2xx8: Difference between revisions

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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=2xx8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2xx8 OCA], [https://pdbe.org/2xx8 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2xx8 RCSB], [https://www.ebi.ac.uk/pdbsum/2xx8 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2xx8 ProSAT]</span></td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=2xx8 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2xx8 OCA], [https://pdbe.org/2xx8 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2xx8 RCSB], [https://www.ebi.ac.uk/pdbsum/2xx8 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2xx8 ProSAT]</span></td></tr>
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== Function ==
[https://www.uniprot.org/uniprot/GRIA2_RAT GRIA2_RAT] Receptor for glutamate that functions as ligand-gated ion channel in the central nervous system and plays an important role in excitatory synaptic transmission. L-glutamate acts as an excitatory neurotransmitter at many synapses in the central nervous system. Binding of the excitatory neurotransmitter L-glutamate induces a conformation change, leading to the opening of the cation channel, and thereby converts the chemical signal to an electrical impulse. The receptor then desensitizes rapidly and enters a transient inactive state, characterized by the presence of bound agonist. In the presence of CACNG4 or CACNG7 or CACNG8, shows resensitization which is characterized by a delayed accumulation of current flux upon continued application of glutamate.<ref>PMID:9351977</ref> <ref>PMID:19265014</ref> <ref>PMID:21172611</ref> <ref>PMID:12501192</ref> <ref>PMID:12015593</ref> <ref>PMID:12872125</ref> <ref>PMID:12730367</ref> <ref>PMID:16192394</ref> <ref>PMID:15591246</ref> <ref>PMID:17018279</ref> <ref>PMID:16483599</ref> <ref>PMID:19946266</ref> <ref>PMID:21317873</ref> <ref>PMID:21846932</ref>
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== Publication Abstract from PubMed ==
== Publication Abstract from PubMed ==