ReviewFrontiers in endocrinology2013
Nitric Oxide-Induced Calcium Release: Activation of Type 1 Ryanodine Receptor, a Calcium Release Channel, through Non-Enzymatic Post-Translational Modification by Nitric Oxide.
Review in Frontiers in endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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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
9 citing papers in PubMed, 26 citations in OpenAlex.
- Involvement of ROS signal in aging and regulation of brain functions.The journal of physiological sciences : JPS · 2025Review
- Posttranslational Modifications ofPharmacological reviews · 2024Review
- Placental Protein 13: Vasomodulatory Effects onInternational journal of molecular sciences · 2024Article
- Carbon Monoxide, a Retrograde Messenger Generated in Postsynaptic Mushroom Body Neurons, Evokes Noncanonical Dopamine Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Regulation of boar sperm functionality by the nitric oxide synthase/nitric oxide system.Journal of assisted reproduction and genetics · 2019Article
- Protein Posttranslational Modifications: Roles in Aging and Age-Related Disease.Oxidative medicine and cellular longevity · 2017Review
- Posttranslational modification of intercellular messenger systems.Frontiers in endocrinology · 2014Article
- Influence of nitric oxide signaling mechanisms in cancer.International journal of immunopathology and pharmacologyArticle
- Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO) is a typical gaseous messenger involved in a wide range of biological processes. In our classical knowledge, effects of NO are largely achieved by activation of soluble guanylyl cyclase to form cyclic guanosine-3', 5'-monophosphate. However, emerging evidences have suggested another signaling mechanism mediated by NO: "S-nitrosylation" of target proteins. S-nitrosylation is a covalent addition of an NO group to a cysteine thiol/sulfhydryl (RSH), and categorized into non-enzymatic post-translational modification (PTM) of proteins, contrasted to enzymatic PTM of proteins, such as phosphorylation mediated by various protein kinases. Very recently, we found novel intracellular calcium (Ca(2+)) mobilizing mechanism, NO-induced Ca(2+) release (NICR) in cerebellar Purkinje cells. NICR is mediated by type 1 ryanodine receptor (RyR1), a Ca(2+) release channel expressed in endoplasmic-reticular membrane. Furthermore, NICR is indicated to be dependent on S-nitrosylation of RyR1, and involved in synaptic plasticity in the cerebellum. In this review, molecular mechanisms and functional significance of NICR, as well as non-enzymatic PTM of proteins by gaseous signals, are described.
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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.