ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Molecular regulation of NADPH oxidase 5 via the MAPK pathway.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 55 citations in OpenAlex.
- Oxidative stress driven airway mesenchymal reprogramming in asthma: mechanistic insights and evidence from botanical drug formulations.Frontiers in pharmacology · 2026Review
- Structure, regulation, and physiological functions of NADPH oxidase 5 (NOX5).Journal of physiology and biochemistry · 2023Review
- Oxidative Stress and Hypertension.Circulation research · 2021Review
- NADPH oxidases and oxidase crosstalk in cardiovascular diseases: novel therapeutic targets.Nature reviews. Cardiology · 2020Review
- Redox Regulation of PPARPPAR research · 2020Article
- Evaluation of the NOX5 protein expression and oxidative stress in sperm from asthenozoospermic men compared to normozoospermic men.Journal of endocrinological investigation · 2019Article
- Endothelial or vascular smooth muscle cell-specific expression of human NOX5 exacerbates renal inflammation, fibrosis and albuminuria in the Akita mouse.Diabetologia · 2019Article
- NOX5: Molecular biology and pathophysiology.Experimental physiology · 2019Review
- Carcinogenesis and Reactive Oxygen Species Signaling: Interaction of the NADPH Oxidase NOX1-5 and Superoxide Dismutase 1-3 Signal Transduction Pathways.Antioxidants & redox signaling · 2019Review
- Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their RegulationPhysiological reviews · 2019Review
- NADPH oxidase 5 (NOX5)-induced reactive oxygen signaling modulates normoxic HIF-1α and p27Molecular carcinogenesis · 2017Article
- Inhibition of histone deacetylase reduces transcription of NADPH oxidases and ROS production and ameliorates pulmonary arterial hypertension.Free radical biology & medicine · 2016Article
- Modulation of cellular redox homeostasis by the endocannabinoid system.Open biology · 2016Review
- Cloning, Characteristics, and Functional Analysis of Rabbit NADPH Oxidase 5.Frontiers in physiology · 2016Article
- ROS signaling by NADPH oxidase 5 modulates the proliferation and survival of prostate carcinoma cells.Molecular carcinogenesis · 2016Article
- Nox5 stability and superoxide production is regulated by C-terminal binding of Hsp90 and CO-chaperones.Free radical biology & medicine · 2015Article
- Redox signaling, Nox5 and vascular remodeling in hypertension.Current opinion in nephrology and hypertension · 2015Review
- The NADPH oxidase NOX5 protects against apoptosis in ALK-positive anaplastic large-cell lymphoma cell lines.Free radical biology & medicine · 2015Article
- Alpha-Lipoic Acid Attenuates Cerebral Ischemia and Reperfusion Injury via Insulin Receptor and PI3K/Akt-Dependent Inhibition of NADPH Oxidase.International journal of endocrinology · 2015Article
- Enzymatic regulation and functional relevance of NOX5.Current pharmaceutical design · 2015Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The mechanisms controlling the activity of NADPH oxidase 5 (Nox5) are unique in that they are independent of the protein: protein interactions that coordinate the activation of other Nox isoforms. Instead, the primary driving force for Nox5 activity is calcium. However, in a previous study we reported that the protein kinase C (PKC)-agonist PMA could induce a sustained activation of Nox5 that was independent of calcium changes. This apparent calcium-independent activation was found to be mediated by the PKC-dependent phosphorylation of specific serine and threonine residues on Nox5 which increased the calcium sensitivity of the enzyme and enabled activation at resting levels of calcium. However, the specific kinase(s) mediating the phosphorylation and activation of Nox5 are not known. As PKC can activate the MEK/ERK1/2 signaling pathway, we hypothesized that Nox5 is activated by the coordinated phosphorylation of both MAPK and PKC pathways. The inhibition of MEK1 using PD-98059 and U-0126 significantly reduced the phosphorylation and activity of Nox5 in response to PMA but not to the calcium-mobilizing stimulus ionomycin. Dominant negative MEK1 and knockdown of endogenous MEK1/2 using a specific small interfering RNA also inhibited Nox5 activity in response to PMA. The mutation of S498 to a nonphosphorylatable residue and to a lesser degree T494 blocked the ability of ERK to stimulate Nox5 activity. However, a constitutively active form of MEK1 failed to increase Nox5 activity in the absence of PMA stimulation. These results suggest that the MEK/ERK1/2 pathway is necessary but not sufficient to regulate the PMA-dependent activation of Nox5.
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