Abstract：
:The slow Wallerian degeneration protein (WldS), 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 WldS is due to Nmnat1 or other portion. We generated WldS or Nmnat1-overexpressing Neuro2A cell lines, in which neuronal differentiation including neurite elongation can be induced by retinoic acid. The overexpression of WldS delayed the neurite degeneration by vincristine, whereas that of Nmnat1 did not delay it much. Taken together, Nmnat1 is considerably weaker than WldS for protection from toxic injury in vitro, suggesting that amino-terminal region of WldS is likely to be more significant for protection from axonal degeneration.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Watanabe M,Tsukiyama T,Hatakeyama Sdoi
10.1016/j.neulet.2006.09.068subject
Has Abstractpub_date
2007-01-16 00:00:00pages
228-32issue
3eissn
0304-3940issn
1872-7972pii
S0304-3940(06)01044-5journal_volume
411pub_type
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