ArticleScientific reports2013
Deletions within its subcellular targeting domain enhance the axon protective capacity of Nmnat2 in vivo.
Article in Scientific reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 44 citations in OpenAlex.
- Article
- Programmed axon degeneration: mechanism, inhibition and therapeutic potential.Nature reviews. Neuroscience · 2026Review
- Bridging the Gap: Contemporary Paradigms in Nerve Scaffolds and Regeneration.Advances in wound care · 2025Review
- The Roles of Moonlighting Nicotinamide Mononucleotide Adenylyl Transferases in Cell Physiology.International journal of molecular sciences · 2025Review
- NMNAT2 is a druggable target to drive neuronal NAD production.Nature communications · 2024Article
- Programmed axon death: a promising target for treating retinal and optic nerve disorders.Eye (London, England) · 2024Review
- The Role of NMNAT2/SARM1 in Neuropathy Development.Biology · 2024Review
- NADInternational journal of molecular sciences · 2024Article
- Article
- Microglia-mediated demyelination protects against CD8Nature communications · 2023Article
- A SARM1-mitochondrial feedback loop drives neuropathogenesis in a Charcot-Marie-Tooth disease type 2A rat model.The Journal of clinical investigation · 2022Article
- The key role of the NAD biosynthetic enzyme nicotinamide mononucleotide adenylyltransferase in regulating cell functions.IUBMB life · 2022Review
- NMNAT2 is downregulated in glaucomatous RGCs, and RGC-specific gene therapy rescues neurodegeneration and visual function.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Lessons from Injury: How Nerve Injury Studies Reveal Basic Biological Mechanisms and Therapeutic Opportunities for Peripheral Nerve Diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- Article
- Caffeine and NADAntioxidants (Basel, Switzerland) · 2020Article
- Programmed axon degeneration: from mouse to mechanism to medicine.Nature reviews. Neuroscience · 2020Review
- Review
- Increased ROS Level in Spinal Cord of Wobbler Mice due to Nmnat2 Downregulation.Molecular neurobiology · 2018Article
- Screening with an NMNAT2-MSD platform identifies small molecules that modulate NMNAT2 levels in cortical neurons.Scientific reports · 2017Article
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4 authors at 3 institutions in 2 countries.
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Abstract
The NAD-synthesising enzyme Nmnat2 is a critical survival factor for axons in vitro and in vivo. We recently reported that loss of axonal transport vesicle association through mutations in its isoform-specific targeting and interaction domain (ISTID) reduces Nmnat2 ubiquitination, prolongs its half-life and boosts its axon protective capacity in primary culture neurons. Here, we report evidence for a role of ISTID sequences in tuning Nmnat2 localisation, stability and protective capacity in vivo. Deletion of central ISTID sequences abolishes vesicle association and increases protein stability of fluorescently tagged, transgenic Nmnat2 in mouse peripheral axons in vivo. Overexpression of fluorescently tagged Nmnat2 significantly delays Wallerian degeneration in these mice. Furthermore, while mammalian Nmnat2 is unable to protect transected Drosophila olfactory receptor neuron axons in vivo, mutant Nmnat2s lacking ISTID regions substantially delay Wallerian degeneration. Together, our results establish Nmnat2 localisation and turnover as a valuable target for modulating axon degeneration in vivo.
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