ArticleJournal of agricultural and food chemistry2025
Selenoprotein K Confers Protection against Iron Dyshomeostasis-Related Neurotoxicity by Regulating the Palmitoylation of TfR-1.
Article in Journal of agricultural and food chemistry, 2025. 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.
- Geno-guided targeting of ferroptosis: a multi-layered network to overcome radioresistance in lung cancer.Frontiers in cell and developmental biology · 2026Review
- Effects of prenatal iron deficiency on neurological development and related disorders in offspring.Frontiers in nutrition · 2025Review
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Authors and funding
7 authors.
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Abstract
Selenoprotein K (SELENOK), a protein residing in the endoplasmic reticulum (ER), is modulated by dietary selenium and is expressed at elevated levels in neurons. SELENOK has been shown to participate in cellular antioxidant activity and posttranslational palmitoylation. This study presents both in vivo and in vitro evidence that SELENOK deficiency reduces the palmitoylation of TfR-1, thereby impairing transferrin transport and ultimately leading to a decrease in the intracellular iron content, impaired mitochondrial respiratory chain activity and decreased ATP production. Remarkably, restoring SELENOK levels significantly enhanced TfR-1 palmitoylation, increased intracellular iron levels, and restored mitochondrial function, thus ameliorating cognitive deficits in 7 month-old SELENOK knockout mice. Consistent with these findings, iron supplementation also improved mitochondrial function by elevating intracellular iron levels, thereby improving cognitive deficits in 7 month-old SELENOK knockout mice. Therefore, SELENOK exerts its neuroprotective effect by regulating the palmitoylation of TfR-1 to maintain iron homeostasis, thereby protecting mitochondrial function in neurons.
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