Endothelial nitric oxide synthase (eNOS) S1176 phosphorylation status governs atherosclerotic lesion formation
Nguyen T, Rahman N, Sessa W, Lee M. Endothelial nitric oxide synthase (eNOS) S1176 phosphorylation status governs atherosclerotic lesion formation. Frontiers In Cardiovascular Medicine 2023, 10: 1279868. PMID: 38034389, PMCID: PMC10683645, DOI: 10.3389/fcvm.2023.1279868.Peer-Reviewed Original ResearchAtherosclerotic plaque formationPlaque formationAkt1 null miceSingle amino acid substitutionMutant miceLesion formationImportance of AktUnique expression patternGene expression analysisIndex of atherosclerosisFavorable lipid profileVascular protective roleAtherosclerotic lesion formationAthero-protective effectsEndothelial NO generationAmino acid substitutionsDouble knockout miceDeletion backgroundPhosphorylation sitesAspartate substitutionPhosphorylation statusExpression analysisEnzyme functionExpression patternsENOS deletionAn optogenetic-phosphoproteomic study reveals dynamic Akt1 signaling profiles in endothelial cells
Zhou W, Li W, Wang S, Salovska B, Hu Z, Tao B, Di Y, Punyamurtula U, Turk B, Sessa W, Liu Y. An optogenetic-phosphoproteomic study reveals dynamic Akt1 signaling profiles in endothelial cells. Nature Communications 2023, 14: 3803. PMID: 37365174, PMCID: PMC10293293, DOI: 10.1038/s41467-023-39514-1.Peer-Reviewed Original ResearchConceptsPhosphorylation sitesSerine/threonine kinase AktMass spectrometry-based phosphoproteomicsThreonine kinase AktAkt-dependent phosphorylationAberrant Akt activationEndothelial cellsKinase substrateKinase AktCell signalingPhosphorylation profilePhenotypic outcomesDownstream signalingAkt activationAkt1 phosphorylationHuman diseasesSystem-level analysisAKT1Vascular endothelial cellsRich resourcePhosphorylationSignalingGrowth factorAktCells