PKC–NF-κB are involved in CCL2-induced Nav1.8 expression and channel function in dorsal root ganglion neurons
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Title
PKC–NF-κB are involved in CCL2-induced Nav1.8 expression and channel function in dorsal root ganglion neurons
Authors
Keywords
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Journal
BIOSCIENCE REPORTS
Volume 34, Issue 3, Pages 237-245
Publisher
Portland Press Ltd.
Online
2014-04-14
DOI
10.1042/bsr20140005
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- PKCε phosphorylation of the sodium channel NaV1.8 increases channel function and produces mechanical hyperalgesia in mice
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- CC chemokine ligand 2 upregulates the current density and expression of TRPV1 channels and Nav1.8 sodium channels in dorsal root ganglion neurons
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- Neurochemokines: a menage a trois providing new insights on the functions of chemokines in the central nervous system
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- Are Voltage-Gated Sodium Channels on the Dorsal Root Ganglion Involved in the Development of Neuropathic Pain?
- (2011) Wei Wang et al. Molecular Pain
- Involvement of glutamate NMDA and AMPA receptors, glial cells and IL-1β in the spinal hyperalgesia evoked by the chemokine CCL2 in mice
- (2011) Ana Baamonde et al. NEUROSCIENCE LETTERS
- Exploring the role of nociceptor-specific sodium channels in pain transmission using Nav1.8 and Nav1.9 knockout mice
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- PKC∊-Dependent Potentiation of TTX-Resistant NaV1.8 Current by Neurokinin-1 Receptor Activation in Rat Dorsal Root Ganglion Neurons
- (2009) Chun-Lei Cang et al. Molecular Pain
- Spinal CCL2 pronociceptive action is no longer effective in CCR2 receptor antagonist-treated rats
- (2008) Marc-Andr Dansereau et al. JOURNAL OF NEUROCHEMISTRY
- Phosphorylation of Sodium Channel Nav1.8 by p38 Mitogen-Activated Protein Kinase Increases Current Density in Dorsal Root Ganglion Neurons
- (2008) A. Hudmon et al. JOURNAL OF NEUROSCIENCE
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