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Relevant bibliographies by topics / Nrf2-mediated antioxidant response

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Academic literature on the topic 'Nrf2-mediated antioxidant response'

Author: Grafiati

Published: 5 June 2025

Last updated: 2 August 2025

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Journal articles on the topic "Nrf2-mediated antioxidant response"

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Li, Wenge, and Ah-Ng Kong. "Molecular mechanisms of Nrf2-mediated antioxidant response." Molecular Carcinogenesis 48, no. 2 (2009): 91–104. http://dx.doi.org/10.1002/mc.20465.

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Sun, Zheng, Y. Eugene Chin, and Donna D. Zhang. "Acetylation of Nrf2 by p300/CBP Augments Promoter-Specific DNA Binding of Nrf2 during the Antioxidant Response." Molecular and Cellular Biology 29, no. 10 (2009): 2658–72. http://dx.doi.org/10.1128/mcb.01639-08.

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ABSTRACT To maintain intracellular redox homeostasis, genes encoding many antioxidants and detoxification enzymes are transcriptionally upregulated upon deleterious oxidative stress through the cis antioxidant responsive elements (AREs) in their promoter regions. Nrf2 is the critical transcription factor responsible for ARE-dependent transcription. We and others have previously demonstrated that Nrf2 is targeted for ubiquitin-mediated degradation by Keap1 in a redox-sensitive manner through modifications of distinct cysteine residues of Keap1. Here, we report that p300/CBP directly acetylates

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Chhunchha, Bhavana, Eri Kubo, and Dhirendra P. Singh. "Obligatory Role of AMPK Activation and Antioxidant Defense Pathway in the Regulatory Effects of Metformin on Cellular Protection and Prevention of Lens Opacity." Cells 11, no. 19 (2022): 3021. http://dx.doi.org/10.3390/cells11193021.

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Increasing levels of oxidative-stress due to deterioration of the Nrf2 (NFE2-related factor)/ARE (antioxidant response element) pathway is found to be a primary cause of aging pathobiology. Metformin having anti-aging effects can delay/halt aging-related diseases. Herein, using lens epithelial cell lines (LECs) of human (h) or mouse (m) and aging h/m primary LECs along with lenses as model systems, we demonstrated that Metformin could correct deteriorated Bmal1/Nrf2/ARE pathway by reviving AMPK-activation, and transcriptional activities of Bmal1/Nrf2, resulting in increased antioxidants enzyma

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Banerjee, Nivedita, Hui Wang, Gangduo Wang, and M. Firoze Khan. "Enhancing the Nrf2 Antioxidant Signaling Provides Protection Against Trichloroethene-mediated Inflammation and Autoimmune Response." Toxicological Sciences 175, no. 1 (2020): 64–74. http://dx.doi.org/10.1093/toxsci/kfaa022.

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Abstract Trichloroethene (trichloroethylene, TCE) and one of its reactive metabolites dichloroacetyl chloride (DCAC) are associated with the induction of autoimmunity in MRL+/+ mice. Although oxidative stress plays a major role in TCE-/DCAC-mediated autoimmunity, the underlying molecular mechanisms still need to be delineated. Nuclear factor (erythroid-derived 2)-like2 (Nrf2) is an oxidative stress-responsive transcription factor that binds to antioxidant responsive element (ARE) and provides protection by regulating cytoprotective and antioxidant gene expression. However, the potential of Nrf

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Kasai, Shuya, Sunao Shimizu, Yota Tatara, Junsei Mimura, and Ken Itoh. "Regulation of Nrf2 by Mitochondrial Reactive Oxygen Species in Physiology and Pathology." Biomolecules 10, no. 2 (2020): 320. http://dx.doi.org/10.3390/biom10020320.

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Reactive oxygen species (ROS) are byproducts of aerobic respiration and signaling molecules that control various cellular functions. Nrf2 governs the gene expression of endogenous antioxidant synthesis and ROS-eliminating enzymes in response to various electrophilic compounds that inactivate the negative regulator Keap1. Accumulating evidence has shown that mitochondrial ROS (mtROS) activate Nrf2, often mediated by certain protein kinases, and induce the expression of antioxidant genes and genes involved in mitochondrial quality/quantity control. Mild physiological stress, such as caloric rest

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Fan, Xian, Bashar S. Staitieh, J. Spencer Jensen, et al. "Activating the Nrf2-mediated antioxidant response element restores barrier function in the alveolar epithelium of HIV-1 transgenic rats." American Journal of Physiology-Lung Cellular and Molecular Physiology 305, no. 3 (2013): L267—L277. http://dx.doi.org/10.1152/ajplung.00288.2012.

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The master transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2) regulates the expression of antioxidant and phase II-metabolizing enzymes by activating the antioxidant response element (ARE) and thereby protects cells and tissues from oxidative stress. Pulmonary complications remain the leading cause of death in human immunodeficiency virus (HIV)-1-infected individuals, who display systemic oxidative stress and glutathione deficiency that can be modeled in transgenic rats where HIV-1-related viral proteins decrease glutathione levels and cause epithelial barrier dysfunction

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Alam, Md Morshedul, Keito Okazaki, Linh Thi Thao Nguyen, et al. "Glucocorticoid receptor signaling represses the antioxidant response by inhibiting histone acetylation mediated by the transcriptional activator NRF2." Journal of Biological Chemistry 292, no. 18 (2017): 7519–30. http://dx.doi.org/10.1074/jbc.m116.773960.

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NRF2 (nuclear factor erythroid 2-related factor 2) is a key transcriptional activator that mediates the inducible expression of antioxidant genes. NRF2 is normally ubiquitinated by KEAP1 (Kelch-like ECH-associated protein 1) and subsequently degraded by proteasomes. Inactivation of KEAP1 by oxidative stress or electrophilic chemicals allows NRF2 to activate transcription through binding to antioxidant response elements (AREs) and recruiting histone acetyltransferase CBP (CREB-binding protein). Whereas KEAP1-dependent regulation is a major determinant of NRF2 activity, NRF2-mediated transcripti

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Garzón-Castaño, Sandra C., Iván A. Lopera-Castrillón, Francisco J. Jiménez-González, Fernando Siller-López, Luz A. Veloza, and Juan Carlos Sepúlveda-Arias. "Nrf2-Mediated Antioxidant Activity of the inner bark extracts obtained from Tabebuia rosea (Bertol) DC and Tabebuia chrysantha (JACQ) G. Nicholson." F1000Research 7 (December 16, 2018): 1937. http://dx.doi.org/10.12688/f1000research.17165.1.

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Background: Several ethnobotanical and ethnopharmacological studies have shown the therapeutic potential of plants from the genus Tabebuia, which have long been used in traditional medicine in rural areas of South America, for the treatment of several human diseases. This study aimed to evaluate the Nrf2-mediated antioxidant activity of the inner bark extracts obtained from Tabebuia rosea and Tabebuia chrysantha. Methods: The antioxidant activity of extracts obtained from the inner bark of T. rosea and T. chrysantha was evaluated using the Oxygen radical absorbance capacity (ORAC) technique. T

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Garzón-Castaño, Sandra C., Iván A. Lopera-Castrillón, Francisco J. Jiménez-González, Fernando Siller-López, Luz A. Veloza, and Juan Carlos Sepúlveda-Arias. "Nrf2-Mediated Antioxidant Activity of the inner bark extracts obtained from Tabebuia rosea (Bertol) DC and Tabebuia chrysantha (JACQ) G. Nicholson." F1000Research 7 (February 12, 2019): 1937. http://dx.doi.org/10.12688/f1000research.17165.2.

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Background: Several ethnobotanical and ethnopharmacological studies have shown the therapeutic potential of plants from the genus Tabebuia, which have long been used in traditional medicine in rural areas of South America, for the treatment of several human diseases. This study aimed to evaluate the Nrf2-mediated antioxidant activity of the inner bark extracts obtained from Tabebuia rosea and Tabebuia chrysantha. Methods: The antioxidant activity of extracts obtained from the inner bark of T. rosea and T. chrysantha was evaluated using the Oxygen radical absorbance capacity (ORAC) technique. T

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Xue, Peng, Xiangxiang Hu, Emily Chang, et al. "Deficiency of optineurin enhances osteoclast differentiation by attenuating the NRF2-mediated antioxidant response." Experimental & Molecular Medicine 53, no. 4 (2021): 667–80. http://dx.doi.org/10.1038/s12276-021-00596-w.

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AbstractAbnormally increased resorption contributes to bone degenerative diseases such as Paget’s disease of bone (PDB) through unclear mechanisms. Recently, the optineurin (OPTN) gene has been implicated in PDB, and global OPTN knockout mice (Optn−/−) were shown to exhibit increased formation of osteoclasts (osteoclastogenesis). Growing evidence, including our own, has demonstrated that intracellular reactive oxygen species (ROS) stimulated by receptor activator of nuclear factor kappa-B ligand (RANKL) can act as signaling molecules to promote osteoclastogenesis. Here, we report that OPTN int

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Book chapters on the topic "Nrf2-mediated antioxidant response"

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Chen, Shao-yu. "Analysis of Nrf2-Mediated Transcriptional Induction of Antioxidant Response in Early Embryos." In Methods in Molecular Biology. Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-867-2_17.

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Yildiz, Mustafa, and Hatice Segmen. "Two Faces of Nrf2 in Cancer." In Oncogenes and Tumor Suppressor Genes [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102753.

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Nuclear factor erythroid 2–related factor 2 (Nrf2) serves as a “main regulator” in response to internal or external cell stressors through coordinated induction of a wide range of cytoprotective genes. In cancer cells, Nrf2 increases expression of cytoprotective genes and, as a result, promotes proliferation through inhibition of apoptosis and metabolic reprogramming. Therefore, the activation of Nrf2 is an important regulator for prevention of cancer triggered by stresses and toxins. Defense system is activated by cellular pathways to ensure that response to stresses and toxins is sufficient

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Zhou, Xian, Gerald Münch, and Dennis Chang. "Cognitive Impairment in Diabetes Mellitus and Its Management by Transcription Factor Nrf2-Mediated Antioxidant Defense System." In Importance of Oxidative Stress and Antioxidant System in Health and Disease [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.108733.

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Diabetes mellitus has been an epidemic in the twenty-first century and an approximately 50% risk of diabetes predisposed to cognitive decline leading to dementia in humans. There is an urgent need to understand the pathophysiology and identify molecular targets of cognitive impairment in diabetes mellitus that might lead to improved therapy. Mounting evidence indicates that nuclear factor erythroid 2-related factor 2 (Nrf2) and its regulated downstream antioxidant genes are emerging therapeutic targets. In this chapter, we introduce cognitive dysfunction in diabetes mellitus and its hallmarks,

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Conference papers on the topic "Nrf2-mediated antioxidant response"

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Campbell, Michelle R., Brian N. Chorley, Xuting Wang, Hye‐Youn Cho, Steve R. Kleeberger, and Douglas A. Bell. "Abstract B51: Discovery of novel genomic targets in the NRF2‐mediated antioxidant response pathway by ChIP‐on‐chip and ChIP‐seq." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Dec 6–9, 2009; Houston, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1940-6207.prev-09-b51.

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Michaeloudes, Charalambos, Po-Jui Chang, and Kian Fan Chung. "TGF-Beta Modulates NRF2-Mediated Antioxidant Responses In Airway Smooth Muscle Cells." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4059.

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