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Open AccessJournal ArticleDOI

Molecular basis of the Keap1–Nrf2 system

TLDR
Cross talk between Nrf2 and other signaling pathways is identified, which provides new insights into the mechanisms by which the Keap1-Nrf2 system serves as a potent regulator of the authors' health and disease.
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This article is published in Free Radical Biology and Medicine.The article was published on 2015-11-01 and is currently open access. It has received 688 citations till now. The article focuses on the topics: Ubiquitin ligase & Regulator.

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Short-term effects of deoxynivalenol, T-2 toxin, fumonisin B1 or ochratoxin on lipid peroxidation and glutathione redox system and its regulatory genes in common carp (Cyprinus carpio L.) liver

TL;DR: The lack of an increase in the expression of nrf2, except as the effect of DON at 8 h, and a decrease in the keap1 expression suggests that the antioxidant defence system was activated at gene and protein levels through Keap1–Nrf2 independent pathways.
Journal ArticleDOI

Theaflavin Attenuates TBHP-Induced Endothelial Cells Oxidative Stress by Activating PI3K/AKT/Nrf2 and Accelerates Wound Healing in Rats

TL;DR: In this study, in vitro work discovered that human umbilical vein endothelial cells exposed to Theaflavin can alleviate apoptosis and cell dysfunction induced by tert-butyl hydroperoxide (TBHP), and certified the potential mechanism of TheAFlavin, which can be used as a potential agent for cutaneous wound therapy.
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Emodin resists to Cyprinid herpesvirus 3 replication via the pathways of Nrf2/Keap1-ARE and NF-κB in the ornamental koi carp (Cyprinus carpio haematopterus)

TL;DR: In this paper, the authors investigated the preventive effects and mechanism of emodin on CyHV-3 infection in ornamental koi carp (Cyprinus carpio haematopterus).
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Activation of KEAP1/NRF2 stress signaling involved in the molecular basis of hemin-induced cytotoxicity in human pro-erythroid K562 cells.

TL;DR: The KEAP1/NRF2 system can be revealed as a basic homeostatic mechanism, activated in cells encountering free heme, both in healthy and diseased state, and provides a multi-target cytoprotective platform to develop agents preventing heme toxicity.
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Based on Activation of p62-Keap1-Nrf2 Pathway, Hesperidin Protects Arsenic-Trioxide-Induced Cardiotoxicity in Mice.

TL;DR: In this article, the authors investigated the effect of Hesperidin (HES) on ATO-induced cardiotoxicity and found that HES significantly reduced the levels of reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), catalase (CAT), tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), B-cell lymphoma-2 (Bcl-2), Bcl-
References
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Journal ArticleDOI

An nrf2/small maf heterodimer mediates the induction of phase ii detoxifying enzyme genes through antioxidant response elements

TL;DR: It is demonstrated that Nrf2 is essential for the transcriptional induction of phase II enzymes and the presence of a coordinate transcriptional regulatory mechanism for phase II enzyme genes and the nrf2-deficient mice may prove to be a very useful model for the in vivo analysis of chemical carcinogenesis and resistance to anti-cancer drugs.
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Keap1 represses nuclear activation of antioxidant responsive elements by Nrf2 through binding to the amino-terminal Neh2 domain

TL;DR: It is postulate that Keap1 and Nrf2 constitute a crucial cellular sensor for oxidative stress, and together mediate a key step in the signaling pathway that leads to transcriptional activation by this novel NRF2 nuclear shuttling mechanism.
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Oxidative Stress Sensor Keap1 Functions as an Adaptor for Cul3-Based E3 Ligase To Regulate Proteasomal Degradation of Nrf2

TL;DR: It is found that both the BTB and intervening-region (IVR) domains are crucial for Nrf2 degradation, implying that these two domains act to recruit ubiquitin-proteasome factors.
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Oncogene-induced Nrf2 transcription promotes ROS detoxification and tumorigenesis

TL;DR: Oncogene-directed increased expression of Nrf2 is a new mechanism for the activation of the NRF2 antioxidant program, and is evident in primary cells and tissues of mice expressing K-RasG12D and B-RafV619E, and in human pancreatic cancer.
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