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Article

UCP2 overexpression worsens mitochondrial dysfunction and accelerates disease progression in a mouse model of amyotrophic lateral sclerosis.

Molecular and cellular neurosciences - 1 Nov 2013

Peixoto Pablo M, Kim Hyun-Jeong, Sider Brittany, Starkov Anatoly, Horvath Tamas L, Manfredi Giovanni

Abstract excerpt

Mitochondrial dysfunction leading to deficits in energy production, Ca(2+) uptake capacity, and free radical generation has been implicated in the pathogenesis of familial amyotrophic lateral sclerosis (ALS) caused by mutations in Cu,Zn superoxide dismutase (SOD1). Numerous studies link UCP2, a member of the uncoupling protein family, to protection of neurons from mitochondrial dysfunction and oxidative damage in...

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Identifiers

PMID: 24141050
DOI: 10.1016/j.mcn.2013.10.002
PMCID: PMC3891658

Genes

UCP2
SOD1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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