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</table>

== Function ==

[https://www.uniprot.org/uniprot/~~NMDZ1_RAT NMDZ1_RAT~~] NMDA receptor subtype of glutamate-gated ion channels ~~possesses~~ high calcium permeability and voltage-dependent sensitivity to magnesium. Mediated by glycine. ~~Plays~~ a ~~key role in~~ synaptic ~~plasticity~~, ~~synaptogenesis, excitotoxicity, memory acquisition and learning. It mediates~~ neuronal ~~functions in glutamate neurotransmission. Is involved in the cell surface targeting of NMDA receptors~~.~~<ref>PMID:15996549</ref>~~

[https://www.uniprot.org/uniprot/NMDE2_RAT NMDE2_RAT] NMDA receptor subtype of glutamate-gated ion channels with high calcium permeability and voltage-dependent sensitivity to magnesium. Mediated by glycine. In concert with DAPK1 at extrasynaptic sites, acts as a central mediator for stroke damage. Its phosphorylation at Ser-1303 by DAPK1 enhances synaptic NMDA receptor channel activity inducing injurious Ca2+ influx through them, resulting in an irreversible neuronal death (By similarity).

== Publication Abstract from PubMed ==

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 </table>
 == Function ==
-[https://www.uniprot.org/uniprot/NMDZ1_RAT NMDZ1_RAT] NMDA receptor subtype of glutamate-gated ion channels possesses high calcium permeability and voltage-dependent sensitivity to magnesium. Mediated by glycine. Plays a key role in synaptic plasticity, synaptogenesis, excitotoxicity, memory acquisition and learning. It mediates neuronal functions in glutamate neurotransmission. Is involved in the cell surface targeting of NMDA receptors.<ref>PMID:15996549</ref>
+[https://www.uniprot.org/uniprot/NMDE2_RAT NMDE2_RAT] NMDA receptor subtype of glutamate-gated ion channels with high calcium permeability and voltage-dependent sensitivity to magnesium. Mediated by glycine. In concert with DAPK1 at extrasynaptic sites, acts as a central mediator for stroke damage. Its phosphorylation at Ser-1303 by DAPK1 enhances synaptic NMDA receptor channel activity inducing injurious Ca2+ influx through them, resulting in an irreversible neuronal death (By similarity).
 <div style="background-color:#fffaf0;">
 == Publication Abstract from PubMed ==