DNA strand breaks and TDP-43 mislocation are absent in the murine hSOD1G93A model of amyotrophic lateral sclerosis in vivo and in vitro

Mutations in the human Cu/Zn superoxide dismutase type-1 (hSOD1) gene are common in familial amyotrophic lateral sclerosis (fALS). The pathophysiology has been linked to, e.g., organelle dysfunction, RNA metabolism and oxidative DNA damage conferred by SOD1 malfunction. However, apart from metabolic...

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Veröffentlicht in:	PloS one 2017, Vol.12 (8), p.e0183684-e0183684
Hauptverfasser:	Penndorf, Diane, Tadić, Vedrana, Witte, Otto W, Grosskreutz, Julian, Kretz, Alexandra
Format:	Artikel
Sprache:	eng
Schlagworte:	Activation Amyotrophic lateral sclerosis Amyotrophic Lateral Sclerosis - genetics Amyotrophic Lateral Sclerosis - pathology Animals Astrocytes Biology and life sciences Biotechnology Breakage Comet Assay Damage assessment Deoxyribonucleic acid Disease Models, Animal Disintegration DNA DNA biosynthesis DNA Damage DNA methylation DNA Repair DNA Transposable Elements DNA-Binding Proteins - metabolism Genotoxicity In vitro methods and tests In Vitro Techniques Integrity Male Medicine and Health Sciences Metabolism Mice Mice, Inbred C57BL Mice, Transgenic Motor neurons Motor Neurons - physiology Motor task performance Mutation Neurodegeneration Neurons Oxidation Oxidative metabolism Real-Time Polymerase Chain Reaction Research and Analysis Methods Ribonucleic acid RNA Silence Spinal Cord - metabolism Spinal Cord - pathology Superoxide dismutase Superoxide Dismutase-1 - genetics Zinc
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