Title : Homocysteine-NMDA receptor-mediated activation of extracellular signal-regulated kinase leads to neuronal cell death.

Pub. Date : 2009 Aug

PMID : 19508427






8 Functional Relationships(s)
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1 The study also shows that homocysteine-dependent NMDA receptor stimulation and resultant Ca2+ influx leads to rapid and sustained phosphorylation of ERK-MAP kinase. Homocysteine mitogen-activated protein kinase 1 Homo sapiens
2 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. Homocysteine mitogen-activated protein kinase 1 Homo sapiens
3 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. Homocysteine mitogen-activated protein kinase 1 Homo sapiens
4 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. Homocysteine mitogen-activated protein kinase 1 Homo sapiens
5 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. Homocysteine mitogen-activated protein kinase 1 Homo sapiens
6 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. Homocysteine mitogen-activated protein kinase 1 Homo sapiens
7 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. Homocysteine mitogen-activated protein kinase 1 Homo sapiens
8 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. Homocysteine mitogen-activated protein kinase 1 Homo sapiens