Declines in Drp1 and parkin expression underlie DNA damage-induced changes in mitochondrial length and neuronal death

Maintaining proper mitochondrial length is essential for normal mitochondrial function in neurons. Mitochondrial fragmentation has been associated with neuronal cell death caused by a variety of experimental toxic stressors. Despite the fact that oxidative stress is a hallmark of neurodegenerative c...

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Veröffentlicht in:	The Journal of neuroscience 2013-01, Vol.33 (4), p.1357-1365
Hauptverfasser:	Wang, David B, Garden, Gwenn A, Kinoshita, Chizuru, Wyles, Cody, Babazadeh, Nasim, Sopher, Bryce, Kinoshita, Yoshito, Morrison, Richard S
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Cell Death - physiology Cells, Cultured DNA Damage - physiology Fluorescent Antibody Technique GTP Phosphohydrolases - biosynthesis GTP Phosphohydrolases - genetics Humans Immunoblotting Mice Mice, Knockout Microtubule-Associated Proteins - biosynthesis Microtubule-Associated Proteins - genetics Mitochondria - pathology Mitochondrial Proteins - biosynthesis Mitochondrial Proteins - genetics Neurons - metabolism Neurons - pathology Oxidative Stress - physiology Real-Time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Transfection Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Ubiquitin-Protein Ligases - biosynthesis Ubiquitin-Protein Ligases - genetics
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