Title : Coaction of hepatic thioredoxin and glutathione systems in iron overload-induced oxidative stress.

Pub. Date : 2021 Apr

PMID : 33393188






4 Functional Relationships(s)
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1 To confirm the iron overload model in the liver, the increased gene expression levels of hepcidin (Hamp), ferroportin (Fpn1), and ferritin (Fth1), which regulate iron trafficking, were observed by a quantitative polymerase chain reaction. Iron hepcidin antimicrobial peptide Mus musculus
2 To confirm the iron overload model in the liver, the increased gene expression levels of hepcidin (Hamp), ferroportin (Fpn1), and ferritin (Fth1), which regulate iron trafficking, were observed by a quantitative polymerase chain reaction. Iron hepcidin antimicrobial peptide Mus musculus
3 To confirm the iron overload model in the liver, the increased gene expression levels of hepcidin (Hamp), ferroportin (Fpn1), and ferritin (Fth1), which regulate iron trafficking, were observed by a quantitative polymerase chain reaction. Iron hepcidin antimicrobial peptide Mus musculus
4 To confirm the iron overload model in the liver, the increased gene expression levels of hepcidin (Hamp), ferroportin (Fpn1), and ferritin (Fth1), which regulate iron trafficking, were observed by a quantitative polymerase chain reaction. Iron hepcidin antimicrobial peptide Mus musculus