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| 1 | Generation of iPSCs from mouse fibroblasts with a single gene, Oct4, and small molecules显示文摘由病毒的 transduction 的四抄写因素 Oct4, Klf4, Sox2 和 c-Myc 的介绍能导致体的房间的 reprogramming 进导致的 pluripotent 干细胞(iPSCs ) ,但是 iPSCs 的使用被病毒的交货系统的使用妨碍。导致化学药品的 reprogramming 把一条新奇途径提供给没有任何病毒的基于向量的基因修正,产生 iPSCs。尽管,以前的报告证明几个小分子能代替一些 reprogramming 因素至少二个抄写因素, Oct4 和 Klf4,仍然被要求从老鼠产生 iPSCs 胚胎的成纤维细胞。这里,我们识别特定的化学联合,它是足够的面对一个单个抄写因素从胚胎的老鼠和成年成纤维细胞允许 reprogramming, Oct4 在 20 天以内,代替 Sox2, Klf4 和 c-Myc。用这个处理产生的 iPSCs 类似于胚胎的干细胞以全球基因表示介绍的老鼠,在 vitro 并且在 vivo 的 epigenetic 地位和 pluripotency。我们也发现那 8 天 Oct4 正式就职是足够的面对小分子启用导致 Oct4 的 reprogramming,它建议 reprogramming 在开始的 8 天以内被开始并且独立于连续外长的 Oct4 表示。没有基因修正,这些发现将帮助 iPSCs 的未来产生,以及阐明位于 reprogramming 过程下面的分子的机制。 | Yanqin Li Qiang Zhang Xiaolei Yin Weifeng Yang Yuanyuan Du Pingping Hou Jian Ge Chun Liu Weiqi Zhang Xu Zhang Yetao Wu Honggang Li Kang Liu Chen Wu Zhihua Song Yang Zhao Yan Shi Hongkui Deng | 2011 | Cell Research2011，21，1： | 51 |
| 2 | Two Supporting Factors Greatly Improve the Efficiency of Human iPSC Generation显示文摘 | Yang Zhao Xiaolei Yin Han Qin Fangfang Zhu Haisong Liu Weifeng Yang Qiang Zhang Chengang Xiang Pingping Hou Zhihua Song Yanxia Liu Jun Yong Pengbo Zhang Jun Cai Meng Liu Honggang Li Yanqin Li Xiuxia Qu Kai Cui Weiqi Zhang Tingting Xiang Yetao Wu Yiding Zh | 2008 | Cell Stem Cell2008，，5： | 1 |
| 3 | Induction of Pluripotency in Mouse Somatic Cells with Lineage Specifiers显示文摘 | Jian Shu Chen Wu Yetao Wu Zhiyuan Li Sida Shao Wenhui Zhao Xing Tang Huan Yang Lijun Shen Xiaohan Zuo Weifeng Yang Yan Shi Xiaochun Chi Hongquan Zhang Ge Gao Youmin Shu Kehu Yuan Weiwu He Chao Tang Yang Zhao Hongkui Deng | 2013 | Cell2013，，5： | 1 |
| 4 | Lead, zinc and cadmium accumulation in herbaceous species and soils in Lanping Pb/Zn mining area,Yunnan Province, China显示文摘 | Yetao TANG Rongliang QIU Xiaowen ZENG Xiaohang FANG Xiaoyong ZHOU Fangming YU Yudu WU | 2006 | Chinese Journal Of Geochemistry2006，25，B08： | 1 |
| 5 | Bone morphogenetic protein 4 (BMP4) promotes hepatic glycogen accumulation and reduces glucose level in hepatocytes through mTORC2 signaling pathway显示文摘Liver is an important organ for regulating glucose and lipid metabolism.Recent studies have shown that bone morphogenetic proteins(BMPs)may play important roles in regu-lating glucose and lipid metabolism.Inour previous studies,we demonstrated that BMP4 signif-icantly inhibits hepatic steatosis and lowers serum triglycerides,playing a protective role against the progression of non-alcoholic fatty liver disease(NAFLD).However,the direct impact of BMP4 on hepatic glucose metabolism is poorly understood.Here,we investigated the regulatory roles of BMP4 in hepatic glucose metabolism.Through a comprehensive analysis of the 14 types of BMPs,we found that BMP4 was one of the most potent BMPs in promoting hepatic glycogen accumulation,reducing the level of glucose in hepatocytes and effecting the expression of genes related to glucose metabolism.Mechanistically,we demonstrated that BMP4 reduced the hepatic glucose lewels through the activation of mTORC2 signaling pathway in vitro and in wivo.Collectively,our findings strongly suggest that BMP4 may play an essential role in regulating hepatic glucose metabolism.This knowledge should aid us to understand the molecular pathogenesis of NAFLD,and may lead to the development of novel therapeutics by exploiting the inhibitory effects of BMPs on hepatic glucose and lipid metabolism. | Liqin An Qiong Shi Ying Zhu Hao Wang Qi Peng Jinghong Wu Yu Cheng Wei Zhang Yanyu Yi Zihao Bao Hui Zhang Yetao Luo Jiaming Fan | 2021 | Genes & Diseases2021，8，4： | 1 |
| 6 | Functionalized selenium nanoparticles ameliorated acetaminophen-induced hepatotoxicity through synergistically triggering PKCδ/Nrf2 signaling pathway and inhibiting CYP 2E1显示文摘Selenium nanoparticles(SeNPs)have been demonstrated potential for use in diseases associated with oxidative stress.Functionalized SeNPs with lower toxicity and higher biocompatibility could bring better therapeutic activity and clinical application value.Herein,this work was conducted to investigate the protective effect of Pleurotus tuber-regium polysaccharide-protein complex funtionnalized SeNPs(PTR-SeNPs)against acetaminophen(APAP)-induced oxidative injure in HepG2 cells and C57BL/6J mouse liver.Further elucidation of the underlying molecular mechanism,in particular their modulation of Nrf2 signaling pathway was also performed.The results showed that PTR-SeNPs could significantly ameliorate APAP-induced oxidative injury as evidenced by a range of biochemical analysis,histopathological examination and immunoblotting study.PTR-SeNPs could hosphorylate and activate PKCδ,depress Keap1,and increase nuclear accumulation of Nrf2,resulting in upregulation of GCLC,GCLM,HO-1 and NQO-1 expression.Besides,PTR-SeNPs suppressed the biotransformation of APAP to generate intracellular ROS through CYP 2E1 inhibition,restoring the mitochondrial morphology.Furthermore,the protective effect of PTR-SeNPs against APAP induced hepatotoxicity was weakened as Nrf2 was depleted in vivo,indicating the pivotal role of Nrf2 signaling pathway in PTR-SeNPs mediated hepatoprotective efficacy.Being a potential hepatic protectant,PTR-SeNPs could serve as a new source of selenium supplement for health-promoting and biomedical applications. | Si Zou Yetao Gong Xiujie Li Yanbin Wu Jinzhong Wu Jianguo Wu Ka-Hing Wong | 2024 | Food Science and Human Wellness2024，13，2： | 0 |
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