Glutamate receptor antibodies activate a subset of receptors and reveal an agonist binding site

@article{Twyman1995GlutamateRA,
  title={Glutamate receptor antibodies activate a subset of receptors and reveal an agonist binding site},
  author={Roy E. Twyman and Lorise C Gahring and Joachim Spiess and Scott W. Rogers},
  journal={Neuron},
  year={1995},
  volume={14},
  pages={755-762}
}
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211 Citations
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211 Citations

Autoantibodies to the glutamate receptor kill neurons via activation of the receptor ion channel.
TLDR
Results show that antibodies to a specific peptide of the GluR can kill neurons by an excitotoxic mechanism, thus mimicking the effects of excess of glutamate, the first example that antibodies can lead to neuronal death in a non-classical complement-independent manner.
Autoantibodies Against an Extracellular Peptide of the GluR3 Subtype of AMPA Receptors Activate Both Homomeric and Heteromeric AMPA Receptor Channels
TLDR
It is reported here that the affinity-purified anti-GluR3B Abs directly activate GluR 3-containing homomeric and heteromeric AMPA receptor complexes without the requirement of neuronal, glial or blood ancillary molecules.
Identification of Amino Acids in the Glutamate Receptor, GluR3, Important for Antibody-binding and Receptor-specific Activation*
TLDR
This study produced additional rabbit anti-GluR3B-specific antibodies, ranked them according to their ability to function as GluR agonists and characterized the immunoreactivity using deletion and alanine substitution mutagenesis to conclude that antibody contacts with key residues in the Glu R3B region define a novel GLUR subunit-specific agonist binding site and impart sub unit-specific immunore activity.
Antibodies Against the NH2-Terminus of the GluA Subunits Affect the AMPA-Evoked Releasing Activity: The Role of Complement
TLDR
The results suggest the presence of GluA2/GluA3-containing release-regulating AMPA autoreceptors in cortical synaptosomes, which could be relevant to the development of autoimmune diseases typified by an overproduction of anti-GLUA subunits.
Glutamate receptor antibodies directed against AMPA receptors subunit 3 peptide B (GluR3B) can be produced in DBA/2J mice, lower seizure threshold and induce abnormal behavior
Glutamate Receptor GluR 3 Antibodies and Death of Cortical Cells gliosis
TLDR
The goal of this work was to determine whether cirbodies (anti-GluR3) suggested that anti-GLUR3 gained culating anti-R3 antibodies destroyed cortical cells access to the central nervous system where it exerted and if so, by what mechanism, and to confirm and deleterious effects.
Glutamate receptor antibodies directed against AMPA receptors subunit 3 peptide B (GluR3B) associate with some cognitive/psychiatric/behavioral abnormalities in epilepsy patients
Immunization with the glutamate receptor-derived peptide GluR3B induces neuronal death and reactive gliosis, but confers partial protection from pentylenetetrazole-induced seizures
Glutamate Receptor GluR3 Antibodies and Death of Cortical Cells
Antibodies prepared to neuronal glutamate receptor subunit3 bind IFNalpha-receptors: implications for an autoimmune process.
TLDR
It is proposed that the IFNAR-1 may be an heteroclitic antigen of GluR3, which may contribute to variable clinical characteristics of certain autoimmune diseases.
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