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Cited by 347

The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.

Regulatory mechanisms of cellular response to oxidative stress

Itoh, Ken, Ishii, Tetsuro, Wakabayashi, Nobunao, Yamamoto, Masayuki·1999·Free Radical Research

Abstract

An antioxidant responsive element (ARE) or electrophile responsive element (EpRE) mediates the transcriptional activation of genes encoding phase II drug metabolizing enzymes. The ARE consensus sequence shows high similarity to an erythroid gene regulatory element, and based on the observation, we have recently found that transcription factor Nrf2 is essential for the coordinate induction of phase II detoxifying enzymes. The expression of anti-oxidative stress enzyme genes is also regulated by Nrf2. Detailed analysis of the regulatory mechanisms of Nrf2 activity has ultimately led us to the identification of a new protein, which we have named Keap1, that suppresses Nrf2 activity by specific binding to its evolutionarily-conserved N-terminal Neh2 regulatory domain.

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Metadata

Authors
Itoh, K., Ishii, T., Wakabayashi, N., & Yamamoto, M.
Venue
Free Radical Research
Published
1999-01
Volume
31
Issue
4
Pages
319-324
ISSN
  • 1029-2470 (ISSN-L)
  • 1071-5762
OpenAlex
W2005568856
Cited by
347
References
32
FWCI
2.07
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Regulatory mechanisms of cellular response to oxidative stress. https://app.cochat.ai/papers/10.1080/10715769900300881
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Itoh, K., Ishii, T., Wakabayashi, N., & Yamamoto, M. (1999). Regulatory mechanisms of cellular response to oxidative stress. Free Radical Research. https://doi.org/10.1080/10715769900300881

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.