Impairment of GABAB receptor dimer by endogenous 14-3-3ζ in chronic pain conditions-Reference-Cited by-同舟云学术

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Impairment of GABAB receptor dimer by endogenous 14-3-3ζ in chronic pain conditions

Published:2012-06-12 Issue:15 Volume:31 Page:3239-3251
ISSN:0261-4189
Container-title:The EMBO Journal
language:en
Short-container-title:

Author:

Laffray Sophie¹²,Bouali-Benazzouz Rabia¹²,Papon Marie-Amélie¹²,Favereaux Alexandre¹²,Jiang Yang³,Holm Tina³,Spriet Corentin⁴,Desbarats Pascal⁵,Fossat Pascal¹²,Le Feuvre Yves¹²,Decossas Marion⁶,Héliot Laurent⁴,Langel Ulo³,Nagy Frédéric¹²,Landry Marc¹²

Affiliation:

1. Bordeaux University; Bordeaux France

2. IINS, CNRS UMR 5297; Bordeaux France

3. Department of Neurochemistry, Stockholm University; Stockholm Sweden

4. Laboratoire d‧Imagerie Cellulaire Fonctionnelle, Institut de Recherche Interdisciplinaire; Lille France

5. LaBRi, CNRS UMR 5800, Bordeaux University; Bordeaux France

6. Bordeaux Imaging Center, Bordeaux University; Bordeaux France

Publisher

Wiley

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,Molecular Biology,General Neuroscience

Reference55 articles.

1. EFNS guidelines on pharmacological treatment of neuropathic pain;Attal;Eur J Neurol,2006

2. BDNF-mediated modulation of GABA and glycine release in dorsal horn lamina II from postnatal rats;Bardoni;Dev Neurobiol,2007

3. gamma-aminobutyric acid type B receptor splice variant proteins GBR1a and GBR1b are both associated with GBR2 in situ and display differential regional and subcellular distribution;Benke;J Biol Chem,1999

4. 14-3-3 proteins in the nervous system;Berg;Nat Rev Neurosci,2003

5. Oligomerization of G-protein-coupled transmitter receptors;Bouvier;Nat Rev Neurosci,2001

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