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Literature summary for 3.1.3.77 extracted from

  • Zhang, Y.; Wang, T.; Yang, K.; Xu, J.; Ren, L.; Li, W.; Liu, W.
    Cerebral microvascular endothelial cell apoptosis after ischemia Role of enolase-phosphatase 1 activation and aci-reductone dioxygenase 1 translocation (2016), Front. Mol. Neurosci., 9, 79 .
    View publication on PubMedView publication on EuropePMC
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Organism

Organism UniProt Comment Textmining
Rattus norvegicus Q5PPH0
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-

Source Tissue

Source Tissue Comment Organism Textmining
brain
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 Rattus norvegicus
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microvessel
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 Rattus norvegicus
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Synonyms

Synonyms Comment Organism
Enoph1
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 Rattus norvegicus

Expression

Organism Comment Expression
Rattus norvegicus focal cerebral ischemia induces Enoph1 mRNA and protein expression in ischemic hemispheric microvessels. Exposure of cultured brain microvascular endothelial cells to oxygen-glucose deprivation also induces Enoph1 upregulation up

General Information

General Information Comment Organism
physiological 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 Rattus norvegicus