Send to:

Choose Destination
See comment in PubMed Commons below
Cell Signal. 2010 Oct;22(10):1477-84. doi: 10.1016/j.cellsig.2010.05.016. Epub 2010 May 31.

G93A SOD1 alters cell cycle in a cellular model of Amyotrophic Lateral Sclerosis.

Author information

  • 1Laboratory of Experimental Neurobiology, IRCCS, National Neurological Institute C. Mondino, Via Mondino, 2, 27100 Pavia, Italy.


Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative multifactorial disease characterized, like other diseases such as Alzheimer's disease (AD), Parkinson's disease (PD) or frontotemporal dementia (FTD), by the degeneration of specific neuronal cell populations. Motor neuron loss is distinctive of ALS. However, the causes of onset and progression of motor neuron death are still largely unknown. In about 2% of all cases, mutations in the gene encoding for the Cu/Zn superoxide dismutase (SOD1) are implicated in the disease. Several alterations in the expression or activation of cell cycle proteins have been described in the neurodegenerative diseases and related to cell death. In this work we show that mutant SOD1 can alter cell cycle in a cellular model of ALS. Our findings suggest that modifications in the cell cycle progression could be due to an increased interaction between mutant G93A SOD1 and Bcl-2 through the cyclins regulator p27. As previously described in post mitotic neurons, cell cycle alterations could fatally lead to cell death.

Copyright 2010 Elsevier Inc. All rights reserved.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk