Divergent Effects of p47
            <sup>phox</sup>
            Phosphorylation at S303-4 or S379 on Tumor Necrosis Factor-α Signaling via TRAF4 and MAPK in Endothelial Cells

Teng, Lichen; Fan, Lampson M.; Meijles, Daniel N.; Li, Jian-Mei

doi:10.1161/atvbaha.112.247775

Cited by 22 publications

(29 citation statements)

References 31 publications

(27 reference statements)

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“…We observed here that the phosphorylation of p47 phox at Ser345 was enhanced in cells exposed intermittently to high that can phosphorylate p47 phox . High glucose-mediated ER stress can increase intracellular Ca 2 + release from the ER, which, in turn, can cause the activation of protein kinase C [35] which was recently reported to promote the serine phosphorylation of p47 phox [36]. However, the exact role of this phosphorylation and the activation of NADPH oxidase warrants further investigation to establish a clear mechanistic link between HO-1, ER stress and activation of NADPH oxidase.…”

Section: Discussionmentioning

confidence: 99%

Heme oxygenase (HO)-1 induction prevents Endoplasmic Reticulum stress-mediated endothelial cell death and impaired angiogenic capacity

Maamoun

Zachariah

McVey

et al. 2017

Biochemical Pharmacology

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Most of diabetic cardiovascular complications are attributed to endothelial dysfunction and impaired angiogenesis. Endoplasmic Reticulum (ER) and oxidative stresses were shown to play a pivotal role in the development of endothelial dysfunction in diabetes.Hemeoxygenase-1 (HO-1) was shown to protect against oxidative stress in diabetes; however, its role in alleviating ER stress-induced endothelial dysfunction remains not fully elucidated. We aim here to test the protective role of HO-1 against high glucose-mediated ER stress and endothelial dysfunction and understand the underlying mechanisms with special emphasis on oxidative stress, inflammation and cell death. Altogether, we show here the critical role of ER stress-mediated cell death in diabetesinduced endothelial dysfunction and impaired angiogenesis and underscore the role of HO-1 induction as a key therapeutic modulator for ER stress response in ischemic disorders and diabetes. Our results also highlight the complex interplay between ER stress response and oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Heme oxygenase (HO)-1 induction prevents Endoplasmic Reticulum stress-mediated endothelial cell death and impaired angiogenic capacity

Maamoun

Zachariah

McVey

et al. 2017

Biochemical Pharmacology

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“…phox activation due to the recent demonstration that p47 phox may still translocate to the plasma membrane independently of the indicated ebselen site of inhibition (157). Moreover, until which time a congener can be found that is devoid of peroxidase mimetic activity, some caution should be applied when interpreting its effects.…”

Section: Ebselenmentioning

confidence: 99%

The Quest for Selective Nox Inhibitors and Therapeutics: Challenges, Triumphs and Pitfalls

Cifuentes-Pagano

Meijles

Pagano

2014

Antioxidants & Redox Signaling

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“…It had been shown previously that phosphorylation of Ser-379 is a key step required for p47 phox membrane translocation and interactions with other proteins, and a single substitution of Ser-379 almost abolished leukocyte NADPH oxidase activity (16, 17), and TNFα-induced NADPH oxidase-dependent O 2 ⨪ production in endothelial cells (18). However, the molecular mechanism of how a single serine (Ser-379) phosphorylation can promote NADPH oxidase activation is unknown.…”

Section: Introductionmentioning

confidence: 99%

Molecular Insights of p47phox Phosphorylation Dynamics in the Regulation of NADPH Oxidase Activation and Superoxide Production

Meijles

Fan

Howlin

et al. 2014

Journal of Biological Chemistry

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Background: p47phox is a regulatory subunit of NADPH oxidase, which produces superoxide.Results: We propose a molecular dynamics model of p47phox phosphorylation and assembly with p22phox in NADPH oxidase activation supported by biochemical experiments.Conclusion: Ser-379 phosphorylation in the C-terminal tail is a molecular switch in p47phox activation.Significance: This report provides novel structural and mechanistic information of p47phox activation.

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Divergent Effects of p47 ^phox Phosphorylation at S303-4 or S379 on Tumor Necrosis Factor-α Signaling via TRAF4 and MAPK in Endothelial Cells

Abstract: Objective-To define the mechanism of p47 phox phosphorylation in regulating endothelial cell response to tumor necrosis factor- (TNF) stimulation.

Cited by 22 publications

References 31 publications

Heme oxygenase (HO)-1 induction prevents Endoplasmic Reticulum stress-mediated endothelial cell death and impaired angiogenic capacity

Heme oxygenase (HO)-1 induction prevents Endoplasmic Reticulum stress-mediated endothelial cell death and impaired angiogenic capacity

The Quest for Selective Nox Inhibitors and Therapeutics: Challenges, Triumphs and Pitfalls

Molecular Insights of p47phox Phosphorylation Dynamics in the Regulation of NADPH Oxidase Activation and Superoxide Production

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Divergent Effects of p47 phox Phosphorylation at S303-4 or S379 on Tumor Necrosis Factor-α Signaling via TRAF4 and MAPK in Endothelial Cells

Abstract: Objective-To define the mechanism of p47 phox phosphorylation in regulating endothelial cell response to tumor necrosis factor- (TNF) stimulation.

Cited by 22 publications

References 31 publications

Heme oxygenase (HO)-1 induction prevents Endoplasmic Reticulum stress-mediated endothelial cell death and impaired angiogenic capacity

Heme oxygenase (HO)-1 induction prevents Endoplasmic Reticulum stress-mediated endothelial cell death and impaired angiogenic capacity

The Quest for Selective Nox Inhibitors and Therapeutics: Challenges, Triumphs and Pitfalls

Molecular Insights of p47phox Phosphorylation Dynamics in the Regulation of NADPH Oxidase Activation and Superoxide Production

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Divergent Effects of p47 ^phox Phosphorylation at S303-4 or S379 on Tumor Necrosis Factor-α Signaling via TRAF4 and MAPK in Endothelial Cells