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| 1 | A small natural molecule promotes mitochondrial fusion through inhibition of the deubiquitinase USP30显示文摘Mitochondrial 熔化是为正常 mitochondrial 功能和 mitochondrial DNA 继承混合并且统一 mitochondrial 分隔空间的一个高度协调的过程。Dysregulated mitochondrial 熔化原因 mitochondrial 破碎,反常 mitochondrial 生理学和继承,并且有原因地与很多 neuronal 疾病被连接了。这里,我们识别了 potently 导致了 mitochondrial 熔化在在 Mfn1 或 Mfn2 是缺乏的房间恢复 mitochondrial 网络和氧化呼吸的 diterpenoid 衍生物 15-oxospiramilactone (S3 ) 。线粒体局部性的 deubiquitinase USP30 是 S3 的一个目标。由 S3 的 USP30 的抑制导致 Mfn1/2 的 non-degradative ubiquitination 的增加,它提高 Mfn1 和 Mfn2 活动并且支持 mitochondrial 熔化。通过 USP30 的一个禁止者的使用,因此,我们的学习揭开在支持 mitochondrial 的 Mfns 的 non-degradative ubiquitination 的异乎寻常的功能熔化。 | Wen Yue Ziheng Chen HaiYang Li Chen Yan Ming Chen Du Feng Chaojun Yan Hao Wu Lei Du Yueying Wang Jinhua Liu Xiaohu Huang Laixin Xia Lei Liu Xiaohui Wang Haijing Jin Jun Wang Zhiyin Song Xiaojiang Hao Quan Chen | 2014 | Cell Research2014，24，4： | 18 |
| 2 | Beclin 1 cleavage by caspase-3 inactivates autophagy and promotes apoptosis显示文摘Autophagy and apoptosis are both highly regulated biological processes that play essential roles in tissue homeostasis,development and diseases.Autophagy is also described as a mechanism of death pathways,however,the precise mechanism of how autophagy links to cell death remains to be fully understood.Beclin 1 is a dual regulator for both autophagy and apoptosis.In this study we found that Beclin 1 was a substrate of caspase-3 with two cleavage sites at positions 124 and 149,respectively.Furthermore,the autophagosome formation occurred,followed by the appearance of morphological hallmarks of apoptosis after staurosporine treatment.The cleavage products of Beclin 1 reduced autophagy and promoted apoptosis in HeLa cells and the cells in which Beclin 1 was stably knocked down by specific shRNA.In addition,the cleavage of Beclin 1 resulted in abrogating the interaction between Bcl-2 with Beclin 1,which could be blocked by z-VAD-fmk.Thus,our results suggest that the cleavage of Beclin 1 by caspase-3 may contribute to inactivate autophagy leading towards augmented apoptosis. | Yushan Zhu Lixia Zhao Lei Liu Ping Gao Weili Tian Xiaohui Wang Haijing Jin Haidong Xu Quan Chen | 2010 | Protein & Cell2010，1，5： | 17 |
| 3 | Association of WNK1 exon 1 polymorphisms with essential hypertension in Hani and Yi minorities of China显示文摘在有在少数的必要高血压的 1 WNK1 基因中国的 Hani 和 Yi 组织的 exon 的多型性的协会在盒子控制学习被调查。包含 WNK1 基因 exon 的 1257 bp 的顺序 1 在 1307 个个人(649 个必要高血压题目和 658 控制) 被决定在 Hani 和 Yi 少数组识别 SNP。十一以前已知的 SNP (rs3168640, rs11885, rs11554421 和 rs34880640 ) 中的四个被识别。SNP 分析显示 SNP rs11885 和 rs11554421 显著地在 Hani 和 Yi 人口与高血压被联系,并且 rs34880640 显著地在 Hani 然而并非在 Yi 人口与高血压被联系,为 covariates 调整了。Haplotype 分析显示 haplotype H1 显著地减少了在两张人口的高血压的风险。这些结果建议 WNK1 多型性在 Hani 和 Yi 人口涉及必要高血压的倾向,它的效果显示出清楚的人口特性。这发现在决定基因因素把疾病治疗与疾病并且这样联系了支持了人口特性的重要性。 | Yina Cun Jin Li Wenru Tang Xiaozhi Sheng Haijing Yu Bingrong Zheng Chunjie Xiao | 2011 | Journal of Genetics and Genomics2011，38，4： | 7 |
| 4 | Redox status of thioredoxin-1 (TRX1) determines the sensitivity of human liver carcinoma cells (HepG2) to arsenic trioxide-induced cell death显示文摘细胞内部的氧化还原作用动态平衡在决定肿瘤房间的敏感到导致药的 apoptosis 起一个关键作用。这里,我们调查了 thioredoxin-1 (TRX1 ) 的角色,氧化还原作用规定的一个关键部件,在砷三氧化物(作为(2 ) O (3 )) 导致的 apoptosis。在 HepG ( 2 )房间的野类型的 TRX1 的在表示上导致了抑制当( 2 ) O ( 3 )导致了细胞色素 c ( cyto c ),释放, caspase 激活和 apoptosis ,并且由 RNAi 的 TRX1 表示的绒毛规定敏化 HepG ( 2 )房间到当( 2 ) O ( 3 )导致了 apoptosis 。有趣地,到重量的单位(32/35 ) 的从 Cys (32/35 ) 的 TRX1 的活跃地点的变化从一个 apoptotic 保护者把这个分子变换成一个 apoptotic 倡导者。以理解这变换的机制,我们从老鼠肝使用了孤立的线粒体并且发现了野类型的 TRX1 能保护的那重组体从 apoptotic 的线粒体变化。相反, TRX1 的变异的形式独自得到了线粒体相关的 apoptotic 变化,包括 mitochondrial 渗透转变毛孔(mPTP ) 洞, mitochondrial 膜潜力的损失,和 cyto 从线粒体的 c 版本。这些 apoptotic 效果被 cyclosporine A (CsA ) 禁止,显示指向到 mPTP 的那变异的 TRX1。到由 2,4-dinitrochlorobenzene (DNCB ) 的氧化形式体内的从它的减少的形式的 TRX1 的改变, TRX reductase 的一个特定的禁止者,也敏化的 HepG (2 ) 房间到当(2 ) O (3 ) 导致了 apoptosis。这些数据建议 TRX1 由任何一个变化在由堵住 cyto c 版本调整 apoptosis,并且在 TRX1 的激活起一个中央作用或活跃地点半胱氨酸的氧化可以敏化肿瘤房间到当(2 ) O (3 ) 导致了 apoptosis。 | Changhai Tian Ping Gao Yanhua Zheng Wen Yue Xiaohui Wang Haijing Jin Quan Chen | 2008 | Cell Research2008，18，4： | 7 |
| 5 | Caspase cleavage of cytochrome cl disrupts mitochondrial function and enhances cytochrome c release显示文摘 | Yushan Zhu Min Li Xiaohui Wang Haijing Jin Shusen Liu Jianxin Xu Quan Chen | 2012 | Cell Research2012，22，1： | 6 |
| 6 | Bid BH3 peptide,but not its mutant form G^(94)E, induces permeability transition pore opening and cytochrome c release in vitro显示文摘It has been shown that Bid and its truncated form tBid could induce cytochrome c (cyt c) release without impacting on PTP. We first show that Bid BH3 peptide, but not its mutant form of Bid BH3 peptide G94E, which is unable to bind to Bcl-xL, induces permeability transition pore (PTP) opening in a dose dependent manner. Bid BH3 peptide also induces the reduction of mitochondria membrane potential (Ψm) and cyt c release from mitochondrial in vitro. PTP opening and the loss of Ψm, were inhibited by Bcl-xL, cyclosporin A and ruthenium red, and the latter was an inhibitor of Ca2+ uniporter in the mitochondrial membrane. These results indicate that Bid BH3 peptide could antagonize Bcl-xL to induced PTP opening and mitochondrial dysfunction. | XIATian, JIANG Chunsun, LI Linjiang, ZHANG Yong, JIN Haijing, LIU Shusen, WU Caihong & CHEN QuanThe National Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100080, China The National Ke | 2002 | Chinese Science Bulletin2002，47，7： | 1 |
| 7 | Real-time cellular analysis for quantitative detection of functional Clostridium difficile toxin in stool显示文摘 | Huang Bin Li Haijing Jin Dazhi | 2014 | Expert Rev Mol Diagn2014，14，3： | 1 |
| 8 | A possible endoscopic therapy for large hiatal hernia complicated with refractory gastroesophageal reflux disease显示文摘A hiatal hernia(HH)is usually associated with gastroesophageal reflux disease(GERD).An HH can increase the incidence of GERD.[1]The coexistence of these diseases increases the difficulty of treatment and can be challenging for endoscopic treatment.Therapeutic methods for small HHs(≤2 cm)combined with refractory GERD have recently been emerging.However,there are still knowledge gaps in the endoscopic treatment of large HHs(≥3cm)combined with refractory GERD.We developed a new endoscopic method called hiatal hernia-endoscopic submucosal dissection(HH-ESD)and performed the present study to clarify the efficacy and safety of HH-ESD. | Haijing Zhang Haiping Zhao Mingxing Hou Chunlu Jin Rui Rui Baiyinbatu Xie Ying Li Zhiguang Hu Guanlan Liu Feng Guo Haiqing Hu | 2022 | Chinese Medical Journal2022，，8： | 1 |
| 9 | A tumor-penetrable drug nanococktail made from human histones for interventional nucleus-targeted chemophotothermal therapy of drug-resistant tumors显示文摘Nanoparticle-based chemophotothermal therapy(CPT)is a promising treatment for multidrug resistant tumors.In this study,a drug nanococktail of DIR825@histone was developed by employing doxorubicin(DOX),NIR dye IR825 and human histones for interventional nucleus-targeted CPT of multidrug resistant tumors with an interventional laser.After localized intervention,DIR825@histone penetrated tumor tissues by transcytosis,efficiently entered tumor cells and targeted the cell nuclei.DIR825@histone also exhibited good photothermal performance and thermal-triggered drug release.Efficient multidrug resistant tumor inhibition was achieved by enhanced CPT sensitization and MDR reversion via nuclear targeting.Moreover,an interventional laser assisted DIR825@histone in inhibiting multidrug resistant tumors by promoting the sufficient delivery of laser energy inside the tumor while reducing skin injury.Therefore,DIR825@histone together with this interventional nucleus-targeted CPT strategy holds great promise for treating multidrug resistant tumors. | Jianquan Guo Dongsheng Tan Chenmei Lou Shiying Guo Xing Jin Haijing Qu Lijia Jing Sijin Li | 2022 | Bioactive Materials2022，7，3： | 0 |
| 10 | The effect of subbranch for the quantification of local hemodynamic environment in the coronary artery:a computed tomography angiography–based computational fluid dynamic analysis显示文摘Background:Hemodynamic parameters derived from computed tomography angiography–based computational fluid dynamics(CFD)analysis have been widely used for clinical decision-making and researches to assess the vulnerability of atherosclerotic plaques and explain the initialization and development of atherosclerosis.Subbranches in the CFD model might affect the accuracy of hemodynamic parameters,but the effectiveness has been least quantified.Methods:A coronary artery baseline model was generated with focal stenosis at the proximal left anterior descending artery.Nineteen comparing models were created by systematically removing various subbranches to examine the changes in hemodynamic parameters,including time-averaged pressure(TAP),time-averaged wall shear stress(TAWSS),oscillatory shear index(OSI),and particle relative residence time(RRT).Changes in these parameters were assessed quantitatively around the stenosis and near the region where subbranches were removed.Results:The removal of subbranches caused a significant change in outflow rate,and there was generally a decrease in all CFD parameters in the regions of interest with a decrease in outflow rate.The subbranch removal had a significant impact on the calculation of TAWSS,OSI,and RRT,whereas TAP was insensitive to the removal with approximately 0.25%variation in all 19 models.The local effect from removing branch segments generally became negligible after 5 diameters away from the cutting-off position,but the decrease could be affected by other factors,such as a large curvature.Conclusion:The outflow rate is a dominant factor for the calculation of TAP,TAWSS,OSI,and RRT.Removal of subbranches has a minor effect on the TAP calculation,but its effect is considerable on the TAWSS,OSI,and RRT.The effect of subbranch removal is limited in a region with 5 local diameters. | Yibing Shi Jin Zheng Ning Yang Yang Chen Jingxi Sun Ying Zhang Xuanxuan Zhou Yongguang Gao Suqing Li Haijing Zhu Julio Acosta-Cabronero Ping Xia Zhongzhao Teng | 2022 | Emergency and Critical Care Medicine2022，2，4： | 0 |
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