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Post-translational Regulation of High Output NO and Endothelial Barrier Dysfuncti

Post-translational Regulation of High Output NO and Endothelial Barrier Dysfuncti
高输出 NO 和内皮屏障功能障碍的翻译后调节
批准号：
8059128
负责人：
Randal A Skidgel
金额：
$34.51万
依托单位：
UNIVERSITY OF ILLINOIS AT CHICAGO
依托单位国家：
美国
项目类别：
财政年份：
2011
资助国家：
美国
项目状态：
已结题
起止时间：
2011-03-01 至 2016-02-29
来源：
https://reporter.nih.gov/project-details/8059128
关键词：
AddressAdherens JunctionBindingBinding SitesCell Culture TechniquesClathrinCollaborationsComplexDimerizationDissociationEndocytosisEndothelial CellsFunctional disorderG-Protein-Coupled ReceptorsGTP-Binding ProteinsGenerationsHumanInflammationInflammatoryKininsLungMediatingMitogen-Activated Protein KinasesModelingModificationMolecular ConformationMusNADPH OxidaseNitric OxideNitric Oxide SynthaseOutputPathway interactionsPeptidesPeptidylprolyl IsomerasePermeabilityPeroxonitritePhosphorylationPhosphotransferasesPinus (genus)Post-Translational RegulationPrincipal InvestigatorProductionProtein DephosphorylationProteinsReceptor ActivationRoleScaffolding ProteinSignal PathwaySignal TransductionSourceStimulusTailTranslational ActivationTranslationscadherin 5cytokinehuman NOS2A proteinlung injurylung vascular injurynitrationnovelnovel therapeuticsprogramsreceptorscaffoldseryl-proline

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中文摘要
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英文摘要
The major source of "high-output" nitric oxide (NO) during inflannmatton is inducible NO synthase (iNOS). Although iNOS is a transcriptionally-regulated generator of high NO, we have discovered a novel mode of post- translational, G protein coupled receptor (GPCR)-mediated activation of iNOS via ERK-dependent phosphorylation in endothelial cells. Post-translational activation of INOS results in a further 3- to 5-fold increase in NO concentration over its already high basal amount. In
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