Regulatory mechanisms controlling gene expression mediated by the antioxidant response element.

By Truyen Nguyen, Philip J. Sherratt, C. B. Pickett. Annual Review of Pharmacology and Toxicology, 2003

1,173 citations recorded by the source corpus.

Subfields: Molecular Biology, Organic Chemistry

View Paper: https://www.semanticscholar.org/paper/0497bd61b5f1001b9a57999ecc303024a8388a80

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Citations in the corpus

Physiological effects of broccoli consumption (2008, background): “For example, it is not known if SF triggers the direct phosphorylation of Keap-1 by PKC, or has an effect on the role that PI3 kinase plays in activation of Nrf2 (Nguyen et al. 2003).”
The Nrf2 cell defence pathway: Keap1-dependent and -independent mechanisms of regulation. (2013, background): “promoter region of Nrf2-regulated genes [11,12] (Fig.”
ROS and ROS-Mediated Cellular Signaling (2016, background): “However, under oxidizing conditions, the increased level of intracellular ROS promotes the dissociation of Nrf2 and Keap1, either by the oxidization of key reactive cysteine residues (Cys273, Cys288, and Cys151) that govern Keap1 activity or via the activation of kinases, such as protein kinase C (P”
Keap1 Recruits Neh2 through Binding to ETGE and DLG Motifs: Characterization of the Two-Site Molecular Recognition Model (2006, background): “Nrf2 (nuclear factor E2-related factor 2) has been found to be the central transcription factor that interacts with the ARE/EpRE to transactivate cytoprotective gene expression constitutively or to induce the expression in response to oxidative stress signals (19, 21, 42).”
Oxidative Stress Sensor Keap1 Functions as an Adaptor for Cul3-Based E3 Ligase To Regulate Proteasomal Degradation of Nrf2 (2004, background): “Transcription factors then induce or regulate the expression of genes encoding cytoprotective enzymes and proteins (16, 23).”
Molecular Mechanisms of Nrf2-Mediated Antioxidant Response (2009, background): “located in the promoter of a battery of cytoprotective genes [42,46].”
Distinct Cysteine Residues in Keap1 Are Required for Keap1-Dependent Ubiquitination of Nrf2 and for Stabilization of Nrf2 by Chemopreventive Agents and Oxidative Stress (2003, background): “Several different protein kinase-dependent signal transduction pathways have been implicated in the release of Nrf2 from Keap1mediated repression, including the ERK and JNK mitogenactivated protein kinase pathways, protein kinase C, and the phosphatidylinositol 3-kinase-dependent pathway (13, 18, 22”
Oxidative stress in ALS: key role in motor neuron injury and therapeutic target. (2010, neutral): “2) [72] [240].”
Keap1 Is a Redox-Regulated Substrate Adaptor Protein for a Cul3-Dependent Ubiquitin Ligase Complex (2004, background): “One major mechanism for protection against oxidative damage involves the coordinated induction of a group of cytoprotective genes that enable cells to neutralize reactive molecules and restore cellular redox homeostasis (14, 41).”
Novel mechanisms of natural antioxidant compounds in biological systems: involvement of glutathione and glutathione-related enzymes. (2005, background): “There is a fair amount of evidence that ARE/EpRE sequences play a pivotal role in the regulation of the cellular defense system, being in turn strictly regulated by transcriptional factors, such as the E2-related factors Nrf1 and mainly Nrf2, ubiquitously expressed and belonging to the basic region ”
Endoplasmic Reticulum Stress and Oxidative Stress: A Vicious Cycle or a Double-Edged Sword? (2007, positive): “NRF2 binds to the antioxidant response element (ARE) to activate transcription of genes encoding detoxifying enzymes, including A1 and A2 subunits of glutathione S -transferase, NAD(P)H:quinone oxidoreductase, (cid:2) -glutamylcysteine synthetase, HO-1, and UDP-glucoronosyl transferase (95).”
The Impact of Oxidative Stress and Inflammation on RPE Degeneration in Non-neovascular AMD (2017, background): “Nrf2 regulates a coordinated transcriptional program that allows cellular redox homeostasis, yet protects the cell from oxidative injury (Nguyen et al., 2003; Rangasamy et al., 2004; Thimmulappa et al., 2002) (Fig 1).”