ArticleThe Journal of biological chemistry2014
Nuclear recruitment of neuronal nitric-oxide synthase by α-syntrophin is crucial for the induction of mitochondrial biogenesis.
Article in The Journal of biological chemistry, 2014. 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, 52 citations in OpenAlex.
- Protein S-nitrosylation in the heart: Mechanisms, physiological roles, and pathological remodeling.Redox biology · 2026Review
- Neuronal nitric oxide synthase expression in secretory cells of the human parotid and submandibular salivary glands: evidence from light and electron microscopy.Cell and tissue research · 2026Article
- Plasticity and structural alterations of mitochondria and sarcoplasmic organelles in muscles of mice deficient in α-dystrobrevin, a component of the dystrophin-glycoprotein complex.Human molecular genetics · 2024Article
- 2-Methoxyestradiol and Hydrogen Peroxide as Promising Biomarkers in Parkinson's Disease.Molecular neurobiology · 2024Article
- Nitrosative stress in Parkinson's disease.NPJ Parkinson's disease · 2022Review
- Endothelial cell damage is the central part of COVID-19 and a mouse model induced by injection of the S1 subunit of the spike protein.Annals of diagnostic pathology · 2021Article
- Antioxidant supplements and endurance exercise: Current evidence and mechanistic insights.Redox biology · 2020Review
- Nitric oxide in cellular adaptation and disease.Redox biology · 2020Review
- RETRACTION: The Major Heat Shock Proteins, Hsp70 and Hsp90, in 2-Methoxyestradiol-Mediated Osteosarcoma Cell Death Model.International journal of molecular sciences · 2020Article
- Glutathione and Nitric Oxide: Key Team Players in Use and Disuse of Skeletal Muscle.Nutrients · 2019Review
- S-Nitrosylation: An Emerging Paradigm of Redox Signaling.Antioxidants (Basel, Switzerland) · 2019Review
- GSH-C4 Acts as Anti-inflammatory Drug in Different Models of Canonical and Cell Autonomous Inflammation Through NFκB Inhibition.Frontiers in immunology · 2019Article
- Alpha-syntrophin dependent expression of tubulin alpha 8 protein in hepatocytes.Journal of physiology and biochemistry · 2018Article
- l-Citrulline Supplementation: Impact on Cardiometabolic Health.Nutrients · 2018Review
- Relation of nNOS isoforms to mitochondrial density and PGC-1alpha expression in striated muscles of mice.Nitric oxide : biology and chemistry · 2018Article
- miR-708-5p and miR-34c-5p are involved in nNOS regulation in dystrophic context.Skeletal muscle · 2018Article
- NO control of mitochondrial function in normal and transformed cells.Biochimica et biophysica acta. Bioenergetics · 2017Review
- Therapeutic strategies to address neuronal nitric oxide synthase deficiency and the loss of nitric oxide bioavailability in Duchenne Muscular Dystrophy.Orphanet journal of rare diseases · 2017Review
- Attempting to Compensate for Reduced Neuronal Nitric Oxide Synthase Protein with Nitrate Supplementation Cannot Overcome Metabolic Dysfunction but Rather Has Detrimental Effects in Dystrophin-Deficient mdx Muscle.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017Article
- Nitric oxide signalling and neuronal nitric oxide synthase in the heart under stress.F1000Research · 2017Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuronal nitric-oxide synthase (nNOS) has various splicing variants and different subcellular localizations. nNOS can be found also in the nucleus; however, its exact role in this compartment is still not completely defined. In this report, we demonstrate that the PDZ domain allows the recruitment of nNOS to nuclei, thus favoring local NO production, nuclear protein S-nitrosylation, and induction of mitochondrial biogenesis. In particular, overexpression of PDZ-containing nNOS (nNOSα) increases S-nitrosylated CREB with consequent augmented binding on cAMP response element consensus sequence on peroxisome proliferator-activated receptor γ co-activator (PGC)-1α promoter. The resulting PGC-1α induction is accompanied by the expression of mitochondrial genes (e.g., TFAM, MtCO1) and increased mitochondrial mass. Importantly, full active nNOS lacking PDZ domain (nNOSβ) does not localize in nuclei and fails in inducing the expression of PGC-1α. Moreover, we substantiate that the mitochondrial biogenesis normally accompanying myogenesis is associated with nuclear translocation of nNOS. We demonstrate that α-Syntrophin, which resides in nuclei of myocytes, functions as the upstream mediator of nuclear nNOS translocation and nNOS-dependent mitochondrial biogenesis. Overall, our results indicate that altered nNOS splicing and nuclear localization could be contributing factors in human muscular diseases associated with mitochondrial impairment.
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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 Socratic graph.