The aryl hydrocarbon receptor cross-talks with multiple signal transduction pathways.
The aryl hydrocarbon receptor cross-talks with multiple signal transduction pathways.
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DOI：
10.1016/j.bcp.2008.08.031
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发表时间：
2009-02-15
影响因子：
5.8
通讯作者：
Marlowe, Jennifer L.
中科院分区：
文献类型：
--
作者：
Puga, Alvaro;Ma, Ci;Marlowe, Jennifer L.
关键词：
接触有毒的多环芳烃会在实验动物和人类中引起许多毒性和致癌反应，这些反应大部分是由芳基烃或二恶英受体 (AHR) 介导的。 AHR 是一种配体激活的转录因子，其在药物代谢酶诱导中的核心作用早已被认识到。一段时间以来，人们已经清楚，AHR 还在其解毒作用之外的途径中发挥作用，并且异生配体对这些途径的干扰可能是这些化合物毒性的重要组成部分。 AHR 的一些配体激活参与细胞周期调节、丝裂原激活蛋白激酶级联、早期基因诱导、RB/E2F 轴内的串扰以及关键钙储备动员的关键途径。最终，特定 AHR 配体的作用可能既取决于它与特定细胞或组织中表达的途径和蛋白质建立的适应性相互作用，也取决于它引起的毒性反应。
Exposure to toxic polycyclic aromatic hydrocarbons raises a number of toxic and carcinogenic responses in experimental animals and humans mediated for the most part by the aryl hydrocarbon---or dioxin---receptor (AHR). The AHR is a ligand-activated transcription factor whose central role in the induction of drug-metabolizing enzymes has long been recognized. For quite some time now, it has become clear that the AHR also functions in pathways outside of its role in detoxification and that perturbation of these pathways by xenobiotic ligands may be an important part of the toxicity of these compounds. AHR activation by some of its ligands participates among others in pathways critical to cell cycle regulation, mitogen-activated protein kinase cascades, immediate-early gene induction, cross-talk within the RB/E2F axis and mobilization of crucial calcium stores. Ultimately, the effect of a particular AHR ligand may depend as much on the adaptive interactions that it established with pathways and proteins expressed in a specific cell or tissue as on the toxic responses that it raises.
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