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Special Issue "Nrf2 in Redox Signaling: A Double Edged Sword"
Deadline for manuscript submissions: closed (31 October 2017).
Prof. Dr. Andreas Von Knethen E-Mail
Institute of Biochemistry I, Faculty of Medicine, Goethe-University Frankfurt/Main, Germany
Interests: sepsis; Nrf2; PPARγ; redox signaling; autophagy
In inflammatory processes, release of reactive oxygen species and synthesis of electrophilic compounds are sensed intracellularly by the cap ´n´ collar basic region leucine zipper transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2). Nrf2 is mainly regulated posttranslationally via the proteasome. Under control conditions, Nrf2 is bound by the Kelch-like ECH-associated protein 1 (Keap1) dimer, provoking binding of the E3-ligase Cullin-3. Ubiquitination of Nrf2 targets Nrf2 for proteasomal degradation. In response to oxidative or electrophilic stress, Nrf2 is stabilized. Following its translocation to the nucleus it induces the expression of antioxidative and cytoprotective target genes. Therefore, Nrf2 activation is an important therapeutic target in diseases associated with (excessive) inflammation and injury. However, excessive or prolonged Nrf2 activation has also been shown to contribute to tumorigenesis. Taking these important functions of Nrf2 into consideration, understanding the different means of Nrf2 regulation will provide an improved background for setting up new treatment regimes.
This Special Issue, Nrf2 in Redox Signaling: A Double Edged Sword, will cover a selection of recent research topics and current review articles in the field of Nrf2-dependent research about its role in acute and chronic inflammation, and its resolution as well as tumorigenesis. Experimental papers, up-to-date review articles, and commentaries are all welcome.
Prof. Dr. Andreas von Knethen
Manuscript Submission Information
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- chronic inflammation
- acute inflammation,
- resolution of inflammation
- antigen presentation
- foam cells
- redox signalling