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Article

Mislocalization of TDP-43 in the G93A mutant SOD1 transgenic mouse model of ALS

20 Apr 2009

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 19379791
DOI: 10.1016/j.neulet.2009.04.031

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Related research

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Mislocalization of TDP-43 in the G93A mutant SOD1 transgenic mouse model of ALSPMID 19379791Read ↗

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Protein misdirection inside and outside motor neurons in Amyotrophic Lateral Sclerosis (ALS): a possible clue for therapeutic strategies.Semantic proximity Read ↗

Addition of exogenous SOD1 aggregates causes TDP-43 mislocalisation and aggregation.Semantic proximity Read ↗

Rapid and Inducible Mislocalization of Endogenous TDP43 in a Novel Human Model of Amyotrophic Lateral SclerosisSemantic proximity Read ↗

Selective removal of misfolded SOD1 delays disease onset in a mouse model of amyotrophic lateral sclerosisSemantic proximity Read ↗

Lack of TDP-43 abnormalities in mutant SOD1 transgenic mice shows disparity with ALS.Semantic proximity Read ↗

Neuronal over-expression of Oxr1 is protective against ALS-associated mutant TDP-43 mislocalisation in motor neurons and neuromuscular defects in vivoSemantic proximity Read ↗

A robust TDP-43 knock-in mouse model of ALSSemantic proximity Read ↗

Overexpression of ALS-associated p.M337V human TDP-43 in mice worsens disease features compared to wild-type human TDP-43 mice.Semantic proximity Read ↗

Endogenous TDP-43 mislocalization in a novel knock-in mouse model reveals DNA repair impairment, inflammation, and neuronal senescenceSemantic proximity Read ↗

TDP-43 aggregation induced by oxidative stress causes global mitochondrial imbalance in ALSSemantic proximity Read ↗

Progressive motor weakness in transgenic mice expressing human TDP-43Semantic proximity Read ↗

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