Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/43195
Title: GSK3 is involved in the relief of mitochondria pausing in a tau-dependent manner.
Author: Llorens Martín, M.
López Domenech, G.
Soriano García, Eduardo
Avila, Jesús
Keywords: Glicogen
Malaltia de Parkinson
Malalties del sistema nerviós
Glycogen
Parkinson's disease
Nervous System Diseases
Issue Date: 14-Nov-2011
Publisher: Public Library of Science (PLoS)
Abstract: Mitochondrial trafficking deficits have been implicated in the pathogenesis of several neurological diseases, including Alzheimer's disease (AD). The Ser/Thre kinase GSK3β is believed to play a fundamental role in AD pathogenesis. Given that GSK3β substrates include Tau protein, here we studied the impact of GSK3β on mitochondrial trafficking and its dependence on Tau protein. Overexpression of GSK3β in neurons resulted in an increase in motile mitochondria, whereas a decrease in the activity of this kinase produced an increase in mitochondria pausing. These effects were dependent on Tau proteins, as Tau (−/−) neurons did not respond to distinct GSK3β levels. Furthermore, differences in GSK3β expression did not affect other parameters like mitochondria velocity or mitochondria run length. We conclude that GSK3B activity regulates mitochondrial axonal trafficking largely in a Tau-dependent manner.
Note: Reproducció del document publicat a: http://dx.doi.org/10.1371/journal.pone.0027686
It is part of: PLoS One, 2011, vol. 6, num. 11, p. e27686
Related resource: http://dx.doi.org/10.1371/journal.pone.0027686
URI: http://hdl.handle.net/2445/43195
ISSN: 1932-6203
Appears in Collections:Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)

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