Disease relevance of Gria4

• To isolate antibodies against ionotropic glutamate receptors (GluRs), we prepared a phage antibody library from mice immunized with proteoliposomes containing purified alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), a selective GluRD receptor [1].
• In dorsal root ganglia, immunostaining of ganglion cell bodies was moderate to dense with antibody to GluR2/3 and light to moderate with antibody to GluR4 [2].

High impact information on Gria4

• By using Western blot we observed decreased levels of the AMPA receptor subunits GluR2/3 and GluR4 in trkB (-/-) forebrains [3].
• Single-cell RT-PCR showed that CD15+ amacrine cells coexpress several AMPA receptors - GluR1, GluR2, and GluR4 being the most common combination [4].
• GluR4 mRNA was increased throughout the grey matter, presumably in relation to the marked microglia activation reported in the grey matter of the lumbar spinal cord in mnd mice [5].
• About half of the P19 cells were stained with antibodies selective for GluR-D but there was little or no immunoreactivity for the GluR-A subunit [6].
• All of these cell lines expressed the AMPA glutamate receptor subunit genes GluR2 and GluR4, but only the GT1-1 and GT1-7 cells expressed the kainate glutamate receptor subunit gene KA2 [7].

Biological context of Gria4

• The glutamate-mediated transmission efficiency of synaptic AMPA receptors is influenced by their subunit composition (GluR-A to GluR-D), post-transcriptional and post-translational modifications, the number of synaptic AMPA receptors, and auxiliary proteins [8].

Anatomical context of Gria4

• Horizontal cell processes postsynaptic at both rod and cone synaptic terminals preferentially expressed the subunits GluR2, GluR2/3 and GluR4 [9].
• In contrast, these neurons exhibiting both NK-3R and GluR4 immunoreactivity were hardly detected although GluR4-positive neurons were still distributed in the substantia nigra [10].
• Possible neuroglia in the spinal cord (mainly GluR2/3 and 4) and satellite cells in dorsal root ganglia (GluR4) were immunostained [2].
• Immunocytochemical labelling of AMPA receptor subunits GluR2/R3 and GluR4 was detected in neuron cell bodies and proximal neurites and more lightly in glial cells [11].
• However, substantial inter-species differences were found for oligodendrocytes (KA2 in mouse; GluR4 and GluR2/3 in rat) [12].

Associations of Gria4 with chemical compounds

• Using this approach, we obtained a panel of high-affinity antibody fragments that immunoprecipitated both recombinant and native GluRD receptors, but not GluR6, a kainate receptor subunit with a 40% sequence similarity [1].

Other interactions of Gria4

• Potential candidate genes in this region include Penk2 and Gria4 [13].
• Two monoclonal antibodies provided some evidence that GluR2 and/or GluR4, as well as NMDAR1 subunit, are present on the rod bipolar cell [14].
• We detected a slight but statistically significant decrease of the AMPA receptor subunits GluR3 and GluR4 only in end stage disease animals [15].

Analytical, diagnostic and therapeutic context of Gria4

• Quantitative PCR studies suggested the pronounced expression of PEPA-preferring AMPA receptor subunits (GluR3 and GluR4) and a splice variant (flop) in the mPFC [16].

References