Sandbox Reserved 1649: Difference between revisions
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== Regulation == | |||
== NR1/NR2A complex == | |||
== Mutations == | |||
The C-terminal truncation of NR2 subunits in NMDA receptors is an interesting mutation. Indeed, the C-terminal truncation of NR2A influences the functioning of the NMDA receptor. Several experiments were carried out and made it possible to conclude on this influence. | |||
First, mice with truncated NR2A subunits have been shown to still have a functional receptor channel, but NR2A ΔC / ΔC mice appear to be altered in the cellular signal transduction events involved in the induction of LTP (potentiation long-term). Despite the presence of the full-length NR2B subunit, the C-terminal truncation of the NR2A subunit altered the signal transduction mediated by NMDAR. | |||
Second, the C-terminal truncation of NR2A has been shown to alter fear in a particular setting. Indeed, the experiment was to put mutant and wild mice through stepwise avoidance training and put them in water. Thus, the researchers concluded that mutant mice have a significantly reduced latency time to leave the safe platform compared to wild mice and that mutant mice exhibit water balance deficits. | |||
The C-terminal truncation of NR2A therefore has consequences on synaptic plasticity and synaptic reorganization during the recording of hippocampal LTP, on the conditioning of fear and also on motor coordination. <ref name="Cter mutation">DOI 10.1016/S0092-8674(00)80921-6 | |||
</ref> | |||
== Disease == | == Disease == | ||
= | Anti-nuclear antibodies produced in systemic or systemic lupus erythematosus (SLE, SLE) interact with the NR2A subunit of the NMDA receptor. This is because the Asp / Glu-Trp-Asp / Glu-Tyr-Ser / Gly pentapeptide is a molecular mimic of double-stranded DNA, so antibodies produced in a patient with SLE recognize this pentapeptide. The latter is also present in the structure of NR2A. Thus, these antibodies cross-interact with NR2A and therefore the NMDA receptor. This interaction can signal neuronal death by an excitotoxic mechanism. | ||
More generally, NMDA receptor dysfunction is implicated in multiple brain disorders, such as stroke, chronic pain, and schizophrenia. <ref name="antibody">DOI 10.1038/nm1101-1189 | |||
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This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes. | This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes. | ||
