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Chemical genetic screening identifies critical pathways in anthrax lethal toxin-induced pathogenesis
Panchal RG Ruthel G Brittingham KC Lane D Kenny TA Gussio R Lazo JS Bavari S 《Chemistry & biology》2007,14(3):245-255
Anthrax lethal toxin (LT)-induced cell death via mitogen-activated protein kinase kinase (MAPKK) cleavage remains questionable. Here, a chemical genetics approach was used to investigate what pathways mediate LT-induced cell death. Several small molecules were found to protect macrophages from anthrax LT cytotoxicity and MAPKK from cleavage by lethal factor (LF), without inhibiting LF enzymatic activity or cellular proteasome activity. Interestingly, the compounds activated MAPK-signaling molecules, induced proinflammatory cytokine production, and inhibited LT-induced macrophage apoptosis in a concentration-dependent manner. We propose that induction of antiapoptotic responses by MAPK-dependent or -independent pathways and activation of host innate responses may protect macrophages from anthrax LT-induced cell death. Altering host responses through a chemical genetics approach can help identify critical cellular pathways involved in the pathogenesis of anthrax and can be exploited to further explore host-pathogen interactions. 相似文献
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谈谈量子力学中的状态叠加原理 总被引:1,自引:1,他引:0
以对话的形式,介绍并评论了布洛欣采夫、狄拉克以及朗道和栗弗席茨关于状态叠加原理的不同表述. 相似文献
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