Tumor Necrosis Factor α Increases Neuronal Vulnerability to Excitotoxic Necrosis by Inducing Expression of the AMPA–Glutamate Receptor Subunit GluR1 via an Acid Sphingomyelinase- and NF-κB-Dependent Mechanism

Tumor Necrosis Factor α Increases Neuronal Vulnerability to Excitotoxic Necrosis by Inducing Expression of the AMPA–Glutamate Receptor Subunit GluR1 via an Acid Sphingomyelinase- and NF-κB-Dependent Mechanism

Acid sphingomyelinase (ASMase) and NF-κB participate in tumor necrosis factor α (TNFα) signal transduction. Mice in which the genes encoding ASMase or the p50 subunit of NF-κB are disrupted have been reported to be less vulnerable than wild-type mice to focal brain ischemia. We now demonstrate selec...

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Bibliographic Details
Main Authors: ZaiFang Yu, Guanjun Cheng, Xiaoming Wen, Gary D. Wu, Wang-Tso Lee, David Pleasure
Format: Article
Language:English
Published: Elsevier 2002-10-01
Series:Neurobiology of Disease
Subjects:
acid sphingomyelinase
AMPA receptor
neuronal excitotoxicity
NF-κB
tumor necrosis factor α
Online Access:http://www.sciencedirect.com/science/article/pii/S0969996102905309

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http://www.sciencedirect.com/science/article/pii/S0969996102905309

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