Reconstitution of an endothelial nitric-oxide synthase (eNOS), hsp90, and caveolin-1 complex in vitro. Evidence that hsp90 facilitates calmodulin stimulated displacement of eNOS from caveolin-1.
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S-nitrosylation of Hsp90 promotes the inhibition of its ATPase and endothelial nitric oxide synthase regulatory activitiesCaveolae and Caveolin-1 Integrate Reverse Cholesterol Transport and Inflammation in AtherosclerosisEndothelial caveolar subcellular domain regulation of endothelial nitric oxide synthaseRole of caveolin-1 and caveolae signaling in endotoxemia and sepsisNitric oxide synthases: regulation and functionProtein kinase A-dependent translocation of Hsp90 alpha impairs endothelial nitric-oxide synthase activity in high glucose and diabetesAccelerated ubiquitination and proteasome degradation of a genetic variant of inducible nitric oxide synthaseActivation of eNOS in rat portal hypertensive gastric mucosa is mediated by TNF-alpha via the PI 3-kinase-Akt signaling pathwayThe proline-rich domain of dynamin-2 is responsible for dynamin-dependent in vitro potentiation of endothelial nitric-oxide synthase activity via selective effects on reductase domain function.Modulating Vascular Hemodynamics With an Alpha Globin Mimetic Peptide (HbαX).Regulation of obesity and insulin resistance by nitric oxideInteraction between nitric oxide signaling and gap junctions: effects on vascular functionGeldanamycin attenuates NO-mediated dilation in human skin.Induction of nitric oxide synthase-2 proceeds with the concomitant downregulation of the endogenous caveolin levels.Estradiol-17beta stimulates specific receptor and endogenous nitric oxide-dependent dynamic endothelial protein S-nitrosylation: analysis of endothelial nitrosyl-proteome.Posttranscriptional and transcriptional regulation of endothelial nitric-oxide synthase during hypoxia: the role of microRNAs.Endothelial nitric oxide synthase activation is critical for vascular leakage during acute inflammation in vivo.Dissecting the molecular control of endothelial NO synthase by caveolin-1 using cell-permeable peptidesTetrahydrobiopterin, superoxide, and vascular dysfunction.High-density lipoprotein and apolipoprotein AI increase endothelial NO synthase activity by protein association and multisite phosphorylation.Caveolae, caveolins, and cavins: complex control of cellular signalling and inflammation.Structural and mechanistic aspects of flavoproteins: electron transfer through the nitric oxide synthase flavoprotein domain.Distinction between signaling mechanisms in lipid rafts vs. caveolae.Caveolae structure and functionEndogenous urotensin II selectively modulates erectile function through eNOSProtein complex formation with heat shock protein 90 in chronic hypoxia-induced pulmonary hypertension in newborn piglets.The role of caveolae in endothelial cell dysfunction with a focus on nutrition and environmental toxicantsPPAR-γ regulates carnitine homeostasis and mitochondrial function in a lamb model of increased pulmonary blood flowThere's NO binding like NOS binding: protein-protein interactions in NO/cGMP signaling.Caveolin-1 is a negative regulator of NADPH oxidase-derived reactive oxygen species.Proposal for a role of the Hsp90/Hsp70-based chaperone machinery in making triage decisions when proteins undergo oxidative and toxic damage.Eph-B4 prevents venous adaptive remodeling in the adult arterial environment.Κ-opioid receptor stimulation improves endothelial function in hypoxic pulmonary hypertension.Therapeutic levels of the hydroxmethylglutaryl-coenzyme A reductase inhibitor lovastatin activate ras signaling via phospholipase D2.Effect of nanoparticles binding β-amyloid peptide on nitric oxide production by cultured endothelial cells and macrophages.Nitric oxide represses inhibitory kappaB kinase through S-nitrosylationMolecular mechanisms involved in the regulation of the endothelial nitric oxide synthase.Cell-specific dual role of caveolin-1 in pulmonary hypertension.A model in which heat shock protein 90 targets protein-folding clefts: rationale for a new approach to neuroprotective treatment of protein folding diseasesHeme-dependent activation of neuronal nitric oxide synthase by cytosol is due to an Hsp70-dependent, thioredoxin-mediated thiol-disulfide interchange in the heme/substrate binding cleft
P2860
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P2860
Reconstitution of an endothelial nitric-oxide synthase (eNOS), hsp90, and caveolin-1 complex in vitro. Evidence that hsp90 facilitates calmodulin stimulated displacement of eNOS from caveolin-1.
description
2000 nî lūn-bûn
@nan
2000年の論文
@ja
2000年学术文章
@wuu
2000年学术文章
@zh
2000年学术文章
@zh-cn
2000年学术文章
@zh-hans
2000年学术文章
@zh-my
2000年学术文章
@zh-sg
2000年學術文章
@yue
2000年學術文章
@zh-hant
name
Reconstitution of an endotheli ...... ement of eNOS from caveolin-1.
@en
Reconstitution of an endotheli ...... ement of eNOS from caveolin-1.
@nl
type
label
Reconstitution of an endotheli ...... ement of eNOS from caveolin-1.
@en
Reconstitution of an endotheli ...... ement of eNOS from caveolin-1.
@nl
prefLabel
Reconstitution of an endotheli ...... ement of eNOS from caveolin-1.
@en
Reconstitution of an endotheli ...... ement of eNOS from caveolin-1.
@nl
P2093
P2860
P356
P1476
Reconstitution of an endotheli ...... ement of eNOS from caveolin-1.
@en
P2093
Garcia-Cardena G
O'Connor DS
P2860
P304
22268-22272
P356
10.1074/JBC.M001644200
P407
P577
2000-07-01T00:00:00Z