Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 285, Issue 53, Pages 41211-41215Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.C110.193904
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Funding
- National Institutes of Health [NS070053, AG13730, NS065053]
- Muscular Dystrophy Association [10040]
- Craig H. Neilsen Foundation [124030]
- National Institutes of Health Neuroscience Blueprint Center [P30 NS057105]
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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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