ArticleBioarchitecture
Axonal trafficking of NMNAT2 and its roles in axon growth and survival in vivo.
Article in Bioarchitecture. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
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- NMNAT2 is a druggable target to drive neuronal NAD production.Nature communications · 2024Article
- The Role of NMNAT2/SARM1 in Neuropathy Development.Biology · 2024Review
- NADInternational journal of molecular sciences · 2024Article
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- The key role of the NAD biosynthetic enzyme nicotinamide mononucleotide adenylyltransferase in regulating cell functions.IUBMB life · 2022Review
- The Role of Axonal Transport in Glaucoma.International journal of molecular sciences · 2022Review
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- Neuronal NMNAT2 Overexpression Does Not Achieve Significant Neuroprotection in Experimental Autoimmune Encephalomyelitis/Optic Neuritis.Frontiers in cellular neuroscience · 2021Article
- Novel HDAC6 Inhibitors Increase Tubulin Acetylation and Rescue Axonal Transport of Mitochondria in a Model of Charcot-Marie-Tooth Type 2F.ACS chemical neuroscience · 2020Article
- Loss ofFrontiers in neurology · 2020Article
- An axonal stress response pathway: degenerative and regenerative signaling by DLK.Current opinion in neurobiology · 2018Review
- Roles of palmitoylation in axon growth, degeneration and regeneration.Journal of neuroscience research · 2017Review
- KIF1A mediates axonal transport of BACE1 and identification of independently moving cargoes in living SCG neurons.Traffic (Copenhagen, Denmark) · 2016Article
- Review
- Impact of Genetic Reduction of NMNAT2 on Chemotherapy-Induced Losses in Cell Viability In Vitro and Peripheral Neuropathy In Vivo.PloS one · 2016Article
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3 authors at 1 institution in 1 country.
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Abstract
The NAD-synthesizing enzyme NMNAT2 is critical for axon survival in primary culture and its depletion may contribute to axon degeneration in a variety of neurodegenerative disorders. Here we discuss several recent reports from our laboratory that establish a critical role for NMNAT2 in axon growth in vivo in mice and shed light on the delivery and turnover of this survival factor in axons. In the absence of NMNAT2, axons fail to extend more than a short distance beyond the cell body during embryonic development, implying a requirement for NMNAT2 in axon maintenance even during development. Furthermore, we highlight findings regarding the bidirectional trafficking of NMNAT2 in axons on a vesicle population that undergoes fast axonal transport in primary culture neurites and in mouse sciatic nerve axons in vivo. Surprisingly, loss of vesicle association boosts the axon protective capacity of NMNAT2, an effect that is at least partially mediated by a longer protein half-life of cytosolic NMNAT2 variants. Analysis of wild-type and variant NMNAT2 in mouse sciatic nerves and Drosophila olfactory receptor neuron axons supports the existence of a similar mechanism in vivo, highlighting the potential for regulation of NMNAT2 stability and turnover as a mechanism to modulate axon degeneration in vivo.
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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 OpenQuestion graph.