ArticleThe Journal of biological chemistry2010
Axonal degeneration is blocked by nicotinamide mononucleotide adenylyltransferase (Nmnat) protein transduction into transected axons.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 68 citations in OpenAlex.
- Nicotinamide Mononucleotide Adenylyltransferase 1 and NADMetabolites · 2026Review
- Cell-based regenerative interventions in Parkinson's disease: Overcoming pharmacological limitations.Acta pharmaceutica Sinica. B · 2026Review
- Programmed axon degeneration: mechanism, inhibition and therapeutic potential.Nature reviews. Neuroscience · 2026Review
- NADAntioxidants & redox signaling · 2023Review
- The Role of Mitochondria in Mediation of Skeletal Muscle Repair.Muscles (Basel, Switzerland) · 2023Review
- Role of Nuclear NADAdvances in experimental medicine and biology · 2023Review
- Coordinated NADPH oxidase/hydrogen peroxide functions regulate cutaneous sensory axon de- and regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- NADCell insight · 2022Review
- The Putative Drosophila TMEM184B Ortholog Tmep Ensures Proper Locomotion by Restraining Ectopic Firing at the Neuromuscular Junction.Molecular neurobiology · 2022Article
- Mitochondrial Reactive Oxygen Species Mediate Activation of TRPV1 and Calcium Entry Following Peripheral Sensory Axotomy.Frontiers in molecular neuroscience · 2022Article
- Nicotinic acid mononucleotide is an allosteric SARM1 inhibitor promoting axonal protection.Experimental neurology · 2021Article
- Small Molecule SARM1 Inhibitors Recapitulate the SARM1Cell reports · 2021Article
- Programmed axon degeneration: from mouse to mechanism to medicine.Nature reviews. Neuroscience · 2020Review
- Initial Kinetic Characterization of Sterile Alpha and Toll/Interleukin Receptor Motif-Containing Protein 1.Biochemistry · 2020Article
- Emergence of SARM1 as a Potential Therapeutic Target for Wallerian-type Diseases.Cell chemical biology · 2020Review
- MicroRNA miR-1002 Enhances NMNAT-Mediated Stress Response by Modulating Alternative Splicing.iScience · 2019Article
- Review
- Mechanisms of injury-induced axon degeneration.Current opinion in neurobiology · 2019Review
- Review
- Death Receptor 6 Promotes Wallerian Degeneration in Peripheral Axons.Current biology : CB · 2017Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Axonal degeneration is an early and important component of many neurological disorders. Overexpression of nicotinamide mononucleotide adenylyltransferase (Nmnat), a component of the slow Wallerian degeneration (Wld(s)) protein, protects axons from a variety of insults. We found that transduction of Nmnat protein into severed axons via virus-like particles prevented axonal degeneration. The post-injury efficacy of Nmnat indicates that its protective effects occur locally within the axon and provides an opportunity to develop novel agents to treat axonal damage.
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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.