Title : Genetic or pharmacologic activation of Nrf2 signaling fails to protect against aflatoxin genotoxicity in hypersensitive GSTA3 knockout mice.

Pub. Date : 2014 Jun

PMID : 24675090






4 Functional Relationships(s)
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Protein Name
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1 Mice are resistant to aflatoxin hepatotoxicity, primarily due to high expression of glutathione S-transferases (GSTs), and in particular the GSTA3 subunit. Aflatoxins glutathione S-transferase, alpha 3 Mus musculus
2 Mice are resistant to aflatoxin hepatotoxicity, primarily due to high expression of glutathione S-transferases (GSTs), and in particular the GSTA3 subunit. Aflatoxins glutathione S-transferase, alpha 3 Mus musculus
3 Nuclear factor erythroid 2 related factor 2 (Nrf2) signaling, which controls a broad-based cytoprotective response, was activated either genetically or pharmacologically in an attempt to rescue GSTA3 knockout mice from aflatoxin genotoxicity. Aflatoxins glutathione S-transferase, alpha 3 Mus musculus
4 The inability to rescue GSTA3 knockout mice from aflatoxin genotoxicity through the Nrf2 transcriptional program indicates that Gsta3 is unilaterally responsible for the detoxication of aflatoxin in mice. Aflatoxins glutathione S-transferase, alpha 3 Mus musculus