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首页> 外文期刊>Biological trace element research >Stress Responses Against Rare Earth Ions Are Mediated by the JNK and p38 MAPK Pathways in Caenorhabditis elegans
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Stress Responses Against Rare Earth Ions Are Mediated by the JNK and p38 MAPK Pathways in Caenorhabditis elegans

机译:对稀土离子的应力反应由JNK和P38 Mapk途径介导的Caenorhabditis elegans

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摘要

Rare earth (RE) ions at high concentrations are toxic to many organisms as they induce oxidative stress and cause improper incorporation of the ions into calcium-binding proteins. Although the mechanism of action underlying the toxicity of REs has been identified, intracellular signaling pathways involved in stress responses against RE ions still remain unclear. In Caenorhabditis elegans, cellular responses against heavy metal stresses are primarily regulated by the c-Jun N-terminal kinase (JNK)-like mitogen-activated protein kinase (MAPK) pathway with a minor contribution of the p38-like MAPK pathway. In this study, we found that both JNK- and p38-like MAPK pathways were involved in stress responses against RE. Unlike heavy metal responses, mutations in both the JNK and p38 pathways caused similar hypersensitivity to RE ions. Although the signaling pathways used for these stress responses were found to be similar, the degree of their respective contribution slightly differed between heavy metal and RE ions.
机译:在高浓度下稀土(RE)离子对许多生物有毒,因为它们诱导氧化应激并导致离子的不当掺入结合蛋白质中。虽然已经鉴定了res毒性的作用机制,但仍然仍然尚不清楚参与RE离子的压力反应的细胞内信号传导途径。在皮龄杆菌中,针对重金属应力的细胞反应主要由C-JUM N-末端激酶(JNK) - 丝虫活化蛋白激酶(MAPK)途径具有较小的P38样MAPK途径的贡献。在这项研究中,我们发现JNK和P38的MAPK途径都参与了对RE的应力响应。与重金属反应不同,JNK和P38途径中的突变导致对再密封性相似的超敏反应。尽管发现用于这些应力响应的信号传导途径是相似的,但它们各自的贡献程度略有不同于重金属和再离子之间。

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