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排序方式: 共有302条查询结果,搜索用时 15 毫秒
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Jia Liu Yiyuan Kang Suhan Yin Aijie Chen Junrong Wu Huimin Liang Longquan Shao 《Small (Weinheim an der Bergstrasse, Germany)》2019,15(25)
Autophagy is a biological process that has attracted considerable attention as a target for novel therapeutics. Recently, nanomaterials (NMs) have been reported to modulate autophagy, which makes them potential agents for the treatment of autophagy‐related diseases. In this study, zinc oxide nanoparticles (ZNPs) are utilized to evaluate NM‐induced autophagy and debate the mechanisms involved. It is found that ZNPs undergo pH‐dependent ion shedding and that intracellular zinc ions (Zn2+) play a crucial role in autophagy. Autophagy is activated with ZNPs treatment, which is inhibited after Zn2+ sequestration via ethylenediamine tetra‐acetic acid. Lysosome‐based autophagic degradation is halted after ZNPs treatment for more than 3 h and is accompanied by blockage of lysophagy, which renews impaired lysosomes. Furthermore, the microtubule (MT) system participates in ZNP‐induced lysosome–autophagy system changes, especially in the fusion between autophagosomes and lysosomes. MT acetylation is helpful for protecting from ZNP‐induced MT disruption, and it promotes the autophagic degradation process. In conclusion, this study provides valuable information on NM‐induced lysosome–autophagy system changes, particularly with respect to the role of lysophagy and the MT system, which point to some attractive targets for the design of engineered nanoparticles. 相似文献
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A Synthetic Transcriptional Activator of Genes Associated with the Retina in Human Dermal Fibroblasts 下载免费PDF全文
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目的:研究表没食子儿茶素没食子酸酯(EGCG)升高cTnIR193H限制型心肌病模型小鼠未突变cTnI的表达水平。方法:8周龄野生型C57小鼠及8周龄cTnIR193H限制型心肌病模型小鼠分别随机分为EGCG干预组、DMSO干预组以及未干预组。每周干预5 d,3个月后采集小鼠心脏组织。分别以Western blot与RT-PCR分别检测HDAC1、GATA4及cTnI 的mRNA表达水平。组蛋白H3K9乙酰化水平、cTnI基因启动子区域中的GATA4与HDAC1结合水平以ChIP-Q-PCR方式检测。结果:EGCG干预组未突变cTnI蛋白表达水平与mRNA表达水平、GATA4的mRNA表达水平、组蛋白H3K9乙酰化水平、cTnI启动子区域GATA4的结合水平均高于未干预组(P<0.05)。cTnI启动子区域HDAC1结合水平、HDAC1的mRNA表达水平均低于未干预组(P<0.05)。 结论:在EGCG干预R193H模型小鼠实验中,EGCG可抑制HDAC1的表达,抑制cTnI启动子区域HDAC1的结合,促进心脏核心转录因子GATA4的表达、组蛋白H3K9的乙酰化、及cTnI启动子区域GATA4的结合,上调心肌的未突变cTnI的表达水平。 相似文献
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Dr. Tarja Kokkola Dr. Tiina Suuronen Dr. Maija Pesonen Prof. Panagis Filippakopoulos Dr. Antero Salminen Dr. Elina M. Jarho Dr. Maija Lahtela‐Kakkonen 《Chembiochem : a European journal of chemical biology》2015,16(14):1997-2001
Control of histone acetylation is a part of the epigenetic mechanism that regulates gene expression and chromatin architecture. The members of the bromodomain and extra terminal domain (BET) protein family are a group of epigenetic readers that recognize histone acetylation, whereas histone deacetyl‐ ases such as sirtuin 1 (SIRT1) function as epigenetic erasers. We observed that BET inhibition by the specific inhibitor JQ1 upregulated SIRT1 expression and activated SIRT1. Moreover, we observed that BET inhibition functionally reversed the pro‐inflammatory effect of SIRT1 inhibition in a cellular lung disease model. SIRT1 activation is desirable in many age‐related, metabolic and inflammatory diseases; our results suggest that BET protein inhibition would be beneficial in treatment of those conditions. Most importantly, our findings demonstrate a novel mechanism of SIRT1 activation by inhibition of the BET proteins. 相似文献
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José A. Souto Dr. Rosaria Benedetti Katharina Otto Marco Miceli Rosana Álvarez Prof. Dr. Lucia Altucci Prof. Dr. Angel R. de Lera Prof. Dr. 《ChemMedChem》2010,5(9):1530-1540
A series of N‐(4‐cyano‐3‐trifluoromethyl‐phenyl)‐2‐ethoxy‐6‐alkyl (and alkenyl) benzamides related to the anacardic acid derivative CTPB have been prepared from 2,6‐dihydroxybenzoic acid with a Suzuki coupling and addition of the anion of 4‐cyano‐3‐trifluoromethylphenylamine to a benzodioxinone as the key steps. In U937 cells, these analogues, in particular 7 c , 7 d , 7 f and 7 j , induced cell‐cycle arrest in the G1 phase, caused apoptosis in about 20 % of the cells, and increased the acetylation levels of H3. These activities correlate with the enzymatic activation of histone lysine acetyltransferases (KATs): CBP and PCAF. 相似文献