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Literature summary for 6.3.2.2 extracted from

  • Thompson, J.A.; White, C.C.; Cox, D.P.; Chan, J.Y.; Kavanagh, T.J.; Fausto, N.; Franklin, C.C.
    Distinct Nrf1/2-independent mechanisms mediate As 3+-induced glutamate-cysteine ligase subunit gene expression in murine hepatocytes (2009), Free Radic. Biol. Med., 46, 1614-1625.
    View publication on PubMedView publication on EuropePMC
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Metals/Ions

Metals/Ions Comment Organism Structure
As3+ As3+ coordinately upregulates GCL catalytic subunit and GCL modifier subunit mRNA levels resulting in increased GCL subunit protein expression, holoenzyme formation, and activity. As3+ increases the rate of transcription of both the GCL catalytic subunit and GCL modifier subunit genes and induces the posttranscriptional stabilization of GCL modifier subunit mRNA. The antioxidant N-acetylcysteine abolishes As3+-induced GCL catalytic subunit expression and attenuates induction of GCL modifier subunit. As3+ induction of GCL catalytic subunit and GCL modifier subunit is also differentially regulated by the MAPK signaling pathways and occurrs independent of the Nrf1/2 transcription factors Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus
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-
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Source Tissue

Source Tissue Comment Organism Textmining
hepatocyte
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 Mus musculus
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Expression

Organism Comment Expression
Mus musculus As3+ coordinately upregulates GCL catalytic subunit and GCL modifier subunit mRNA levels resulting in increased GCL subunit protein expression, holoenzyme formation, and activity. As3+ increases the rate of transcription of both the GCL catalytic subunit and GCL modifier subunit genes and induces the posttranscriptional stabilization of GCL modifier subunit mRNA. The antioxidant N-acetylcysteine abolishes As3+-induced GCL catalytic subunit expression and attenuates induction of GCL modifier subunit. As3+ induction of GCL catalytic subunit and GCL modifier subunit is also differentially regulated by the MAPK signaling pathways and occurs independent of the Nrf1/2 transcription factors up