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首页> 美国卫生研究院文献>The Journal of Biological Chemistry >The Ras GTPase-activating-like Protein IQGAP1 Mediates Nrf2 Protein Activation via the Mitogen-activated Protein Kinase/Extracellular Signal-regulated Kinase (ERK) Kinase (MEK)-ERK Pathway
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The Ras GTPase-activating-like Protein IQGAP1 Mediates Nrf2 Protein Activation via the Mitogen-activated Protein Kinase/Extracellular Signal-regulated Kinase (ERK) Kinase (MEK)-ERK Pathway

机译：Ras GTPase激活样蛋白IQGAP1通过有丝分裂原激活的蛋白激酶/细胞外信号调节激酶（ERK）激酶（MEK）-ERK途径介导Nrf2蛋白激活

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Nrf2 plays a critical role in the regulation of cellular oxidative stress. MEK-ERK activation has been shown to be one of the major pathways resulting in the activation of Nrf2 and induction of Nrf2 downstream targets, including phase II detoxifying/antioxidant genes in response to oxidative stress and xenobiotics. In this study, IQGAP1 (IQ motif-containing GTPase-activating protein 1), a new Nrf2 interaction partner that we have published previously, was found to modulate MEK-ERK-mediated Nrf2 activation and induction of phase II detoxifying/antioxidant genes. Nrf2 binds directly to the IQ domain (amino acids 699–905) of IQGAP1. Knockdown of IQGAP1 significantly attenuated phenethyl isothiocyanate- or MEK-mediated activation of the MEK-ERK-Nrf2 pathway. Knockdown of IQGAP1 also attenuated MEK-mediated increased stability of Nrf2, which in turn was associated with a decrease in the nuclear translocation of Nrf2 and a decrease in the expression of phase II detoxifying/antioxidant genes. In the aggregate, these results suggest that IQGAP1 may play an important role in the MEK-ERK-Nrf2 signaling pathway.
机译：Nrf2在调节细胞氧化应激中起关键作用。已经证明，MEK-ERK活化是导致Nrf2活化和Nrf2下游靶标诱导的主要途径之一，包括响应氧化应激和异源生物的II期解毒/抗氧化基因。在这项研究中，我们之前发表的新的Nrf2相互作用伙伴IQGAP1（含IQ基序的GTPase激活蛋白1）被发现可调节MEK-ERK介导的Nrf2激活和II期解毒/抗氧化基因的诱导。 Nrf2直接与IQGAP1的IQ域（699-905位氨基酸）结合。敲低IQGAP1显着减弱了异硫氰酸苯乙基酯或MEK介导的MEK-ERK-Nrf2途径的激活。敲低IQGAP1还减弱了MEK介导的Nrf2稳定性的提高，这又与Nrf2核易位的减少和II期解毒/抗氧化剂基因表达的降低有关。总体而言，这些结果表明IQGAP1可能在MEK-ERK-Nrf2信号通路中发挥重要作用。

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