ArticleNature communications2025
AAK1 activation-mediated iron trafficking drives ferroptotic cell death.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Carrier-free nanoparticles in microneedles disrupt endosomal acidification suppress ferroptosis in radiation-induced oral mucositis.Materials today. Bio · 2026Article
- Artesunate in Ferroptosis and Cuproptosis Regulation: Context-Dependent Mechanisms, Interplay, and Therapeutic Implications.International journal of molecular sciences · 2026Review
- The biphasic interactions between ferroptosis and oxidative stress: from molecular mechanisms to disease interventions.Molecular biology reports · 2026Review
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Authors and funding
20 authors.
Funding
Abstract
Ferrous iron is necessary for the occurrence of ferroptosis. The molecular mechanisms that maintain iron homeostasis within cells play a crucial role in the regulation of ferroptosis. However, how cells regulate iron uptake during ferroptosis remains unclear. Here, PKCβII is identified as a key kinase mediating transferrin receptor 1 (TFR1) endocytosis through phosphorylation and activation of AP2-associated protein kinase 1 (AAK1) during the ferroptotic process. Mechanistically, activated AAK1 phosphorylates AP2M1, which facilitates the recruitment of clathrin to mediate the endocytosis of TFR1, increasing the levels of both cellular total iron and ferrous iron and thereby promoting ferroptosis. The non-phosphorylatable mutation of AAK1 inhibits ferroptosis and consequently promotes breast tumor growth in vivo. In conclusion, we identify that the PKCβII-AAK1-AP2M1 pathway is a crucial mechanism for the regulation of cellular iron uptake during ferroptosis, which is correlated with the prognosis of breast cancer patients and presents a potential target for cancer therapy.
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