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

Abstract：

: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.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Cova E,Ghiroldi A,Guareschi S,Mazzini G,Gagliardi S,Davin A,Bianchi M,Ceroni M,Cereda C

doi

10.1016/j.cellsig.2010.05.016

subject

Has Abstract

pub_date

2010-10-01 00:00:00

pages

1477-84

issue

10

eissn

0898-6568

issn

1873-3913

pii

S0898-6568(10)00146-4

journal_volume

22

pub_type

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