P38 MAPK Inhibition Protects Against Glutamate Neurotoxicity and Modifies NMDA and AMPA Receptor Subunit Expression
Published 2014 View Full Article
- Home
- Publications
- Publication Search
- Publication Details
Title
P38 MAPK Inhibition Protects Against Glutamate Neurotoxicity and Modifies NMDA and AMPA Receptor Subunit Expression
Authors
Keywords
P38 MAPK, Glutamate, Excitotoxicity, Glu-R expression, Cell signaling
Journal
JOURNAL OF MOLECULAR NEUROSCIENCE
Volume 55, Issue 3, Pages 596-608
Publisher
Springer Nature
Online
2014-08-29
DOI
10.1007/s12031-014-0398-0
References
Ask authors/readers for more resources
Related references
Note: Only part of the references are listed.- Salvianolic acid B protects human endothelial progenitor cells against oxidative stress-mediated dysfunction by modulating Akt/mTOR/4EBP1, p38 MAPK/ATF2, and ERK1/2 signaling pathways
- (2014) Yubo Tang et al. BIOCHEMICAL PHARMACOLOGY
- Disruption of the GluR2/GAPDH complex protects against ischemia-induced neuronal damage
- (2013) Dongxu Zhai et al. NEUROBIOLOGY OF DISEASE
- Inhibition of p38 MAPK reduces loss of primary sensory neurons after nerve transection
- (2012) Sithiporn Agthong et al. NEUROLOGICAL RESEARCH
- Reactive oxygen species participate in the p38-mediated apoptosis induced by potassium deprivation and staurosporine in cerebellar granule neurons
- (2011) Yazmín Ramiro-Cortés et al. INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
- Postischemic Oxidative Stress Promotes Mitochondrial Metabolic Failure in Neurons and Astrocytes
- (2010) Gary Fiskum et al. Annals of the New York Academy of Sciences
- Activation of p38 MAPK participates in brain ischemic tolerance induced by limb ischemic preconditioning by up-regulating HSP 70
- (2010) Xiao-Cai Sun et al. EXPERIMENTAL NEUROLOGY
- Differential Roles of NMDA Receptor Subtypes NR2A and NR2B in Dendritic Branch Development and Requirement of RasGRF1
- (2010) Fernando J. Sepulveda et al. JOURNAL OF NEUROPHYSIOLOGY
- Excitotoxicity through Ca2+-permeable AMPA receptors requires Ca2+-dependent JNK activation
- (2010) M. Vieira et al. NEUROBIOLOGY OF DISEASE
- Long-Term Potentiation in the CA1 Hippocampus Induced by NR2A Subunit-Containing NMDA Glutamate Receptors Is Mediated by Ras-GRF2/Erk Map Kinase Signaling
- (2010) Shan-xue Jin et al. PLoS One
- Dynamic and specific interaction between synaptic NR2-NMDA receptor and PDZ proteins
- (2010) L. Bard et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Homocysteine-NMDA receptor-mediated activation of extracellular signal-regulated kinase leads to neuronal cell death
- (2009) Ranjana Poddar et al. JOURNAL OF NEUROCHEMISTRY
- Traumatic Injury Activates MAP Kinases in Astrocytes: Mechanisms of Hypothermia and Hyperthermia
- (2009) Tingting Huang et al. JOURNAL OF NEUROTRAUMA
- Opposing Roles for ATF2 and c-Fos in c-Jun-Mediated Neuronal Apoptosis
- (2009) Z. Yuan et al. MOLECULAR AND CELLULAR BIOLOGY
- AMPA Receptor Incorporation into Synapses during LTP: The Role of Lateral Movement and Exocytosis
- (2009) Hiroshi Makino et al. NEURON
- Role of p38 MAPK and pro-inflammatory cytokines expression in glutamate-induced neuronal death of neonatal rats
- (2008) V. Chaparro-Huerta et al. INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE
- Changes in hippocampal NMDA-R subunit composition induced by exposure of neonatal rats to l-glutamate
- (2008) M.C. Rivera-Cervantes et al. INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE
- Glutamate Receptor Dynamics in Dendritic Microdomains
- (2008) Thomas M. Newpher et al. NEURON
- Postsynaptic mechanisms of excitotoxicity: Involvement of postsynaptic density proteins, radicals, and oxidant molecules
- (2008) J.P. Forder et al. NEUROSCIENCE
- Apoptosis induced by domoic acid in mouse cerebellar granule neurons involves activation of p38 and JNK MAP kinases
- (2007) G. Giordano et al. NEUROCHEMISTRY INTERNATIONAL
Discover Peeref hubs
Discuss science. Find collaborators. Network.
Join a conversationAsk a Question. Answer a Question.
Quickly pose questions to the entire community. Debate answers and get clarity on the most important issues facing researchers.
Get Started