is present in ALT cancer cells,leading to apoptosis stress by activating p53-independent,but JNK/c-IVIyc-dependent apoptotic pathway.Notably,ALT cells expressing wild-type p53 show much lower apoptosis than p53-deficient ALT cells.Mechanistically,we find that intrinsic DNA damage in ALT cells induces low level of p53 that is insufficient to initiate the transcription of apoptosis-related genes,but is sufficient to stimulate the expression of key components of mTORC2(mTOR and Rictor),which in turn leads to phosphorylation of AKT.Activated AKT(p-AKT)thereby stimulates downstream anti-apoptotic events.Therefore,p53 and AKT are the key factors that suppress sponta?neous apoptosis in ALT cells.Indeed,inhibition of p53 or AKT selectively induces rapid death of ALT cells in vitro,and p53 inhibitor severely suppresses the growth of ALT-cell xenograft tumors in mice.These findings reveal a previously unrecognized function of p53 in antiapoptosis and identify that the inhibition of p53 or AKT has a potential as therapeutics for specifically targeting ALT cancers. | Yuanlong Ge Shu Wu Zepeng Zhang Xiaocui Li Feng Li Siyu Yan Haiying Liu Junjiu Huang Yong Zhao | 2019 | Protein & Cell2019，10，11： | 2 |
| 13 | Production of non-mosaic genome edited porcine embryos by injection of CRISPR/Cas9 into germinal vesicle oocytes显示文摘Genetically modified pigs represent a great promise for generating models of human diseases and producing new breeds.Generation of genetically edited pigs using somatic cell nuclear transfer(SCNT)or zygote cytoplasmic microinjection is a tedious process due to the low developmental rate or mosaicism of the founder(FO).Herein,we developed a method termed germinal vesicle oocyte gene editing(GVGE)to produce non-mosaic porcine embryos by editing maternal alleles during the GV to MII transition.Injection of Cas9 mRNA and X-linked Dmd gene-specific gRNA into GV oocytes did not affect their developmental potential.The MII oocytes edited during in vitro maturation(IVM)could develop into blastocysts after parthenogenetic activation(PA)or in vitro fertilization(IVF).Genotyping results indicated that the maternal gene X-linked Dmd could be efficiently edited during oocyte maturation.Up to81.3% of the edited IVF embryos were non-mosaic Dmd gene mutant embryos.In conclusion,GVGE might be a valuable method for the generation of non-mosaic maternal allele edited FO embryos in a short simple step. | Xiaohu Su Wei Chen Qingqing Cai Puping Liang Yaosheng Chen Peiqing Cong Junjiu Huang | 2019 | Journal of Genetics and Genomics2019，46，7： | 2 |
| 14 | TPP1 as a versatile player at the ends of chromosomes显示文摘Telomeres,线性真核细胞的染色体的结束,是双人脚踏车 DNA 重复并且由各种各样的 telomeric 蛋白质盖住。这些核蛋白建筑群保护 telomeres 免受 DNA 的伤害损坏反应(DDR ) ,再结合,和端对端的熔化,保证染色体稳定性。人的 telosome/shelterin 建筑群是学习最好的联系 telomere 的蛋白质建筑群之一,由六核心 telomeric 蛋白质 TRF1, TRF2, TIN2, RAP1, POT1,和 TPP1 组成。TPP1,也已知的同样肾上腺皮质的发育异常蛋白质相当或相同的事物(ACD ) ,是 TEBP- 的一个通常认为的哺乳动物的相当或相同的事物并且属于 oligonucleotide 绑定(OB )-fold-containing 蛋白质家庭。三功能的域在 TPP1, N 终端 OB 褶层, POT1 有约束力的招募域(RD ) ,和 carboxyl 终端交往 TIN2 域(TID ) 以内被识别了。TPP1 能与 POT1 和 TIN2 交往维持 telomere 结构,并且调停为 telomere 延伸的 telomerase 招募。这些特征显示了 TPP1 玩在 telomere 的一个必要角色维护。这里,我们将考察重要调查结果加亮 TPP1 的功能的意义,与它和另外的 telosome 部件和 telomerase 的相互作用的一个焦点。我们将也在疾病治疗讨论潜在的含意。 | Sijie ZHANG | 2014 | Frontiers in Biology2014，9，3： | 1 |
| 15 | Bend family proteins mark chromatin boundaries and synergistically promote early germ cell differentiation显示文摘Understanding the regulatory networks for germ cell fate specification is necessary to developing strategies for improving the efficiency of germ cell production in vitro.In this study,we developed a coupled screening strategy that took advantage of an arrayed bi-molecular fluorescence complementation(BiFC)platform for protein-protein interaction screens and epiblast-like cell(EpiLC)-induction assays using reporter mouse embryonic stem cells(mESCs).Investigation of candidate interaction partners of core human pluripotent factors OCT4,NANOG,KLF4 and SOX2 in EpiLC differentiation assays identified novel primordial germ cell(PGC)-inducing factors including BEN-domain(BEND/Bend)family members.Through RNA-seq,ChIP-seq,and ATAC-seq analyses,we showed that Bend5 worked together with Bend4 and helped mark chromatin boundaries to promote EpiLC induction in vitro.Our findings suggest that BEND/Bend proteins represent a new family of transcriptional modulators and chromatin boundary factors that participate in gene expression regulation during early germline development. | Guang Shi Yaofu Bai Xiya Zhang Junfeng Su Junjie Pang Quanyuan He Pengguihang Zeng Junjun Ding Yuanyan Xiong Jingran Zhang Jingwen Wang Dan Liu Wenbin Ma Junjiu Huang Zhou Songyang | 2022 | Protein & Cell2022，13，10： | 1 |
| 16 | Effective generation of maternal genome point mutated porcine embryos by injection of cytosine base editor into germinal vesicle oocytes显示文摘Cytosine and adenine base editors are promising new tools for introducing precise genetic modifications that are required to generate disease models and to improve traits in pigs. Base editors can catalyze the conversion of C→T(C>T) or A→G(A>G) in the target site through a single guide RNA. Injection of base editors into the zygote cytoplasm can result in the production of offspring with precise point mutations, but most F0 are mosaic, and breeding of F1 heterozygous pigs is time-intensive. Here, we developed a method called germinal vesicle oocyte base editing(GVBE) to produce point mutant F0 porcine embryos by editing the maternal alleles during the GV to MⅡ transition. Injection of cytosine base editor 3(BE3) mRNA and X-linked Dmdspecific guide RNAs into GVoocytes efficiently edited maternal Dmd during in vitro maturation and did not affect the maturation potential of the oocytes. The edited MⅡ oocytes developed into blastocysts after parthenogenetic activation(PA) or in vitro fertilization(IVF). However, BE3 may reduce the developmental potential of IVF blastocysts from 31.5%±0.8% to 20.4%±2.1%. There 40%–78.3% diploid PA blastocysts had no more than two different alleles, including up to 10% embryos that had only C>T mutation alleles. Genotyping of IVF blastocysts indicated that over 70% of the edited embryos had one allele or two different alleles of Dmd. Since the male embryos had only a copy of Dmd allele, all five(5/19) F0 male embryos are homozygous and three of them were Dmd precise C>T mutation. Nine(9/19) female IVF embryos had two different alleles including a WT and a C>T mutation. DNA sequencing showed that some of them might be heterozygous embryos. In conclusion, the GVBE method is a valuable method for generating F0 embryos with maternal point mutated alleles in a single step. | Xiaohu Su Wei Chen Qingqing Cai Puping Liang Yaosheng Chen Peiqing Cong Junjiu Huang | 2020 | Science China(Life Sciences)2020，63，7： | 1 |
| 17 | Cost-effective generation of A-to-G mutant mice by zygote electroporation of adenine base editor ribonucleoproteins显示文摘More than 32,000 pathogenic single nucleotide polymorphisms(SNPs)have been identified in the human genome(Gaudelli et al.,2017).Genetically modified mice with pathogenic SNPs are good models for studies of disease pathogenesis and the development of new therapeutics.Accordingly,an efficient,high-throughput method for the generation of mouse models with SNPs is needed. | Hongwei Sun Shengyao Zhi Guifang Wu Guanglan Wu Tianqi Cao Hu Hao Zhou Songyang Puping Liang Junjiu Huang | 2020 | Journal of Genetics and Genomics2020，47，6： | 1 |
| 18 | DeepNitro: Prediction of Protein Nitration and Nitrosylation Sites by Deep Learning显示文摘Protein nitration and nitrosylation are essential post-translational modifications(PTMs)involved in many fundamental cellular processes. Recent studies have revealed that excessive levels of nitration and nitrosylation in some critical proteins are linked to numerous chronic diseases.Therefore, the identification of substrates that undergo such modifications in a site-specific manner is an important research topic in the community and will provide candidates for targeted therapy. In this study, we aimed to develop a computational tool for predicting nitration and nitrosylation sites in proteins. We first constructed four types of encoding features, including positional amino acid distributions, sequence contextual dependencies, physicochemical properties, and position-specificscoring features, to represent the modified residues. Based on these encoding features, we established a predictor called DeepNitro using deep learning methods for predicting protein nitration and nitrosylation. Using n-fold cross-validation, our evaluation shows great AUC values for DeepNitro, 0.65 for tyrosine nitration, 0.80 for tryptophan nitration, and 0.70 for cysteine nitrosylation, respectively,demonstrating the robustness and reliability of our tool. Also, when tested in the independent dataset, DeepNitro is substantially superior to other similar tools with a 7%à42% improvement in the prediction performance. Taken together, the application of deep learning method and novel encoding schemes, especially the position-specific scoring feature, greatly improves the accuracy of nitration and nitrosylation site prediction and may facilitate the prediction of other PTM sites. DeepNitro is implemented in JAVA and PHP and is freely available for academic research at http://gffzz99614c6466484d9dhnxcv9bw0c0qc6owp.ffgz.tsg.suse.edu.cn. | Yubin Xie Xiaotong Luo Yupeng Li Li Chen Wenbin Ma Junjiu Huang Jun Cui Yong Zhao Yu Xue Zhixiang Zuo Jian Ren | 2018 | Genomics, Proteomics & Bioinformatics2018，16，4： | 1 |
| 19 | TERC suppresses PD-L1 expression by downregulating RNA binding protein HuR显示文摘TERC is the RNA component of telomerase,and provides a template for TERT to synthesize telomere repeats at chromosome ends.Increasing evidence has revealed that TERC is involved in other biological processes beyond telomerase.Here,we found that the expression level of TERC is negatively correlated with PD-L1 and that ectopic expression of TERC but not TERT in ALT cells significantly inhibits PD-L1,suggesting that TERC suppresses PD-L1 expression in a telomerase-independent manner.Mechanistically,instead of regulating PD-L1 m RNA directly,TERC accelerates PD-L1 m RNA degradation by inhibiting the expression of Hu R,which binds to the 3′UTR of PD-L1 m RNA and maintains its stability.We also found that the small molecule AS1842856,a Fox O1 inhibitor,promotes TERC expression and reverses the PD-L1 upregulation caused by chemotherapy,providing a potential combination cancer therapy that avoids cancer immune escape during chemotherapy. | Heping Jin Yanlian Chen Jian Ren Junjiu Huang Yong Zhao Haiying Liu | 2022 | Science China(Life Sciences)2022，65，12： | 0 |
| 20 | Endogenous reverse transcriptase and RNase H-mediated antiviral mechanism in embryonic stem cells显示文摘Nucleic acid-based systems play important roles in antiviral defense,including CRISPR/Cas that adopts RNA-guided DNA cleavage to prevent DNA phage infection and RNA interference(RNAi)that employs RNA-guided RNA cleavage to defend against RNA virus infection.Here,we report a novel type of nucleic acid-based antiviral system that exists in mouse embryonic stem cells(mESCs),which suppresses RNA virus infection by DNA-mediated RNA cleavage.We found that the viral RNA of encephalomyocarditis virus can be reverse transcribed into complementary DNA(vcDNA)by the reverse transcriptase(RTase)encoded by endogenous retrovirus-like elements in mESCs.The vcDNA is negative-sense single-stranded and forms DNA/RNA hybrid with viral RNA.The viral RNA in the heteroduplex is subsequently destroyed by cellular RNase H1,leading to robust suppression of viral growth. | Junyu Wu Chunyan Wu Fan Xing Liu Cao Weijie Zeng Liping Guo Ping Li Yongheng Zhong Hualian Jiang Manhui Luo Guang Shi Lang Bu Yanxi Ji Panpan Hou Hong Peng Junjiu Huang Chunmei Li Deyin Guo | 2021 | Cell Research2021，31，9： | 0 |
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