Protection of vincristine-induced neuropathy by WldS expression and the independence of the activity of Nmnat1
Section snippets
Acknowledgements
We thank G. Wilmot and T. Kitamura for the plasmids and cell lines and Y. Soida for her help in preparing the manuscript. This work was supported in part by a research grant from Grant-in-Aid for Scientific Research on Priority Areas from the Ministry of Education, Culture, Sports, Science and Technology (18023003, 18659252) and the General Insurance Association of Japan.
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Cited by (24)
NMNATs, evolutionarily conserved neuronal maintenance factors
2013, Trends in NeurosciencesDifferential protection of neuromuscular sensory and motor axons and their endings in Wld<sup>S</sup> mutant mice
2012, NeuroscienceCitation Excerpt :Several attempts have been made to transfer the neuroprotective benefits of WldS expression to animal models of neurodegenerative disease, with variable success. Crossbreeding WldS mice with models of peripheral neuropathy or axonopathy disease mitigates the onset and progression of disease signs (Wang et al., 2001, 2002; Ferri et al., 2003; Samsam et al., 2003; Watanabe et al., 2007; Meyer zu Horste et al., 2011). However, not all models of neurodegeneration are protected by co-expression of WldS (Vande Velde et al., 2004; Fischer et al., 2005; Kariya et al., 2009).
Sirtuins in aging and age-related diseases
2011, Handbook of the Biology of AgingVitamin B3, the nicotinamide adenine dinucleotides and aging
2010, Mechanisms of Ageing and DevelopmentDifferential proteomics analysis of synaptic proteins identifies potential cellular targets and protein mediators of synaptic neuroprotection conferred by the slow Wallerian degeneration (Wld<sup>s</sup>) gene
2007, Molecular and Cellular ProteomicsCitation Excerpt :Similarly VDAC1 is a known component of the NAD pathway, affecting cellular equilibrium via maintenance of cellular redox homeostasis (55). NAD levels, which can be manipulated by changing expression levels of Nmnat1, have been shown previously to at least partially replicate the Wlds phenotype in vitro (Refs. 21–23, but see Refs. 24 and 25). It is possible, therefore, that NAD-mediated neuroprotection of non-somatic compartments may be acting through modulating Aralar1 and/or VDAC1 levels.