共查询到20条相似文献,搜索用时 15 毫秒
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Site-specific Srb10-dependent phosphorylation of the yeast Mediator subunit Med2 regulates gene expression from the 2-microm plasmid 下载免费PDF全文
Hallberg M Polozkov GV Hu GZ Beve J Gustafsson CM Ronne H Björklund S 《Proceedings of the National Academy of Sciences of the United States of America》2004,101(10):3370-3375
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TRAP230/ARC240 and TRAP240/ARC250 Mediator subunits are functionally conserved through evolution 总被引:6,自引:0,他引:6 下载免费PDF全文
Samuelsen CO Baraznenok V Khorosjutina O Spahr H Kieselbach T Holmberg S Gustafsson CM 《Proceedings of the National Academy of Sciences of the United States of America》2003,100(11):6422-6427
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Schmid-Schönbein GW Hugli TE Kistler EB Sofianos A Mitsuoka H 《Microcirculation (New York, N.Y. : 1994)》2001,8(1):5-14
Cell activation in the microcirculation leads to an inflammatory cascade and is accompanied by many cardiovascular complications. There is a need to identify the trigger mechanisms that lead to the production of in vivo activating factors. We review here mechanisms for cell activation in the microcirculation and specifically the production of humoral cell activators in physiological shock. The elevated levels of activating factors in plasma could be traced to the action of pancreatic enzymes in the ischemic intestine. New interventions against the production of the activators are proposed. The evidence suggests that pancreatic enzymes in the ischemic intestine may attack several tissue components and generate cellular activators that are associated with multiorgan dysfunction in physiological shock. 相似文献
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Dietary restriction is one of the several ways which could putatively extend organisms’ lifespan, ranging from Saccharomyces cerevisiae to rodents, by activating the AMP-activated protein kinase (AMPK), an ATP/AMP sensor. Extensive researches have shown that aging reduces sensibility of AMPK and eventually causes energy imbalance in cells. Research in mammals’ AMPK depicts that this signaling molecule could control autophagy, improve cellular stress resistance and suppress inflammatory responses. Hence, in this study we performed a drug repurposing of 1908 FDA-approved drugs in order to discover putative safe activators of AMPK and to find new applications for existing drugs. For this purpose, FDA-approved drugs were screened by virtual screening and the ligand–protein interactions were carefully inspected. Moreover, through MM/PBSA analysis, the binding affinity of hit compounds in γ and αβ binding sites were investigated. As Cangrelor, Nacitentan, Levoleucovorin and Glisoxepide had lower binding affinities; we predicted that they would probably prove to be more potential activators than C2. However, hit-compounds in αβ binding site, exhibited higher unfavorable binding affinity. Hence, present findings can prove to be valuable for discovering new activators for AMPK. 相似文献
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