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EC Number General Information Commentary Reference
Show all pathways known for 3.1.3.77Display the word mapDisplay the reaction diagram Show all sequences 3.1.3.77metabolism methionine salvage pathway 701951
Show all pathways known for 3.1.3.77Display the word mapDisplay the reaction diagram Show all sequences 3.1.3.77physiological function exposure of cultured brain microvascular endothelial cells to oxygen-glucose deprivation induced Enoph1 upregulation, which is accompanied by increased cell death and apoptosis. Knockdown of Enoph1 expression or overexpressing Enoph1 attenuates or potentiates oxygen-glucose deprivation-induced endothelial cell death, respectively. Enoph1 knockdown or overexpression results in a significant reduction or augmentation of reactive oxygen species generation, apoptosis-associated proteins and endoplasmic reticulum stress proteins in oxygen-glucose deprivation-treated endothelial cells. Oxygen-glucose deprivation upregulates the expression of Enoph1's downstream protein acireductone dioxygenase 1 and enhances its interaction with Enoph1 750658
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