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Literature summary for 3.4.21.35 extracted from

  • Liu, L.; Zhang, R.; Liu, K.; Zhou, H.; Tang, Y.; Su, J.; Yu, X.; Yang, X.; Tang, M.; Dong, Q.
    Tissue kallikrein alleviates glutamate-induced neurotoxicity by activating ERK1 (2009), J. Neurosci. Res., 87, 3576-3590.
    View publication on PubMed

Application

Application Comment Organism
drug development tissue kallikrein represents a promising therapeutic strategy for ischemic stroke Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
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Synonyms

Synonyms Comment Organism
tissue kallikrein
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Homo sapiens

General Information

General Information Comment Organism
physiological function pretreatment of cultured cortical neurons from rats with tissue kallikrein largely prevents glutamate-induced morphological changes and cell death: tissue kallikrein pretreatment alleviates glutamate-induced oxidative stress by inhibiting neuronal nitric oxide synthase activity, thereby reducing the generation of nitric oxide and reactive oxygen species. Extracellular signal-regulated kinase 1/2 cascade (ERK1/2), particularly ERK1, and nuclear factor-kappaB are involved in tissue kallikrein neuroprotection against glutamate-induced neurotoxicity. Tissue kallikrein pretreatment activates ERK1 and nuclear factor-kappaB, leading to enhanced expression of brain-derived neurotrophic factor mRNA and antiapoptotic gene Bcl-2 protein Homo sapiens