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| 1 | Highly efficient differentiation of human ES cells and iPS cells into mature pancreatic insulin-producing cells显示文摘人的 pluripotent 干细胞代表功能的胰腺的内分泌的系房间的潜在地无限的来源。这里,我们报导一条高度有效的途径导致人的胚胎的茎(ES ) 细胞和导致的 pluripotent 茎(iPS ) 在一个定义化学药品的文化系统区分进成熟生产胰岛素的细胞的细胞。这条途径获得的区分的人的 ES 房间由流动 cytometry 分析作为 assayed 包括了将近 25% 胰岛素积极的房间,它以比得上成年人的小岛的一种方式响应葡萄糖刺激释放了 insulin/C-peptide。大多数这些生产胰岛素的房间共同表示成熟尾房间特定的标记象 NKX6-1 和 PDX1 那样,在 vivo 显示一个类似的基因表示模式到成年小岛尾房间。在这研究,我们也证明 EGF 便于 PDX1 积极的胰腺的祖先的扩大。而且,我们的协议也成功了高效地导致人的 iPS 房间区分进生产胰岛素的房间。因此,这个工作不仅提供一个新模型在 vitro 学习人的胰腺的专门化和成熟的机制,而且提高为糖尿病的处理利用病人特定的 iPS 房间的可能性。 | Donghui Zhang Wei Jiang Meng Liu Xin Sui Xiaolei Yin Song Chen Yan Shi Hongkui Deng | 2009 | Cell Research2009，19，4： | 90 |
| 2 | Mammalian WTAP is a regulatory subunit of the RNA N6-methyladenosine methyltransferase显示文摘包含 methyltransferase 建筑群的象 3 一样的 methyltransferase (METTL3 ) 催化 N6-methyladenosine (m6A ) 形成,一个新奇 epitranscriptomic 标记;然而,这建筑群的性质仍然保持大部分未知。这里,我们报导人的 m6A methyltransferase 建筑群, Wilm 的肿瘤 1 伙伴蛋白质(WTAP ) 和象 14 一样的 methyltransferase (METTL14 ) 的二个新部件。WTAP 与 METTL3 和 METTL14 交往,并且为他们的本地化被要求进在 vivo 与处理因素的 pre-mRNA 并且为 m6A methyltransferase 的催化活动充实的原子点缀。RNA 的多数在 vivo 由 WTAP 和 METTL3 跳了代表包含一致 m6A 主题的 mRNAs。当 WTAP 不在时, METTL3 的 RNA 有约束力的能力强烈被减少,建议 WTAP 可以工作调整到 mRNA 目标的 m6A methyltransferase 建筑群的招募。而且,在有 photoactivatable-ribonucleoside-enhanced crosslinking 和 immunoprecipitation (同等片断) 的联合的 transcriptomic 分析说明那 WTAP 和 METTL3 调整涉及抄写并且 RNA 处理的基因拼接的表示和选择。在 zebrafish 胚胎的调停 Morpholino 的击倒的指向 WTAP 或 METTL3 引起了织物区别缺点并且增加了 apoptosis。这些调查结果提供 WTAP 可以在 m6A methyltransferase 建筑群作为一个规章的子单元工作并且在 RNA 的 epitranscriptomic 规定起一个关键作用的充分证据新陈代谢。 | Xiao-Li Ping Bao-Fa Sun Lu Wang Wen Xiao Xin Yang Wen-Jia Wang Samir Adhikari Yue Shi Ying Lv Yu-Sheng Chen Xu Zhao Ang Li Ying Yang Ujwal Dahal Xiao-Min Lou Xi Liu Jun Huang Wei-Ping Yuan Xiao-Fan Zhu Tao Cheng Yong-Liang Zhao Xinquan Wang Jannie M Rendtlew Danielsen Feng Liu Yun-Gui Yang | 2014 | Cell Research2014，24，2： | 244 |
| 3 | FTO-dependent demethylation of N6-methyladenosine regulates mRNA splicing and is required for adipogenesis显示文摘 | Xu Zhao Ying Yang Bao-Fa Sun Yue Shi Xin Yang Wen Xiao Ya-Juan Hao Xiao-Li Ping Yu-Sheng Chen Wen-Jia Wang Kang-Xuan Jin Xing Wang Chun-Min Huang Yu Fu Xiao-Meng Ge Shu-Hui Song Hyun Seok Jeong Hiroyuki Yanagisawa Yamei Niu Gui-Fang Jia Wei Wu Wei-Min Tong Akimitsu Okamoto Chuan He Jannie M Rendtlew Danielsen Xiu-Jie Wang Yun-Gui Yang | 2014 | Cell Research2014，24，12： | 109 |
| 4 | Gasdermin D is an executor of pyroptosis and required for interleukin-lp secretion显示文摘 | Wan-ting He Haoqiang Wan Lichen Hu Pengda Chen Xin Wang Zhe Huang Zhang-Hua Yang Chuan-Qi Zhong Jiahuai Han | 2015 | Cell Research2015，25，12： | 195 |
| 5 | Pyroptosis is driven by non-selective gasdermin-D pore and its morphology is different from MLKL channel-mediated necroptosis显示文摘Necroptosis 和 pyroptosis 是有血浆膜破裂的一个普通特征的规划房间死亡的二种形式。这里,我们与 necroptosis 比较学习了 pyroptosis 的形态学和机制。与 necroptosis 不同, pyroptosis 经历膜 blebbing 并且生产 apoptotic 在血浆膜以前的像身体的房间伸出(称为的 pyroptotic 身体) 破裂。在 necroptosis 的破裂是像爆炸的,而在 pyroptosis 它导致房间变平。necroptosis 的实行被混合的系 kinase 调停,这被知道像域(MLKL ) 在血浆膜的 oligomers,而 gasdermin-D (GSDMD ) 调停在它由 caspase-1 或 caspase-11 的劈开以后的 pyroptosis。我们显示出那 N 终端碎片 caspase 劈开产生的 GSDMD (GSDMD-N ) 也形成 oligomer 并且移居到血浆膜杀死房间。MLKL 和 GSDMD-N 是脂性的,两蛋白质的 N 终端序列为他们的 oligomerization 和血浆膜 translocation 是重要的。不同于在血浆膜上形成隧道的 MLKL,那导致渗透地胀大的选择离子的流入冲破的房间, GSDMD-N 形成非选择的毛孔并且不依靠增加的 osmolarity 破坏房间。我们的学习表明 GSDMD 的形成毛孔的活动和 MLKL 的形成隧道的活动在 pyroptosis 和 necroptosis 决定血浆膜破裂的不同方法。 | Xin Chen Wan-ting He Lichen Hu Jingxian Li Yuan Fang Xin Wang Xiaozheng Xu Zhuo Wang Kai Huang Jiahuai Han | 2016 | Cell Research2016，26，9： | 110 |
| 6 | Cytoplasmic m6A reader YTHDF3 promotes mRNA translation显示文摘 | Ang Li Yu-Sheng Chen Xiao-Li Ping Xin Yang Wen Xiao Ying Yang Hui-Ying Sun Qin Zhu Poonam Baidya Xing Wang Devi Prasad Bhattarai Yong-Liang Zhao Bao-Fa Sun Yun-Gui Yang | 2017 | Cell Research2017，27，3： | 82 |
| 7 | Single-cell RNA-seq data analysis on the receptor ACE2 expression reveals the potential risk of different human organs vulnerable to 2019-nCoV infection显示文摘It has been known that,the novel coronavirus,2019-nCoV,which is considered similar to SARS-CoV,invades human cells via the receptor angiotensin converting enzyme II(ACE2).Moreover,lung cells that have ACE2 expression may be the main target cells during 2019-nCoV infection.However,some patients also exhibit non-respiratory symptoms,such as kidney failure,implying that 2019-nCoV could also invade other organs.To construct a risk map of different human organs,we analyzed the single-cell RNA sequencing(scRNA-seq)datasets derived from major human physiological systems,including the respiratory,cardiovascular,digestive,and urinary systems.Through scRNA-seq data analyses,we identified the organs at risk,such as lung,heart,esophagus,kidney,bladder,and ileum,and located specific cell types(i.e.,type II alveolar cells(AT2),myocardial cells,proximal tubule cells of the kidney,ileum and esophagus epithelial cells,and bladder urothelial cells),which are vulnerable to 2019-nCoV infection.Based on the findings,we constructed a risk map indicating the vulnerability of different organs to 2019-nCoV infection.This study may provide potential clues for further investigation of the pathogenesis and route of 2019-nCoV infection. | Xin Zou Ke Chen Jiawei Zou Peiyi Han Jie Hao Zeguang Han | 2020 | Frontiers of Medicine2020，14，2： | 193 |
| 8 | Ferroptosis:molecular mechanisms and health implications显示文摘Cell death can be executed through different subroutines.Since the description of ferroptosis as an iron-dependent form of nonapoptotic cell death in 2012,there has been mounting interest in the process and function of ferroptosis.Ferroptosis can occur through two major pathways,the extrinsic or transporter-dependent pathway and the intrinsic or enzyme-regulated pathway.Ferroptosis is caused by a redox imbalance between the production of oxidants and antioxidants,which is driven by the abnormal expression and activity of multiple redox-active enzymes that produce or detoxify free radicals and lipid oxidation products.Accordingly,ferroptosis is precisely regulated at multiple levels,including epigenetic,transcriptional,posttranscriptional and posttranslational layers.The transcription factor NFE2L2 plays a central role in upregulating anti-ferroptotic defense,whereas selective autophagy may promote ferroptotic death.Here,we review current knowledge on the integrated molecular machinery of ferroptosis and describe how dysregulated ferroptosis is involved in cancer,neurodegeneration,tissue injury,inflammation,and infection. | Daolin Tang Xin Chen Rui Kang Guido Kroemer | 2021 | Cell Research2021，31，2： | 182 |
| 9 | PTEN encoding product:a marker for tumorigenesis and progression of gastric carcinoma显示文摘AIM: To detect the expression of PTEN encoding productin normal mucosa, intestinal metaplasia (IM), dysplasia andcarcinoma of the stomach, and to investigate its clinicalimplication in tumorigenesis and progression of gastriccarcinoma.METHODS: Formalin-fixed paraffin embedded specimens from184 cases of gastric carcinoma, their adjacent normal mucosa,IM and dysplasia were evaluated for PTEN protein expressionby SABC immunohistochemistry. PTEN expression wascompared with tumor stage, lymph node metastasis, Lauren'sand WHO's histological classification of gastric carcinoma.Expression of VEGF was also detected in 60 cases of gastriccarcinoma and its correlation with PTEN was concerned.RESULTS: The positive rates of PTEN protein were 100 %(102/102), 98.5 %(65/66), 66.7 % (4/6) and 47.8 %(88/184)in normal mucosa, IM, dysplasia and carcinoma of the stomach,respectively. The positive rates in dysplasia and carcinomawere lower than in normal mucosa and IM (P<0.01).Advanced gastric cancers expressed less frequent PTEN thanearly gastric cancer (42.9 % v567.6 %, P<0.01). The positiverate of PTEN protein was lower in gastric cancer with thanwithout lymph node metastasis (40.3 % v563.3 %, P<0.01).PTEN was less expressed in diffuse-type than in intestinal-type gastric cancer (41.5 % v557.8 %,P<0.05). Signet ringcell carcinoma showed the expression of PTEN at the lowestlevel (25.0 %, 7/28); less than well and moderatelydifferentiated ones (P<0.01). Expression of PTEN was notcorrelated with expression of VEGF (P>0.05).CONCLUSION: Loss or reduced expression of PTEN proteinoccures commonly in tumorigenesis and progression of gastriccarcinoma. It is suggested that PTEN can be an objective markerfor pathologically biological behaviors of gastric carcinoma. | Lin Yang Li-Ge Kuang Hua-Chuan Zheng Jin-Yi Li Dong-Ying Wu Su-Min Zhang Yan Xin No.4 Lab,Cancer Institute,The First Affiliated Hospital,China Medical University,Shenyang 110001,China Ying Chen Shen Yang Gynecology & Obstetrics Hospital,Shenyang 110014,China | 2003 | World Journal of Gastroenterology2003，9，1： | 127 |
| 10 | Multimodality treatment in hepatocellular carcinoma patients with tumor thrombi in portal vein显示文摘AIM To compare the therapeutic effect andsignificances of multimodality treatment forhepatocellular carcinoma (HCC) with tumorthrombi in portal vein (PVTT).METHODS HCC patients (n = 147) with tumortrombi in the main portal vein or the first branchof portal vein were divided into four groups bythe several therapeutic methods. There wereconservative treatment group in 18 out ofpatients (group A); and hepatic artery ligation(HAL) and/or hepatic artery infusion (HAl)group in 18 patients (group B), in whompostoberative chemoembolization was doneperiodically; group of removal of HCC with PVTTin 79 (group C) and group of transcatheterhepatic arterial chemoembolization (TACE) orHAl and/or portal vein infusion (PVI) afteroperation in 32 (group D).RESULTS The median survival period was 12months in our series and the 1-, 3-, and 5-yearsurvival rates were 44.3%, 24.5% and 15.2%,respectively. The median survival times were 2,5, 12 and 16 months in group A, B, C and D,respectively. The 1-, 3- and 5-year survival rateswere 5.6%, 0% and 0% in group A; 22.2%,5.6% and 0% in group B; 53.9%, 26.9% and16.6% in group C; 79.3%, 38.9% and 26.8% ingroup D, respectively. Significant differenceappeared in the survival rates among the groups(P<0.05).CONCLUSION Hepatic resection with removalof tumor thrombi and HCC should increase thecurative effects and be encouraged for theprolongation of life span and quality of life forHCC patients with PVTT, whereas the besttherapeutic method for HCC with PVTT is withregional hepatic chemotherapy orchemoemblization after hepatic resection withremoval of tumor thrombi. | Jia Fan Zhi Quan Wu Zhao You Tang Jian Zhou Shuang Jian Qiu Zeng Chen Ma Xin Da Zhou Sheng Long Ye Liver Cancer Institute, Zhongshan Hospital, Fudan University Medical Center (Former Shanghai University), 136 Yixueyuan Road, Shanghai 200032, China | 2001 | World Journal of Gastroenterology2001，7，1： | 80 |
| 11 | Enhanced efficiency of generating induced pluripotent stem (iPS) cells from human somatic cells by a combination of six transcription factors显示文摘 | Jing Liao Zhao Wu Ying Wang Lu Cheng Chun Cui Yuan Gao Taotao Chen Lingjun Rao Siye Chen Nannan Jia Huiming Dai Shunmei Xin Jiuhong Kang Gang Pei Lei Xiao | 2008 | Cell Research2008，18，5： | 61 |
| 12 | Mesenchymal stem cells: a new strategy for immunosuppression and tissue repair显示文摘间充质的干细胞(MSC ) 为治疗各种各样的疾病有大潜力,特别那些与织物有关损坏包含有免疫力的反应。各种各样的研究证明了 MSC 在 vitro 并且在 vivo 是强烈抑制免疫力的。我们的最近的研究证明了那未刺激的 MSC 确实不能免疫力的抑制;他们与 TNF- 伪, IL-1 伪或 IL-1 尾与激活的淋巴细胞的上层清液,或与 IFN- 纬的联合在刺激之上变得 potently 抑制免疫力。这观察表明在某些情形下面,煽动性的 cytokines 能实际上变得抑制免疫力。我们证明在调停 MSC 的免疫力的抑制的机制有一个种类变化:由告知 cytokine 的老鼠 MSC 的免疫力的抑制被氮的氧化物调停(没有) 而由告知 cytokine 的人的 MSC 的免疫力的抑制通过 indoleamine 被执行 2, 3-dioxygenase (伊多语) 。在有煽动性的 cytokines 的刺激之上,另外,老鼠和人的 MSC 分泌几白血球 chemokines 显然服务与 MSC 吸引有免疫力的房间进最近,在哪儿不或伊多语被预言很活跃。因此,由煽动性的刺激 cytokine 的 MSC 的免疫力的抑制经由 chemokines 的一致行动发生并且免疫者禁止没有或伊多语由 MSC 生产了。因此,我们的结果在对待有免疫力的回答导致的织物损害关于调停 MSC 的免疫力的抑制并且为 MSC 的更好的申请的机制提供新奇信息。 | Yufang Shi Gangzheng Hu Juanjuan Su Wenzhao Li Qing Chen Peishun Shou Chunliang Xu Xiaodong Chen Yin Huang Zhexin Zhu Xin Huang Xiaoyan Han Ningxia Xie Guangwen Ren | 2010 | Cell Research2010，20，5： | 72 |
| 13 | RNA-seq analysis of prostate cancer in the Chinese population identifies recurrent gene fusions, cancer-associated long noncoding RNAs and aberrant alternative splicings显示文摘在有前列腺癌症的不同赛跑的病人之中有显著不同;然而,位于这差别下面的机制仍然保持不清楚。这里,我们在场 transcriptome 的一处全面风景用 RNA-seq,越过关于基因熔化的前列腺癌症 transcriptomes 的揭示巨大的差异,长 noncoding RNA (长 ncRNA ) ,其他的拼接和体的变化从中国人口 14 主要前列腺癌症和他们的配对的正常对应物介绍。14 个肿瘤(21.4%) 中的三个在中国病人怀有 TMPRSS2 尔格熔化,和这熔化的低流行进一步在一个另外的肿瘤集合(10/54=18.5%) 被证实。尤其是,二新奇基因熔化, CTAGE5-KHDRBS3 (20/54=37%) 和 USP9Y-TTTY15 (19/54=35.2%) ,在我们的耐心的队经常发生了。介绍的进一步系统的 transcriptional 识别了是在肿瘤表示的差别的众多的长 ncRNAs。在长 ncRNA 和基因的表示之间的关联的分析建议长 ncRNAs 可以在 transcriptional 规定以外有功能。这研究在中国人口产出新卓见进前列腺癌症的致病。 | Shancheng Ren Zhiyu Peng Jian-Hua Mao Yongwei Yu Changjun Yin Xin Gao Zilian Cui Jibin Zhang Kang Yi Weidong Xu Chao Chen Fubo Wang Xinwu Guo Ji Lu Jun Yang Min Wei Zhijian Tian Yinghui Guan Liang Tang Chuanliang Xu Linhui Wang Xu Gao Wei Tian Jian Wang Huanming Yang Jun Wang Yinghao Sun | 2012 | Cell Research2012，22，5： | 66 |
| 14 | Current pattern of Chinese dialysis units: a cohort study in a representative sample of units显示文摘 | ZHOU Qiu-gen JIANG Jian-ping WU Sheng-jie TIAN Jian-wei CHEN Jiang-hua YU Xue-qing CHEN Ping-yan MEI Chang-lin XIONG Fei SHI Wei ZHOU Wei LIU Xu-sheng SUN Shi-ren XIE Di LIU Jun XU Xin HOU Fan-fan | 2012 | Chinese Medical Journal2012，，19： | 69 |
| 15 | Quality assessment of clinical guidelines in China: 1993-2010显示文摘 | CHEN Yao-long YAO Liang XIAO Xiao-juan WANG Qi WANG Ze-hao LIANG Fu-xiang LIANG Hui WANG Xin SHEN Xi-ping XIE Chang-chun YANG Ke-hu | 2012 | Chinese Medical Journal2012，，20： | 65 |
| 16 | Translocation of mixed lineage kinase domain-like protein to plasma membrane leads to necrotic cell death显示文摘混合的系 kinase 像域的蛋白质(MLKL ) 被识别受体交往下游地工作蛋白质 3 (RIP3 ) 在肿瘤坏死 factor-α(TNF ) 导致了坏死(也叫的 necroptosis ) 。然而, MLKL 怎么工作调停 necroptosis 是未知的。由在 MLKL 大美人房间的 MLKL 功能的宪法,我们证明 MLKL 的 N 终点在 necroptosis 为它的功能被要求。在对待 TNF 的房间的 MLKL 的 oligomerization 为 necroptosis 是必要的,当人工地由使用荷尔蒙绑定领域一起强迫 MLKL (HBD*) 扳机 necroptosis。尤其是,一起强迫 N 终端领域(ND ) 然而并非 MLKL 的 C 终端 kinase 领域引起 necroptosis。进一步的删除分析证明 four-α MLKL (1-130 氨基酸) 的螺旋捆是足够的触发 necroptosis。两 HBD*调停并且 MLKL (ND ) 或 MLKL 的导致 TNF 的建筑群是到血浆膜的类脂化合物椽子的这些建筑群的 tetramers,和 translocation 先于房间死亡。homo-oligomerization 为 MLKL translocation 被要求,为血浆膜地点的信号顺序位于第一和第二 α 的连接; MLKL 的 -helices。MLKL 或 MLKL (ND ) 的血浆膜 translocation 导致钠流入,并且从房间文化媒介的钠的弄空禁止 necroptosis。上述所有现象没在 apoptosis 被看见。因此, MLKL oligomerization 导致 MLKL 的 translocation 到血浆膜,和血浆膜的类脂化合物椽子由自己或经由到增加的另外的蛋白质的 MLKL 复杂行为任何一个钠流入,增加渗透的压力,最后导致膜破裂。 | Xin Chen Wenjuan Li Junming Ren Deli Huang Wan-ting He Yunlong Song Chao Yang Wanyun Li Xinru Zheng PengdaChen Jiahuai Han | 2014 | Cell Research2014，24，1： | 67 |
| 17 | aunalysis of the Genome Sequence of the Medicinal Plant Salvia miltiorrhiza显示文摘 | Haibin Xu Jingyuan Song Hongmei Luo Yujun Zhang Qiushi Li Yingjie Zhu Jiang Xu Ying Li Chi Song Bo Wang Wei Sun Guoan Shen Xin Zhang Jun Qian Aijia Ji Zhichao Xu Xiang Luo Liu He Chuyuan Li Chao Sun Haixia Yah Guanghong Cui Xiwen Li Xian 'en Li Jianhe Wei Juyan Liu Yitao Wang Alice Hayward David Nelson Zemin Ning Reuben J. Peters Xiaoquan Qi Shilin Chen | 2016 | Molecular Plant2016，9，6： | 70 |
| 18 | 5-methylcytosine promotes mRNA export--NSUN2 as the methyltransferase and ALYREF as an m5C reader显示文摘 | Yang, Xin Yang, Ying Sun, Bao-Fa Chen, Yu-Sheng Xu, Jia-Wei Lai, Wei-Yi Li, Ang Wang, Xing Bhattarai, Devi Prasad Xiao, Wen Sun, Hui-Ying Zhu, Qin Ma, Hai-Li Adhikari, Samir Sun, Min Hao, Ya-Juan Zhang, Bing Huang, Chun-Min Huang, Niu Jiang, Gui-Bin Zhao, Yong-Liang Wang, Hai-Lin Sun, Ying-Pu Yang, Yun-Gui | 2017 | Cell Research2017，27，5： | 62 |
| 19 | H7N9 virulent mutants detected in chickens in China pose an increased threat to humans显示文摘 | Jianzhong Shi Guohua Deng Huihui Kong Chunyang Gu Shujie Ma Xin Yin Xianying Zeng Pengfei Cui Yan Chen Huanliang Yang Xiaopeng Wan Xiurong Wang Liling Liu Pucheng Chen Yongping Jiang Jinxiong Liu Yuntao Guan Yasuo Suzuki Mei Li Zhiyuan Qu Lizheng Guan Jinkai Zang Wenli Gu Shuyu Han Yangming Song Yuzhen Hu Zeng Wang Linlin Gu Wenyu Yang Libin Liang Hongmei Bao Guobin Tian Yanbing Li Chuanling Qiao Li Jiang Chengjun Li Zhigao Bu Hualan Chen | 2017 | Cell Research2017，27，12： | 70 |
| 20 | Five-year plans, China finance and their consequences显示文摘An important factor influencing corporate finance and economic growth in China lies in its government sponsored industrial policies. Examining China's five-year plans during 1991–2010, we find that state-owned firms in government supported industries enjoy faster growth in initial public offerings and higher offer prices. Further, they enjoy faster growth in loans granted by major national banks. However, this preferential access to capital by state-owned firms appears to be achieved at the expense of non-state-owned firms which are crowded out. Government support induces more investment but also brings more overinvestment, which mainly comes from the non-state sector.Finally, supported industries have higher stock market returns and cash flow growth that dampen when state ownership increases. | Donghua Chen Oliver Zhen Li Fu Xin | 2017 | China Journal of Accounting Research2017，，3： | 76 |
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