Application | Comment | Organism |
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medicine | 15 lipoxygenase 1 is abundant in asthmatic human airway epithelial cells and binds phosphatidylethanolamine-binding protein 1 (PEBP1), leading to generation of hydroperoxy-phospholipids, which drive ferroptotic cell death. 15LO1, PEBP1, and glutathione peroxidase 4 GPX4 activity drives abnormal asthmatic redox biology, to enhance type 2 inflammatory responses. In vitro, type 2 inflammatory cytokine IL-13 induces 15LO1 generation of hydroperoxy-phospholipids, which lowers intracellular GSH and increased extracellular GSSG levels. Lowering GSH further by inhibiting cystine transporter SLC7A11 enhances type 2 inflammatory protein expression and ferroptosis. Ex vivo, redox imbalances correspond to 15LO1 and SLC7A11 expression, type 2 inflammatory biomarkers, and worsen clinical outcomes | Homo sapiens |
Organism | UniProt | Comment | Textmining |
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Homo sapiens | P16050 | cf. EC 1.13.11.33, EC 1.13.11.12 | - |
General Information | Comment | Organism |
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physiological function | 15 lipoxygenase 1 is abundant in asthmatic human airway epithelial cells and binds phosphatidylethanolamine-binding protein 1 (PEBP1), leading to generation of hydroperoxy-phospholipids, which drive ferroptotic cell death. 15LO1, PEBP1, and glutathione peroxidase 4 GPX4 activity drives abnormal asthmatic redox biology, to enhance type 2 inflammatory responses. In vitro, type 2 inflammatory cytokine IL-13 induces 15LO1 generation of hydroperoxy-phospholipids, which lowers intracellular GSH and increased extracellular GSSG levels. Lowering GSH further by inhibiting cystine transporter SLC7A11 enhances type 2 inflammatory protein expression and ferroptosis. Ex vivo, redox imbalances correspond to 15LO1 and SLC7A11 expression, type 2 inflammatory biomarkers, and worsen clinical outcomes | Homo sapiens |