ArticleThe Journal of biological chemistry2009
Transnitrosylating nitric oxide species directly activate type I protein kinase A, providing a novel adenylate cyclase-independent cross-talk to beta-adrenergic-like signaling.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 59 citations in OpenAlex.
- A redox sensor in protein kinase A regulatory subunit Iα regulates vasodilation and protects against hypertension.Redox biology · 2026Article
- S-Nitrosylation of GPCR Regulatory Machinery as a Mechanism to Bias Signaling.Handbook of experimental pharmacology · 2026Review
- Exercise training rescues impaired HAmerican journal of physiology. Heart and circulatory physiology · 2023Article
- S-nitrosylation is required for βMolecular cell · 2022Article
- Aging-Induced Impairment of Vascular Function: Mitochondrial Redox Contributions and Physiological/Clinical Implications.Antioxidants & redox signaling · 2021Review
- Oxidation of Protein Kinase A Regulatory Subunit PKARIα Protects Against Myocardial Ischemia-Reperfusion Injury by Inhibiting Lysosomal-Triggered Calcium Release.Circulation · 2021Article
- Redox Regulation, Oxidative Stress, and Inflammation in Group 3 Pulmonary Hypertension.Advances in experimental medicine and biology · 2021Review
- Cardiac ischemia-reperfusion injury induces ROS-dependent loss of PKA regulatory subunit RIα.American journal of physiology. Heart and circulatory physiology · 2019Article
- Blood Pressure-Lowering by the Antioxidant Resveratrol Is Counterintuitively Mediated by Oxidation of cGMP-Dependent Protein Kinase.Circulation · 2019Article
- Effects of sulfide and polysulfides transmitted by direct or signal transduction-mediated activation of TRPA1 channels.British journal of pharmacology · 2019Review
- β-adrenergic regulation of late NaJournal of molecular and cellular cardiology · 2018Article
- Nitrosative stress uncovers potent βAmerican journal of physiology. Heart and circulatory physiology · 2018Article
- Article
- Phosphorylation of protein kinase A (PKA) regulatory subunit RIα by protein kinase G (PKG) primes PKA for catalytic activity in cells.The Journal of biological chemistry · 2018Article
- Proof of Principle for a Novel Class of Antihypertensives That Target the Oxidative Activation of PKG Iα (Protein Kinase G Iα).Hypertension (Dallas, Tex. : 1979) · 2017Article
- Nitric oxide signalling and neuronal nitric oxide synthase in the heart under stress.F1000Research · 2017Review
- Old dog, new tricks: novel cardiac targets and stress regulation by protein kinase G.Cardiovascular research · 2016Review
- S-Nitrosylation of Calcium-Handling Proteins in Cardiac Adrenergic Signaling and Hypertrophy.Circulation research · 2015Article
- Deficient angiogenesis in redox-dead Cys17Ser PKARIα knock-in mice.Nature communications · 2015Article
- Obligatory role of neuronal nitric oxide synthase in the heart's antioxidant adaptation with exercise.Journal of molecular and cellular cardiology · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The transnitrosylating nitric oxide (NO) donor nitrocysteine (CysNO) induced a disulfide bond between the two regulatory RI subunits of protein kinase A (PKA). The conventional NO donor S-nitroso-N-acetylpenicillamine failed to do this, consistent with our observation that it also did not promote protein S-nitrosylation. This disulfide oxidation event activated PKA and induced vasorelaxation independently of the classical beta-adrenergic or NO signaling pathway. Activation of PKA had also been anticipated to exert a positive inotropic effect on the myocardium but did not. The lack of positive inotropy was explained by CysNO concomitantly activating protein kinase G (PKG) Ialpha. PKG was found to exert a partial negative inotropic influence regardless of whether PKA was activated by classical beta-receptor stimulation or by disulfide bond formation. This work demonstrates that NO molecules that can induce S-nitrosylation directly activate type I PKA, providing a novel cross-talk to beta-adrenergic-like signaling without receptor or adenylate cyclase stimulation. However, the expected positive inotropic consequences of PKA activation by this novel mechanism are countermanded by the simultaneous dual activation of PKGIalpha, which is also activated by CysNO.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.