Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 김원기 | - |
dc.date.accessioned | 2019-03-06T16:30:02Z | - |
dc.date.available | 2019-03-06T16:30:02Z | - |
dc.date.issued | 1999 | - |
dc.identifier.issn | 0896-6273 | - |
dc.identifier.other | OAK-12535 | - |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/249459 | - |
dc.description.abstract | 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. | - |
dc.language | English | - |
dc.title | Attenuation of NMDA receptor activity and neurotoxicity by nitroxyl anion, NO- | - |
dc.type | Article | - |
dc.relation.issue | 2 | - |
dc.relation.volume | 24 | - |
dc.relation.index | SCI | - |
dc.relation.index | SCIE | - |
dc.relation.index | SCOPUS | - |
dc.relation.startpage | 461 | - |
dc.relation.lastpage | 469 | - |
dc.relation.journaltitle | Neuron | - |
dc.identifier.doi | 10.1016/S0896-6273(00)80859-4 | - |
dc.identifier.scopusid | 2-s2.0-0033213383 | - |
dc.author.google | Kim W.-K. | - |
dc.author.google | Choi Y.-B. | - |
dc.author.google | Rayudu P.V. | - |
dc.author.google | Das P. | - |
dc.author.google | Asaad W. | - |
dc.author.google | Arnelle D.R. | - |
dc.author.google | Stamler J.S. | - |
dc.author.google | Lipton S.A. | - |
dc.contributor.scopusid | 김원기(34770946200) | - |
dc.date.modifydate | 20211210152058 | - |