ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Regulation of the inositol 1,4,5-trisphosphate receptor type I by O-GlcNAc glycosylation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Are You a Friend or an Enemy? The Dual Action of Methylglyoxal on Brain Microvascular Endothelial Cells.International journal of molecular sciences · 2025Article
- Neuronal microRNAs safeguard ER CaCellular and molecular life sciences : CMLS · 2022Article
- CREB regulates the expression of type 1 inositol 1,4,5-trisphosphate receptors.Journal of cell science · 2021Article
- Role ofPhysiological reviews · 2021Review
- Regulation of cardiac O-GlcNAcylation: More than just nutrient availability.Biochimica et biophysica acta. Molecular basis of disease · 2020Review
- The Two-Way Relationship Between Calcium and Metabolism in Cancer.Frontiers in cell and developmental biology · 2020Review
- Review
- Disruption of O-GlcNAc homeostasis during mammalian oocyte meiotic maturation impacts fertilization.Molecular reproduction and development · 2019Article
- The Role of O-GlcNAcylation for Protection against Ischemia-Reperfusion Injury.International journal of molecular sciences · 2019Review
- EOGT andBiochemical Society transactions · 2017Review
- The Role of Stress-Induced O-GlcNAc Protein Modification in the Regulation of Membrane Transport.Oxidative medicine and cellular longevity · 2017Review
- Disruption of O-linked N-Acetylglucosamine Signaling Induces ER Stress and β Cell Failure.Cell reports · 2015Article
- Bioactive nanoparticles improve calcium handling in failing cardiac myocytes.Nanomedicine (London, England) · 2015Article
- Hydrogen peroxide induces vasorelaxation by enhancing 4-aminopyridine-sensitive Kv currents through S-glutathionylation.Pflugers Archiv : European journal of physiology · 2015Article
- S-glutathionylation of ion channels: insights into the regulation of channel functions, thiol modification crosstalk, and mechanosensing.Antioxidants & redox signaling · 2014Review
- Article
- Dynamic O-GlcNAcylation and its roles in the cellular stress response and homeostasis.Cell stress & chaperones · 2013Article
- The roles of O-linked β-N-acetylglucosamine in cardiovascular physiology and disease.American journal of physiology. Heart and circulatory physiology · 2012Review
- Dynamic O-GlcNAc modification regulates CREB-mediated gene expression and memory formation.Nature chemical biology · 2012Article
- Current and calcium responses to local activation of axonal NMDA receptors in developing cerebellar molecular layer interneurons.PloS one · 2012Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inositol 1,4,5-trisphosphate (InsP3) receptor type I (InsP3R-I) is the principle channel for intracellular calcium (Ca2+) release in many cell types, including central neurons. It is regulated by endogenous compounds like Ca2+ and ATP, by protein partners, and by posttranslational modification. We report that the InsP3R-I is modified by O-linked glycosylation of serine or threonine residues with beta-N-acetylglucosamine (O-GlcNAc). The level of O-GlcNAcylation can be altered in vitro by the addition of the enzymes which add [OGT (O-GlcNActransferase)] or remove (O-GlcNAcase) this sugar or by loading cells with UDP-GlcNAc. We monitored the effects of this modification on InsP3R function at the single-channel level and on intracellular Ca2+ transients. Single-channel activity was monitored with InsP3R incorporated into bilayers; Ca2+ signaling was monitored using cells loaded with a Ca2+-sensitive fluorophore. We found that channel activity was decreased by the addition of O-GlcNAc and that this decrease was reversed by removal of the sugar. Similarly, cells loaded with UDP-GlcNAc had an attenuated response to uncaging of InsP3. These results show that O-GlcNAcylation is an important regulator of the InsP3R-I and suggest a mechanism for neuronal dysfunction under conditions in which O-GlcNAc is high, such as diabetes or physiological stress.
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Registered trials
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