Nrf2-Keap1 defines a physiologically important stress response mechanism.
By Hozumi Motohashi, Masayuki Yamamoto. Trends in Molecular Medicine, 2004
1,729 citations recorded by the source corpus.
Subfields: Health, Toxicology and Mutagenesis, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/141b4c3422e2bc477a35a1fdbbc2a96e8e20a394
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Health, Toxicology and Mutagenesis
- Masayuki Yamamoto
- Donna D. Zhang
- D. Bohmann
- Gerasimos P. Sykiotis
- A. Kong
- Wenge Li
- Hozumi Motohashi
- A. Dinkova-Kostova
In Molecular Biology
- Masayuki Yamamoto
- Donna D. Zhang
- Hozumi Motohashi
- Gerasimos P. Sykiotis
- D. Bohmann
- A. Dinkova-Kostova
- K. I. Tong
- K. Taguchi
Citations in the corpus
- Molecular mechanisms of the Keap1–Nrf2 pathway in stress response and cancer evolution (2011, background): “The transcription factor Nrf2 (NF-E2-related factor 2) is a potent transcriptional activator and plays a central role in inducible expression of many cytoprotective genes in response to oxidative and electrophilic stresses (Itoh et al. 1997; Motohashi & Yamamoto 2004) (Fig.”
- Keap1 Recruits Neh2 through Binding to ETGE and DLG Motifs: Characterization of the Two-Site Molecular Recognition Model (2006, background): “The induction of these cytoprotective genes is regulated at the transcriptional level by a specific cis-acting element, the antioxidant/electrophile response element (ARE/EpRE) found in the promoter regions of these genes (21, 39, 40).”
- Dietary Polyphenols and Their Biological Significance (2007, background): “The Nrf2–Kelch-like ECH-asso ciated protein 1 (Keap1)-ARE system is now recognized as one of the major cellular defence mec hanisms against oxidative and xenobiotic stresses [46].”
- Nrf2 is a critical regulator of the innate immune response and survival during experimental sepsis. (2006, neutral): “1 mg glutathione S-transferase–IkBa (1-317) substrate (Santa Cruz Biotech-”
- Inflammation, a Key Event in Cancer Development (2006, background): “The transcription factor Nrf2, which regulates a wide range of detoxifying and antioxidant genes, was identified as a critical system responding to cellular stresses (203).”
- The emerging role of the Nrf2–Keap1 signaling pathway in cancer (2013, background): “…to protect against neurodegenerative diseases, aging, diabetes, photo-oxidative stress, cardiovascular dis- ease, inflammation, pulmonary fibrosis, acute pulmonary injury, and cancer (for review, see Motohashi and Yamamoto 2004; Jeong et al. 2006; Zhang 2006; Kensler et al. 2007; Lau et al. 2008).”
- Oxidative and Electrophilic Stresses Activate Nrf2 through Inhibition of Ubiquitination Activity of Keap1 (2006, background): “In defense, vertebrates have developed multiple stress response systems, including the system regulated by the Nrf2-Keap1 pathway (13, 21, 23, 24, 28, 29).”
- Antioxidant Properties of Probiotic Bacteria (2017, background): “In recent years, both in vivo and in vitro reports have indicated that probiotic bacteria could protect against oxidative stress through regulating the Nrf2-Keap1-ARE pathway.”
- Stress-Activated Cap’n’collar Transcription Factors in Aging and Human Disease (2010, background): “Nrf2 is the central mediator of a prominent antioxidant response system (27, 28).”
- Activation of Nrf2-antioxidant signaling attenuates NF-κB-inflammatory response and elicits apoptosis (2008, background): “enhancer called antioxidant response element (ARE), and eventually recruits the whole transcription machinery including the RNA polymerase II to transcribe phase II/III genes [1].”
- NF-kappaB/p65 antagonizes Nrf2-ARE pathway by depriving CBP from Nrf2 and facilitating recruitment of HDAC3 to MafK. (2008, background): “Nrf2 is amember of theCNC-basic leucine zipper (CNC-bZIP) family of transcription factors, which coordinately regulates the constitutive and inducible expression of antioxidant and phase 2 detoxification enzymes, such as heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1), via a cis-”