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XB-ART-11928
Neuron 1999 Oct 01;242:461-9. doi: 10.1016/s0896-6273(00)80859-4.
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Attenuation of NMDA receptor activity and neurotoxicity by nitroxyl anion, NO-.

Kim WK , Choi YB , Rayudu PV , Das P , Asaad W , Arnelle DR , Stamler JS , Lipton SA .


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Recent evidence indicates that the NO-related species, nitroxyl anion (NO), is produced in physiological systems by several redox metal-containing proteins, including hemoglobin, nitric oxide synthase (NOS), superoxide dismutase, and S-nitrosothiols (SNOs), which have recently been identified in brain. However, the chemical biology of NO- remains largely unknown. Here, we show that NO- -unlike NO*, but reminiscent of NO+ transfer (or S-nitrosylation)- -reacts mainly with Cys-399 in the NR2A subunit of the N-methyl-D-aspartate (NMDA) receptor to curtail excessive Ca2+ influx and thus provide neuroprotection from excitotoxic insults. This effect of NO- closely resembles that of NOS, which also downregulates NMDA receptor activity under similar conditions in culture.

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Species referenced: Xenopus laevis
Genes referenced: grin2a nos1 nos3