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• W2021007638 endingPage "1106" @default.
• W2021007638 startingPage "1095" @default.
• W2021007638 abstract "Hyperhomocysteinemia is an independent risk factor for stroke and neurological abnormalities. However, the underlying cellular mechanisms by which elevated homocysteine can promote neuronal death is not clear. In the present study we have examined the role of NMDA receptor-mediated activation of the extracellular signal-regulated kinase-mitogen-activated protein (ERK-MAP) kinase pathway in homocysteine-dependent neurotoxicity. The study demonstrates that in neurons l-homocysteine-induced cell death was mediated through activation of NMDA receptors. The study also shows that homocysteine-dependent NMDA receptor stimulation and resultant Ca2+ influx leads to rapid and sustained phosphorylation of ERK-MAP kinase. Inhibition of ERK phosphorylation attenuates homocysteine-mediated neuronal cell death thereby demonstrating that activation of ERK-MAP kinase signaling pathway is an intermediate step that couples homocysteine-mediated NMDA receptor stimulation to neuronal death. The findings also show that cAMP response-element binding protein (CREB), a pro-survival transcription factor and a downstream target of ERK, is only transiently activated following homocysteine exposure. The sustained activation of ERK but a transient activation of CREB together suggest that exposure to homocysteine initiates a feedback loop that shuts off CREB signaling without affecting ERK phosphorylation and thereby facilitates homocysteine-mediated neurotoxicity." @default.
• W2021007638 created "2016-06-24" @default.
• W2021007638 creator A5049383731 @default.
• W2021007638 creator A5058498535 @default.
• W2021007638 date "2009-07-13" @default.
• W2021007638 modified "2023-10-17" @default.
• W2021007638 title "Homocysteine-NMDA receptor-mediated activation of extracellular signal-regulated kinase leads to neuronal cell death" @default.
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• W2021007638 doi "https://doi.org/10.1111/j.1471-4159.2009.06207.x" @default.
• W2021007638 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2748669" @default.
• W2021007638 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19508427" @default.
• W2021007638 hasPublicationYear "2009" @default.
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