|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Cationic nanocarriers induce cell necrosis through impairment of Na^+/K^+-ATPase and cause subsequent inflammatory response显示文摘有积极表面费用的 Nanocarriers 以他们限制了他们的临床的应用的毒性著名。位于他们的毒性下面的机制例如煽动性的反应的正式就职,仍然保持大部分未知。在我们发现了 cationic nanocarriers 的那注射的现在的学习,包括 cationic liposomes, PEI,和 chitosan,导致了坏死的房间的快速的外观。cationic nanocarriers 导致的房间坏死依赖于他们的积极表面费用,但是不要求 RIP1 和 Mlkl。相反,细胞内部的 Na + 超载被发现伴随房间死亡。在文化媒介或有 Na +/K+-ATPase 阳离子绑定地点禁止者 ouabain 的房间的预告的处理的 Na + 的弄空,从房间坏死的保护的房间。而且,有 cationic nanocarriers 的处理在 vitro 并且在 vivo 禁止了 Na +/K+-ATPase 活动。计算模拟证明 cationic 搬运人能与 Na +/K+-ATPase 的阳离子绑定地点交往。有 ouabain 的小剂量的老鼠 pretreated 在 cationic nanocarriers 的致命的剂量的注射以后显示出改进幸存。进一步的分析建议 cationic nanocarriers 和 mitochondrial DNA 的产生的漏导致的那房间坏死能在 vivo 触发严重发炎,它被包含 TLR9 并且 MyD88 发信号的一条小径调停。一起拿,我们的结果揭示由此的新奇机制 cationic nanocarriers 通过和 mitochondrial 的随后的暴露的和 Na +/K+-ATPase, 的相互作用导致尖锐房间坏死是的联系损坏的分子的模式调停的一个关键事件煽动性的回答。我们的学习为评估 nanocarriers 的 biocompatibility 并且为药交货设计更好、更安全的有重要含意。 | Xiawei Wei Bin Shao Zhiyao He Tinghong Ye Min Luo Yaxiong Sang Xiao Liang Wei Wang Shuntao Luo Shengyong Yang Shuang Zhang Changyang Gong Maling Gou Hongxing Deng Yinglan Zhao Hanshuo Yang Senyi Deng Chengjian Zhao Li Yang Zhiyong Qian Jiong Li Xun Sun Jiahuai Han Chengyu Jiang Min Wu Zhirong Zhang | 2015 | Cell Research2015，25，2： | 21 |
| 2 | Therapeutic effects of standardized Vitex negundo seeds extract on complete Freund’s adjuvant induced arthritis in rats显示文摘 | Zheng ChengJian Zhao XiangXiang Ai HongWei | 2014 | Phytomedicine2014，21，6： | 1 |
| 3 | Immunotherapy of tumor with vaccine based on basic fibroblast growth factor-activated fibroblasts显示文摘 | Xiuying Li Yongsheng Wang Yuwei Zhao Hengxiu Yang Aiping Tong Chengjian Zhao Huashan Shi Yang Li Zhenlin Wang Yuquan Wei | 2014 | Journal of Cancer Research and Clinical Oncology2014，，2： | 1 |
| 4 | β-decay Study of Tz=-3/2Proton-rich Nucleus 29S显示文摘The exotic decay of nuclei far from the stability has recently become a hot topic of nuclear structure research.The nuclide 29S is not well investigated in the A=4n+1,Tz=-3/2series of strong+β-delayed proton precursors.The decay schemes of these nuclei are characterized | ZHONG Fupeng XU Xinxing LIN Chengjian WANG Jiansong LI Zhihuan YANG Lei MA Nanru WANG Dongxi WEN Peiwei SUN Lijie WU Hongyi LUO Diwen WU Chenguang JIANG Ying LIU Yang ZANG Hongliang LIANG Pengfei LI Pengjie LI Xiaojing ZHAO Qingqing SHI Guozhu MA Junbing MA Peng YU Gongming Dipikap Patel BAI Zhen YANG Feng JIA Huiming ZHANG Huanqiao WANG Jianguo YANG Yanyun MA Weihu HU Qiang JIN Shuya ZHOU Xiaohong LI Ren HOU Dongsheng LIU Minliang HU Zhengguo MA Xinwen YANG Weiqing GAO Zhihao DUAN Fangfang YU Yuechao WANG Yufeng WANG Peng ZHOU Qingwu CUI Danteng WANG Xiang HU Liyuan PAN Min ZHANG Gaolong WANG Xiaoyu | 2017 | Annual Report of China Institute of Atomic Energy2017，，1： | 0 |
| 5 | ETV2 mediates endothelial transdifferentiation of glioblastoma显示文摘Glioblastoma multiforme(GBM)is characterized by extensive endothelial hyperplasia.Recent studies suggest that a subpopulation of endothelial cells originates via vasculogenesis by the transdifferentiation of GBM tumor cells into endothelial cells(endotransdifferentiation).The molecular mechanism underlying this process remains poorly defined.Here,we show that the expression of ETS variant 2(ETV2),a master regulator of endothelial cell development,is highly correlated with malignancy.Functional studies demonstrate that ETV2 is sufficient and necessary for the transdifferentiation of a subpopulation of CD133+/Nestin+GBM/neural stem cells to an endothelial lineage.Combinational studies of ChIP-Seq with gain-of-function RNA-Seq data sets suggest that ETV2,in addition to activating vascular genes,represses proneural genes to direct endo-transdifferentiation.Since endotransdifferentiation by ETV2 is VEGF-A independent,it likely accounts for the observed resistance of GBM tumor cells to antiangiogenesis therapy.Further characterization of the regulatory networks mediated by ETV2 in endo-transdifferentiation of GBM tumor cells should lead to the identification of more effective therapeutic targets for GBM. | Chengjian Zhao Gustavo AGomez Yuwei Zhao Yu Yang Dan Cao Jing Lu Hanshuo Yang Shuo Lin | 2018 | Signal Transduction and Targeted Therapy2018，3，1： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员