ArticleFree radical biology & medicine2023
Response to oxidative stress of AML12 hepatocyte cells with knockout of methionine sulfoxide reductases.
Article in Free radical biology & medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 1 citations in OpenAlex.
- Mg/Mn bi-single-atom carbon dot nanozymes with enhanced SOD-like activity and fluorescence for hepatoprotection.Journal of nanobiotechnology · 2026Article
- Reference Gene Validation for Quantitative PCR Analysis in 2D and 3D AML12 Hepatocyte Models.Biomedicines · 2026Article
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2 authors at 1 institution in 1 country.
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Abstract
Methionine sulfoxide reductases are enzymes that reduce methionine oxidation in the cell. In mammals there are three B-type reductases that act on the R-diastereomer of methionine sulfoxide, and one A-type reductase (MSRA) that acts on the S-diastereomer. Unexpectedly, knocking out the four genes in the mouse protected from oxidative stresses such as ischemia-reperfusion injury and paraquat. To elucidate the mechanism by which lack of the reductases protects against oxidative stresses, we aimed to create a cell culture model with AML12 cells, a differentiated hepatocyte cell line. We employed CRISPR/Cas9 to create lines lacking the four individual reductases. All were viable and their susceptibility to oxidative stresses was the same as the parental strain. The triple knockout lacking all three methionine sulfoxide reductases B was also viable, but the quadruple knockout was lethal. We thus modeled the quadruple knockout mouse by creating an AML12 line lacking the three MSRB and heterozygous for the MSRA (Msrb3KO-Msra
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