Abstract
The slow Wallerian degeneration protein (Wld S), a fusion protein containing amino-terminal E4B and full-length nicotinamide mononucleotide adenylyltransferase 1 (Nmnat1), delays axon degeneration caused by physical damages, toxins and genetic mutations which result in patients being diagnosed with neurodegenerative diseases. It is still controversial whether the suppression of axonal degeneration by Wld S is due to Nmnat1 or other portion. We generated Wld S or Nmnat1-overexpressing Neuro2A cell lines, in which neuronal differentiation including neurite elongation can be induced by retinoic acid. The overexpression of Wld S delayed the neurite degeneration by vincristine, whereas that of Nmnat1 did not delay it much. Taken together, Nmnat1 is considerably weaker than Wld S for protection from toxic injury in vitro, suggesting that amino-terminal region of Wld S is likely to be more significant for protection from axonal degeneration.
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