Gains or losses: molecular mechanisms of TDP43-mediated neurodegeneration
Author:
Publisher
Springer Science and Business Media LLC
Subject
General Neuroscience
Link
http://www.nature.com/articles/nrn3121.pdf
Reference148 articles.
1. Neumann, M. et al. Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis. Science 314, 130–133 (2006). TDP43 protein is identified biochemically, immunohistochemically and by amino acid sequence analysis as the major component of proteinaceous ubiquitin-positive inclusions in FTLD and ALS. Pathologic TDP43 is found to be ubiquitylated, phosphorylated and cleaved, and is associated with nuclear clearance of normal TDP43.
2. Giordana, M. T. et al. TDP-43 redistribution is an early event in sporadic amyotrophic lateral sclerosis. Brain Pathol. 20, 351–360 (2010).
3. Brandmeir, N. J. et al. Severe subcortical TDP-43 pathology in sporadic frontotemporal lobar degeneration with motor neuron disease. Acta Neuropathol. 115, 123–131 (2008).
4. Strong, M. J. et al. TDP43 is a human low molecular weight neurofilament (hNFL) mRNA-binding protein. Mol. Cell. Neurosci. 35, 320–327 (2007).
5. Pamphlett, R., Luquin, N., McLean, C., Jew, S. K. & Adams, L. TDP-43 neuropathology is similar in sporadic amyotrophic lateral sclerosis with or without TDP-43 mutations. Neuropathol. Appl. Neurobiol. 35, 222–225 (2009).
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