WldS, Nmnats and axon degeneration-progress in the past two decades
Author:
Publisher
Springer Science and Business Media LLC
Subject
Cell Biology,Drug Discovery,Biochemistry,Biotechnology
Link
http://link.springer.com/content/pdf/10.1007/s13238-010-0021-2.pdf
Reference72 articles.
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2. Araki, T., Sasaki, Y., and Milbrandt, J. (2004). Increased nuclear NAD biosynthesis and SIRT1 activation prevent axonal degeneration. Science 305, 1010–1013.
3. Avery, M.A., Sheehan, A.E., Kerr, K.S., Wang, J., and Freeman, M.R. (2009). Wld S requires Nmnat1 enzymatic activity and N16-VCP interactions to suppress Wallerian degeneration. J Cell Biol 184, 501–513.
4. Beirowski, B., Babetto, E., Coleman, M.P., and Martin, K.R. (2008). The WldS gene delays axonal but not somatic degeneration in a rat glaucoma model. Eur J Neurosci 28, 1166–1179.
5. Beirowski, B., Babetto, E., Gilley, J., Mazzola, F., Conforti, L., Janeckova, L., Magni, G., Ribchester, R.R., and Coleman, M.P. (2009). Non-nuclear Wld(S) determines its neuroprotective efficacy for axons and synapses in vivo. J Neurosci 29, 653–668.
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