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

Emanuela Cova, Andrea Ghiroldi, Stefania Guareschi, Giuliano Mazzini, Stella Gagliardi, Annalisa Davin, Marika Bianchi, Mauro Ceroni, Cristina Cereda

Research output: Contribution to journalArticle


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.

Original languageEnglish
Pages (from-to)1477-1484
Number of pages8
JournalCellular Signalling
Issue number10
Publication statusPublished - Oct 2010


  • Amyotrophic lateral sclerosis
  • Bcl-2
  • Cell cycle
  • Mutant SOD1

ASJC Scopus subject areas

  • Cell Biology

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