http://www.cnr.it/ontology/cnr/individuo/prodotto/ID199011
Altered gene expression, mitochondrial damage and oxidative stress: converging routes in motor neuron degeneration (Articolo in rivista)
- Type
- Label
- Altered gene expression, mitochondrial damage and oxidative stress: converging routes in motor neuron degeneration (Articolo in rivista) (literal)
- Anno
- 2012-01-01T00:00:00+01:00 (literal)
- Alternative label
Luisa Rossi1; Cristiana Valle2,3; Maria Teresa Carrì1,3 (2012)
Altered gene expression, mitochondrial damage and oxidative stress: converging routes in motor neuron degeneration
in International Journal of Cell Biology (Print)
(literal)
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- Luisa Rossi1; Cristiana Valle2,3; Maria Teresa Carrì1,3 (literal)
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- Review Article - Article ID 908724, 9 pages (literal)
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- Rivista
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- 1 Department of Biology, University of Rome Tor Vergata, Via della Ricerca Scientifica, 00133 Rome, Italy.
2 Institute for Cell Biology and Neurobiology, CNR, 00100 Rome, Italy.
3 RCCS Fondazione Santa Lucia, 00143 Rome, Italy. (literal)
- Titolo
- Altered gene expression, mitochondrial damage and oxidative stress: converging routes in motor neuron degeneration (literal)
- Abstract
- Motor neuron diseases (MNDs) are a rather heterogeneous group of diseases, with either sporadic or genetic origin or both, all characterized by the progressive degeneration of motor neurons. At the cellular level, MNDs share features such as protein misfolding and aggregation, mitochondrial damage and energy deficit, and excitotoxicity and calcium mishandling. This is particularly well demonstrated in ALS, where both sporadic and familial forms share the same symptoms and pathological phenotype, with a prominent role for mitochondrial damage and resulting oxidative stress. Based on recent data, however, altered control of gene expression seems to be a most relevant, and previously overlooked, player in MNDs. Here we discuss which may be the links that make pathways apparently as different as altered gene expression, mitochondrial damage, and oxidative stress converge to generate a similar motoneuron-toxic phenotype. (literal)
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