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| 1 | JMJD3 is a histone H3K27 demethylase显示文摘组蛋白甲基化是参予细胞的过程的一个多样的数组的重要 epigenetic 现象并且被发现了与癌症被联系。几的 Recentidentification 嘘一 demethylases 证明了那嘘一甲基化是一个可逆过程。通过一条候选人途径,我们化学上有简历作为 H3K27demethylase 识别了 JMJD3。进 HeLa 房间的 JMJD3 的 Transfection 引起了整齐的乙醇 H3K27 的特定的减小,但是没在 di- 和单音的甲基 H3K27 上有效果,或嘘 H3K4 和 H3K9 上的一离氨酸 methylations。Theenzymatic 活动要求 JmjC 域和被建议了为余因子绑定重要的保存组氨酸。试管内生物化学的实验证明那 JMJD3directly 催化 demethylation。另外,我们发现 JMJD3 起来在前列腺癌症,和它的表示调整了在变形前列腺癌症是更高的。因此,我们作为能够把整齐的乙醇组从移开的 ademethylase 识别了 JMJD3 嘘一 H3 离氨酸 27 并且起来在前列腺癌症调整了。 | Yang Xiang Ziqi Zhu Gang Han Hanqing Lin Longyong Xu Charlie Degui Chen | 2007 | Cell Research2007，17，10： | 37 |
| 2 | Dual-specificity histone demethylase KIAA1718 (KDM7A) regulates neural differentiation through FGF4显示文摘histone H3 离氨酸的 Dimethylations 9 和离氨酸 27 是与抄写压抑联系的重要 epigenetic 标记。这里,我们作为为这二个镇压标记特定的新奇 histone demethylase 识别了 KIAA1718 (KDM7A ) 。用老鼠胚胎的干细胞,我们证明那 KIAA1718 表情在神经区别的早阶段增加了。基因击倒堵住的神经区别和效果被野类型的人的基因,并且不由催化地不活跃的异种救。另外, KIAA1718 的 overexpression 加速了神经区别。我们提供 KDM7A 的支持 neural 区别效果通过 FGF4 的直接 transcriptional 激活被调停的证据,一个信号分子在神经区别含有。因此,我们的学习识别了通过 FGF4 调整神经区别的双特性的 histone demethylase。 | Chengyang Huang Yang Xiang Yanru Wang Xia Li Longyong Xu Ziqi Zhu Ting Zhang Qingqing Zhu Kejing Zhang Naihe Jing Charlie Degui Chen | 2010 | Cell Research2010，20，2： | 15 |
| 3 | Overexpressed miR-9 promotes tumor metastasis via targeting E-cadherin in serous ovarian cancer显示文摘MicroRNAs (miRNAs ) 玩在在各种各样的癌症的发展和前进的关键角色。不正常的 miR-9 表示仍然保持模糊,并且卵巢的癌症的变形前进上的一致都没被到达。在这研究,从生物信息学分析的结果证明 E-cadherin mRNA 的 3-UTR 被 miR-9 直接调整。酶记者试金结果证实 miR-9 能直接指向这 3-UTR。在卵巢的癌症织物的 miR-9 和 E-cadherin 表示被 qRT-PCR 确定。移植和侵略被在 SKOV3 和 A2780 愈合弯屈和 Transwell 系统试金检测。qRT-PCR 和西方的污点被执行检测上皮 ? 间充质的联系转变的 mRNA 和蛋白质。Immunofluorescence 技术被用来分析表示和 E-cadherin, N-cadherin,和 vimentin 的 subcellular 本地化。结果证明 miR-9 经常与配对的主要的相比是在变形浆液的卵巢的癌症织物的 upregulated。miR-9 的 Upregulation 能 downregulate E-cadherin 的表示但是 upregulate 间充质的标记(N-cadherin 和 vimentin ) 的表示。miR-9 的 Overexpression 能在卵巢的癌症支持房间移植和侵略,并且这些进程能有效地经由 miR-9 禁止者被禁止。因此,我们的学习证明 miR-9 可以经由指向 E-cadherin 和一条新奇潜在的治疗学的途径控制卵巢的癌症的转移支持卵巢的癌症转移。 | Bo Zhou Hongbin Xu Meng Xia Chaoyang Sun Na Li Ensong Guo Lili Guo Wanying Shan Hao Lu Yifan Wu Yuan Li Degui Yang Danhui Weng Li Meng Junbo Hu Ding Ma Gang Chen Kezhen Li | 2017 | Frontiers of Medicine2017，11，2： | 10 |
| 4 | PHF8 is a histone H3K9me2 demethylase regulating rRNA synthesis显示文摘histone H3 离氨酸 9 的 Dimethylation (H3K9me2 ) 是与抄写压抑联系的一个重要 epigenetic 标记。这里,我们识别了 PHF8, JmjC-domain-containing 蛋白质,为这个镇压标记特定的 histone demethylase。Recombinant 全身的野类型蛋白质能把 methylation 从 H3K9me2 移开,但是到丙氨酸 H247A 的保存 histidine 的变化废除 demethylase 活动。Overexpressed 外长的 PHF8 是 colocalized, B23 染色。内长的 PHF8 也是有 B23 和 fibrillarin 的 colocalized,二生长得很好的核蛋白质,建议那 PHF8 在核是局部性的并且可以调整 rRNA 抄写。确实, PHF8 跳了到 rDNA 基因的倡导者区域。减少的 PHF8 击倒 rRNA 的表示,和基因的 overexpression 导致了 rRNA 的 upregulation 抄本。附随地, H3K9me2 水平在 PHF8 击倒的房间在 rDNA 基因的倡导者区域被提高并且当野类型然而并非催化地不活跃的 H247A 变异的 PHF8 是 overexpressed 时,显著地减少了。因此,我们的学习为调整 rRNA 抄写的 H3K9me2 识别了 histone demethylase。 | Ziqi Zhu Yanru Wang Xia Li Yiqin Wang Longyong Xu Xiang Wang Tianliang Sun Xiaobin Dong Lulu Chen Hailei Mao Yi Yu Jingsong Li Pin Adele Chen Charlie Degui Chen | 2010 | Cell Research2010，20，7： | 7 |
| 5 | A sequence of 28S rRNA-derived small RNAs is enriched in mature sperm and various somatic tissues and possibly associates with inflammation显示文摘 | Chu, Chen Yu, Lu Wu, Bin Ma, Li Gou, Lan-Tao He, Miao Guo, Yunli Li, Zhi-Tong Gao, Wei Shi, Huijuan Liu, Mo-Fang Wang, Hongyan Chen, Charlie Degui Drevet, Joel R. Zhou, Yuchuan Zhang, Yonglian | 2017 | Journal of Molecular Cell Biology2017，9，3： | 6 |
| 6 | The histone H3 lysine-27 demethylase Jmjd3 plays a critical role in specific regulation of Th17 cell differentiation显示文摘Interleukin(IL)17-producing T helper(Th17)cells play critical roles in the clearance of extracellular bacteria and fungi as well as the pathogenesis of various autoimmune diseases,such as multiple sclerosis,psoriasis,and ulcerative colitis.Although a global transcriptional regulatory network of Th17 cell differentiation has been mapped recently,the participation of epigenetic modifications in the differentiation process has yet to be elucidated.We demonstrated here that histone H3 lysine-27(H3K27)demethylation,predominantly mediated by the H3K27 demethylase Jmjd3,crucially regulated Th17 cell differentiation.Activation of naı¨ve CD41 T cells immediately induced high expression of Jmjd3.Genetic depletion of Jmjd3 in CD41 T cells specifically impaired Th17 cell differentiation both in vitro and in vivo.Ectopic expression of Jmjd3 largely rescued the impaired differentiation of Th17 cells in vitro in Jmjd3-deficientCD41 T cells.Importantly,Jmjd3-deficient mice were resistant to the induction of experimental autoimmune encephalomyelitis(EAE).Furthermore,inhibition of the H3K27 demethylase activity with the specific inhibitor GSK-J4 dramatically suppressed Th17 cell differentiation in vitro.At the molecular level,Jmjd3 directly bound to and reduced the level of H3K27 trimethylation(me3)at the genomic sites ofRorc,which encodes the masterTh17 transcription factorRorgt,and Th17 cytokine genes such as Il17,Il17f,and Il22.Therefore,our studies established acritical role of Jmjd3-mediatedH3K27demethylation inTh17 cell differentiation andsuggest that Jmjd3 can be a novel therapeutic target for suppressing autoimmune responses. | Zhi Liu Wei Cao Longxia Xu Xi Chen Yu Zhan Qian Yang Sanhong Liu Pengfei Chen Yuhang Jiang Xiaohua Sun Yu Tao Yiming Hu Cuifeng Li Qi Wang Ying Wang Charlie Degui Chen Yufang Shi Xiaoren Zhang | 2015 | Journal of Molecular Cell Biology2015，7，6： | 6 |
| 7 | The androgen receptor in hormone-refractory prostate cancer显示文摘先进前列腺癌症对防碍发信号的雄激素受体(AR ) 的荷尔蒙治疗应答。然而,当将近所有瘤进行到,效果是短命的一荷尔蒙倔强(HR ) 说,疾病的一个致命的阶段。直觉地,因为堵住的荷尔蒙治疗或还原剂 AR 活动不在对待 HR 瘤是有效的, AR 不应该被包含。然而,仍然有一致, AR 玩在 HR 前列腺癌症(HRPC ) 的一个必要角色因为 AR 发信号在 HR 瘤仍然是功能的。发信号的 AR 能通过几机制在 HR 瘤被激活。首先,细胞内部的信号 transduction 小径的激活能敏化 AR 阉割雄激素的层次。另外,在 AR 的变化能改变 AR ligand 特性,从而允许它被非类固醇或反雄激素激活。最后,野类型的 AR 的 overexpression 敏化自己到雄激素的低集中。因此,指向 AR 发信号的药能仍然在对待 HRPC 是有效的。 | Hai-Lei Mao Zhi-Qi Zhu Charlie Degui Chen | 2009 | Asian Journal of Andrology2009，11，1： | 4 |
| 8 | Structural insights into a dual-specificity histone demethylase ceKDM7A from Caenorhabditis elegans显示文摘Histone 离氨酸 methylation 能被 JmjC 包含域的蛋白质在 sequence-state-specific 和 methylation-state-specific 举止移开。然而,底层特性怎么样,决定,酶怎么被调整,大部分是未知的。我们最近发现了那 ceKDM7A,一个哲学博士 -- 并且 JmjC 包含域的蛋白质,是为 H3K9me2 特定的 histone demethylase, H3K27me2,和 PHD 摸绑定到 H3K4me3 指南在 vivo 的 demethylation 活动。为了为酶的活动和 PHD 的功能提供结构的卓见进分子的机制,摸,我们与包含 H3K4me3, H3K9me2,和 H3K27me2 修正的各种各样的联合的单身者或二肽一起在 apo 形式并且在建筑群解决了酶的六水晶结构。结构显示 H3K9me2 和 H3K27me2 以一种类似的方式与 ceKDM7A 交往,并且肽绑定特性被特定的相互作用的一个网络决定。结构的几何测量也揭示了与 PHD 手指和 H3K9me2 界限联系到 JmjC 领域的那 H3K4me3 从二个分开的分子,建议 trans-histone 肽绑定机制。因此,我们的全身的结构的研究重要地由催化领域而且更多揭示底层识别不仅,为 H3K9me2 和 H3K27me2 的 ceDKM7A 的双特性的分子的机制。 | Ying Yang Lulu Hu Ping Wang Haifeng Hou Yan Lin Yi Liu Ze Li Rui Gong Xiang Feng Lu Zhou Wen Zhang Yuhui Dong Huirong Yang Hanqing Lin Yiqin Wang Charlie Degui Chen Yanhui Xu | 2010 | Cell Research2010，20，8： | 3 |
| 9 | Knockout of glutathione peroxidase 5 down-regulates the piRNAs in the caput epididymidis of aged mice显示文摘The mammalian epididymis not only plays a fun dame ntal role in the maturati on of spermatozoa,but also provides protecti on agai nst various stressors.The foremost among these is the threat posed by oxidative stress,which arises from an imbalance in reactive oxygen species and can elicit damage to cellular lipids,proteins,and nucleic acids.In mice,the risk of oxidative damage to spermatozoa is mitigated through the expression and secretion of glutathione peroxidase 5(GPX5)as a major luminal scavenger in the proximal caput epididymidal segment.Accordingly,the loss of GPX5^-/-mediated protection leads to impaired DNA integrity in the spermatozoa of aged Gpx57 mice.To explore the underlying mechanism,we have conducted transcriptomic analysis of caput epididymidal epithelial cells from aged(13 months old)Gpx5^-/-m mice.This analysis revealed the dysregulation of several thousand epididymal mRNA transcripts,in eluding the downregulation of a subgroup of piRNA pathway gen es,in aged Gpx5^-/-mice.In agreeme nt with these fin dings,we also observed the loss of piRNAs,which potentially bind to the P-element-induced wimpy testis(PlWI)-like proteins PIWIL1 and PIWIL2.The absence of these piRNAs was correlated with the elevated mRNA levels of their putative gene targets in the caput epididymidis of Gpx5^-/-mice.Importantly,the oxidative stress response genes tend to have more targeting piRNAs,and many of them were among the top increased genes upon the loss of GPX5^-/-.Taken together,our findings suggest the existence of a previously uncharacterized somatic piRNA pathway in the mammalian epididymis and its possible invoIvement in the aging and oxidative stress-mediated responses. | Chen Chu Lu Yu Joelle Henry-Berger Yan-Fei Ru Ayhan Kocer Alexandre Champroux Zhi-Tong Li Miao He Sheng-Song Xie Wu-Bin Ma Min-Jie Ni Zi-Mei Ni Yun-Li Guo Zhao-Liang Fei Lan-Tao Gou Qiang Liu Samanta Sharma Yu Zhou Mo-Fang Liu Charlie Degui Chen Andrew L Eamens Brett Nixon Yu-Chuan Zhou Joel R Drevet Yong-Lian Zhang | 2020 | Asian Journal of Andrology2020，22，6： | 2 |
| 10 | Mice generated after round spermatid injection into haploid two-cell blastomeres显示文摘 | Hui Yang Linyu Shi Charlie Degui Chen Jinsong Li | 2011 | Cell Research2011，21，5： | 2 |
| 11 | Coordinated regulation of active and repressive histone methylations by a dual-specificity histone demethylase ceKDM7A from Caenorhabditis elegans显示文摘H3K9me2 和 H3K27me2 是与抄写压抑联系的重要 epigenetic 标记,当 H3K4me3 与抄写激活被联系时。活跃、压抑的 histone methylations 以一种互相独占的方式散布,这被显示出,但是内在的机制糟糕被理解。这里,我们识别了 ceKDM7A,一个哲学博士(植物 homeodomain )- 并且 JmjC 包含域的蛋白质,为 H3K9me2 和 H3K27me2 特定的 histone demethylase。我们进一步证明 ceKDM7A 的 PHD 领域在染色体宽的水平绑了 H3K4me3 和与 ceKDM7A co 局部性的 H3K4me3。到 H3K4me3 的 PHD 域绑定的混乱在 vivo 减少了 demethylase 活动,并且 ceKDM7A 的损失减少了它的联系目标基因的表达式。这些结果显示 ceKDM7A 被招募到倡导者到 demethylate H3K9me2 和 H3K27me2 并且通过 PHD 领域的绑定激活基因表示到 H3K4me3。因此,我们的学习识别双特性的 histone demethylase 并且提供新奇卓见进 histone methylation 的规定。 | Hanqing Lin Yiqin Wang Yanru Wang Feng Tian Pu Pu Yi Yu Hailei Mao Ying Yang Ping Wang Lulu Hu Yan Lin Yi Liu Yanhui Xu Charlie Degui Chen | 2010 | Cell Research2010，20，8： | 2 |
| 12 | Effect of magnetic field of arc chamber and operating mechanism on current limiting characteristics of low voltage circuit breakers 显示文摘 | CHEN Degui LIU Hongwu SUN Haitao | 2003 | IEICE Transactions on Electronics2003，86，6： | 1 |
| 13 | Imaging and Spectrum Diagnostics of Air Arc Plasma Characteristics 显示文摘 | LI Xingwen CHEN Degui LIU Hongwu | 2004 | IEEE Trans on Plasma Sci2004，32，6： | 1 |
| 14 | Experimental Investigation on the Arc Motion with Different Configurations of Quenching Chamber in AC Contactor 显示文摘 | CHEN Degui DAI Ruicheng LI Xingwen | 2006 | IEICE Trans on Electronics2006，89，8： | 1 |
| 15 | A Novel Optical Fiber Measurement System of Arc Motion in Molded Case Circuit Breakers 显示文摘 | LI Xingwen CHEN Degui LIU Hongwu | 2004 | IEICE Trans on Electronics2004，87，8： | 1 |
| 16 | Study of the Influence of Arc Ignition Position on Arc Motion in Low Voltage Circuit Breaker 显示文摘 | LI Xingwen CHEN Degui DAI Ruicheng | 2007 | IEEE Trans on Plasma Sci2007，35，2： | 1 |
| 17 | Kernel lysine content does not increase in some maize opaque2 mutants显示文摘 | Gang Zhao Mingshun Li Degui Zhang Xinhai Li Zikai Wu Xiaoke Ci Chuanxiao Xie Li Bai Zhenyu Lu Liang Chen Zhuanfang Hao Shihuang Zhang | 2012 | Planta2012，，1： | 1 |
| 18 | Parallel Digital Simulation for the Control Problem in Differential Algebraic System显示文摘Parallel Digital Simulation for the Control Problem in Differential Algebraic SystemChenLirong&LiuDegui(BeijingInstituteofCom... | Chen Lirong & Liu Degui(Beijing Institute of Computer Application and Simulation Technology,P.O.Box 3929, Beijing 100854, P.R.China) | 1996 | Journal of Systems Engineering and Electronics1996，7，4： | 1 |
| 19 | Genetic and Phenotypic Investigation of a Chinese Pedigree with Lattice Corneal Dystrophy ⅢB Subtype显示文摘Purpose:.To investigate phenotypes and disease-causing mutation in the transforming growth factor b-induced gene(TGFBI) in a Southern Chinese pedigree with lattice corneal dystrophy(LCD) IIIB with complicated cataract.Methods:.A Southern Chinese pedigree with lattice corneal dystrophy IIIB with complicated cataract was recruited. Comprehensive ophthalmic investigations were performed before and after cataract surgery of phacoemulsification and intraocular lens implantation in the proband's both eyes..Peripheral blood was collected from the proband,.and genomic DNA was extracted..All exons of the TGFBI gene were sequenced to screen possible mutations.Results:.A bilateral LCD IIIB subtype was observed in the proband..Optical coherence tomography further revealed superreflective changes in the subepithelial and stroma layers of the cornea,.with reduced central corneal thickness..Notably,bilateral cataract was found in the proband..Direct sequencing detected a recurrent heterozygous missense c.1877A>G mutation in exon 14 of the TGFBI gene,.resulting in substitution of histidine with arginine(p.H626R).Conclusion:.The current study was the first report of the TGFBI p.H626R mutation in Southern Chinese,.suggesting that it could be a mutation hotspot across populations..Moreover,.the mutation was associated with LCD IIIB subtype with complicated cataract,.which had not been reported before,pointing to clinical heterogeneity of the mutation. | Degui Wang Yong Yao Mingzhi Zhang Jianhuan Chen | 2013 | Eye Science2013，28，3： | 1 |
| 20 | A class of twostep continuity Runge-Kutta methods for solving singular delay differential equations and its convergence显示文摘An idea of relaxing the effect of delay when computing the RungeKutta stages in the current step and a class of twostep continuity RungeKutta methods (TSCRK) is presented. Their construction, their order conditions and their convergence are studied. The twostep continuity RungeKutta methods possess good numerical stability properties and higher stageorder, and keep the explicit process of computing the RungeKutta stages. The numerical experiments show that the TSCRK methods are efficient. | Leng Xin Liu Degui Song Xiaoqiu Chen Lirong | 2005 | Journal of Systems Engineering and Electronics2005，16，4： | 1 |
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