ArticleFEBS letters2008
Co-regulation of constitutive nitric oxide synthases and NADPH oxidase by the small GTPase Rac.
Article in FEBS letters, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 44 citations in OpenAlex.
- Redox and actin, a fascinating story.Redox biology · 2025Review
- Oxidative stress in phenylketonuria-evidence from human studies and animal models, and possible implications for redox signaling.Metabolic brain disease · 2021Review
- Cysteine Glutathionylation Acts as a Redox Switch in Endothelial Cells.Antioxidants (Basel, Switzerland) · 2019Review
- The Adverse Effects of Environmental Noise Exposure on Oxidative Stress and Cardiovascular Risk.Antioxidants & redox signaling · 2018Review
- SLC7A11 Overexpression in Glioblastoma Is Associated with Increased Cancer Stem Cell-Like Properties.Stem cells and development · 2017Article
- DOCK2 interacts with FLT3 and modulates the survival of FLT3-expressing leukemia cells.Leukemia · 2017Article
- Redox regulation of Rac1 by thiol oxidation.Free radical biology & medicine · 2015Article
- Smooth muscle specific Rac1 deficiency induces hypertension by preventing p116RIP3-dependent RhoA inhibition.Journal of the American Heart Association · 2014Article
- Rho GTPases, oxidation, and cell redox control.Small GTPases · 2014Review
- Redox regulation of protein damage in plasma.Redox biology · 2014Review
- Involvement of Rho GTPases and their regulators in the pathogenesis of hypertension.Small GTPases · 2014Review
- Neuronal nitric oxide synthase and NADPH oxidase interact to affect cognitive, affective, and social behaviors in mice.Behavioural brain research · 2013Article
- Redox regulation of Ras and Rho GTPases: mechanism and function.Antioxidants & redox signaling · 2013Review
- Cross talk between NADPH oxidase and autophagy in pulmonary artery endothelial cells with intrauterine persistent pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Modulation of RhoGTPases improves the behavioral phenotype and reverses astrocytic deficits in a mouse model of Rett syndrome.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012Article
- Role of reactive oxygen and nitrogen species in the vascular responses to inflammation.Free radical biology & medicine · 2012Review
- The role of Rho protein signaling in hypertension.Nature reviews. Cardiology · 2010Review
- Novel aspects of the roles of Rac1 GTPase in the cardiovascular system.Current opinion in pharmacology · 2010Review
- Mitochondrial energetics and therapeutics.Annual review of pathology · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Nitric oxide (NO), generated by NO synthases (NOSs), has multifarious roles in signal transduction. Reactive oxygen species (ROS), generated by ubiquitous NADPH oxidases (NOXs), also participate in cellular signaling. However, the coordination of signals conveyed by NO and ROS is poorly understood. We show that the small GTPase Rac, a component of some NOXs, also interacts with and regulates the constitutively-expressed NOSs. Cellular NO and O(2)(-) production increase or decrease together following activation or inhibition of Rac, and Rac inhibition reveals transduction mechanisms that depend upon NO (vasodilation), ROS (actin polymerization) or both (cytoskeletal organization). Thus, signaling by NO and ROS may be coordinated through a common control element.
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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.