Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 1.13.11.31 extracted from

  • Nagasaki, T.; Schuyler, A.J.; Zhao, J.; Samovich, S.N.; Yamada, K.; Deng, Y.; Ginebaugh, S.P.; Christenson, S.A.; Woodruff, P.G.; Fahy, J.V.; Trudeau, J.B.; Stoyanovsky, D.; Ray, A.; Tyurina, Y.Y.; Kagan, V.E.; Wenzel, S.E.
    15LO1 dictates glutathione redox changes in asthmatic airway epithelium to worsen type 2 inflammation (2022), J. Clin. Invest., 132, e151685 .
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
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

Organism UniProt Comment Textmining
Homo sapiens P16050 cf. EC 1.13.11.33, EC 1.13.11.12
-

General Information

General Information Comment Organism
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