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本文引用的文献

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Liver-specific inactivation of the Nrf1 gene in adult mouse leads to nonalcoholic steatohepatitis and hepatic neoplasia.成年小鼠肝脏中Nrf1基因的特异性失活会导致非酒精性脂肪性肝炎和肝脏肿瘤。
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A Toll-interleukin 1 repeat protein at the synapse specifies asymmetric odorant receptor expression via ASK1 MAPKKK signaling.突触处的一种Toll样白细胞介素1重复蛋白通过ASK1丝裂原活化蛋白激酶激酶激酶信号通路决定不对称气味受体的表达。
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Nrf2-Keap1 defines a physiologically important stress response mechanism.Nrf2-Keap1定义了一种具有重要生理意义的应激反应机制。
Trends Mol Med. 2004 Nov;10(11):549-57. doi: 10.1016/j.molmed.2004.09.003.
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Requirement for a conserved Toll/interleukin-1 resistance domain protein in the Caenorhabditis elegans immune response.秀丽隐杆线虫免疫反应中对保守的Toll/白细胞介素-1抗性结构域蛋白的需求。
Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6593-8. doi: 10.1073/pnas.0308625101.
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Phosphorylation by the beta-catenin/MAPK complex promotes 14-3-3-mediated nuclear export of TCF/POP-1 in signal-responsive cells in C. elegans.在秀丽隐杆线虫的信号响应细胞中,β-连环蛋白/丝裂原活化蛋白激酶复合物介导的磷酸化作用促进了14-3-3介导的TCF/POP-1的核输出。
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TLR-independent control of innate immunity in Caenorhabditis elegans by the TIR domain adaptor protein TIR-1, an ortholog of human SARM.秀丽隐杆线虫中由TIR结构域衔接蛋白TIR-1(人类SARM的直系同源物)对先天免疫进行的不依赖Toll样受体(TLR)的调控
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SKN-1 links C. elegans mesendodermal specification to a conserved oxidative stress response.SKN-1将秀丽隐杆线虫中胚层和内胚层的特化与保守的氧化应激反应联系起来。
Genes Dev. 2003 Aug 1;17(15):1882-93. doi: 10.1101/gad.1107803. Epub 2003 Jul 17.
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Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases.由细胞外信号调节激酶(ERK)、应激活化蛋白激酶(JNK)和p38蛋白激酶介导的丝裂原活化蛋白激酶信号通路。
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A conserved p38 MAP kinase pathway in Caenorhabditis elegans innate immunity.秀丽隐杆线虫固有免疫中一条保守的p38丝裂原活化蛋白激酶信号通路。
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SEK-1 MAPKK mediates Ca2+ signaling to determine neuronal asymmetric development in Caenorhabditis elegans.SEK-1丝裂原活化蛋白激酶激酶介导钙离子信号传导以决定秀丽隐杆线虫中的神经元不对称发育。
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秀丽隐杆线虫的p38丝裂原活化蛋白激酶(MAPK)信号通路在氧化应激反应中调节转录因子SKN-1的核定位。

The C. elegans p38 MAPK pathway regulates nuclear localization of the transcription factor SKN-1 in oxidative stress response.

作者信息

Inoue Hideki, Hisamoto Naoki, An Jae Hyung, Oliveira Riva P, Nishida Eisuke, Blackwell T Keith, Matsumoto Kunihiro

机构信息

Department of Molecular Biology, Graduate School of Science, Institute for Advanced Research, Nagoya University, Chikusa-ku, Nagoya 464-8602, Japan.

出版信息

Genes Dev. 2005 Oct 1;19(19):2278-83. doi: 10.1101/gad.1324805. Epub 2005 Sep 15.

DOI:10.1101/gad.1324805
PMID:16166371
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1240035/
Abstract

The evolutionarily conserved p38 mitogen-activated protein kinase (MAPK) cascade is an integral part of the response to a variety of environmental stresses. Here we show that the Caenorhabditis elegans PMK-1 p38 MAPK pathway regulates the oxidative stress response via the CNC transcription factor SKN-1. In response to oxidative stress, PMK-1 phosphorylates SKN-1, leading to its accumulation in intestine nuclei, where SKN-1 activates transcription of gcs-1, a phase II detoxification enzyme gene. These results delineate the C. elegans p38 MAPK signaling pathway leading to the nucleus that responds to oxidative stress.

摘要

进化上保守的p38丝裂原活化蛋白激酶(MAPK)级联反应是对多种环境应激反应的一个组成部分。我们在此表明,秀丽隐杆线虫的PMK-1 p38 MAPK途径通过CNC转录因子SKN-1调节氧化应激反应。在氧化应激反应中,PMK-1使SKN-1磷酸化,导致其在肠细胞核中积累,在那里SKN-1激活II期解毒酶基因gcs-1的转录。这些结果描绘了秀丽隐杆线虫中导致对氧化应激作出反应的细胞核的p38 MAPK信号通路。