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Axonal Degeneration Is Blocked by Nicotinamide Mononucleotide Adenylyltransferase (Nmnat) Protein Transduction into Transected Axons

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... Full description

Journal Title: Journal of Biological Chemistry 12/31/2010, Vol.285(53), pp.41211-41215
Main Author: Sasaki, Y.
Other Authors: Milbrandt, J.
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0021-9258 ; E-ISSN: 1083-351X ; DOI: http://dx.doi.org/10.1074/jbc.C110.193904
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recordid: crossref10.1074/jbc.C110.193904
title: Axonal Degeneration Is Blocked by Nicotinamide Mononucleotide Adenylyltransferase (Nmnat) Protein Transduction into Transected Axons
format: Article
creator:
  • Sasaki, Y.
  • Milbrandt, J.
subjects:
  • Chemistry
  • Anatomy & Physiology
ispartof: Journal of Biological Chemistry, 12/31/2010, Vol.285(53), pp.41211-41215
description: 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.
language: eng
source:
identifier: ISSN: 0021-9258 ; E-ISSN: 1083-351X ; DOI: http://dx.doi.org/10.1074/jbc.C110.193904
fulltext: fulltext
issn:
  • 00219258
  • 0021-9258
  • 1083351X
  • 1083-351X
url: Link


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descriptionAxonal 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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