Nitric oxide‐induced mitochondrial fission is regulated by dynamin‐related GTPases in neurons

By M. J. Barsoum, Hua Yuan, A. Gerencser, G. Liot, Yulia Kushnareva, S. Graeber, I. Kovács, Wilson D Lee, J. Waggoner, Jiankun Cui and 8 more. EMBO Journal, 2006

681 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/77d01e452f0904eb2f6d9ca7fd317954068dae31

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In Epidemiology

1. R. Youle
2. W. Ding
3. Xiao-Ming Yin
4. Orian Shirihai
5. D. Suen
6. Xiongwei Zhu
7. George Perry
8. Mark A. Smith

In Molecular Biology

1. R. Youle
2. P. Reddy
3. M. Beal
4. W. Ding
5. Xiao-Ming Yin
6. Orian Shirihai
7. M. Mańczak
8. M. Calkins

In Physiology

1. P. Reddy
2. M. Beal
3. M. Calkins
4. M. Mańczak
5. R. Youle
6. W. Ding
7. Xiongwei Zhu
8. Orian Shirihai

Citations in the corpus

• Impaired Balance of Mitochondria Fission and Fusion in Alzheimer Disease (2009, result): “studies (Barsoum et al., 2006), but also to mitochondrial deple-”
• Mitophagy: mechanisms, pathophysiological roles, and analysis (2012, background): “In nitric oxide-treated cultured cortical neurons, Fis1 was found to be involved in mitophagy (Barsoum et al., 2006). Gomes and Scorrano (2008) found that overexpression of Fis1 itself can induce general autophagy in HeLa cells as demonstrated by increased YFP-LC3 puncta and p62 degradation.”
• Mitochondrial dynamics and apoptosis. (2008, positive): “Drp1 function is required for apoptotic mitochondrial fission, as expression of a dominant negative mutant (Drp1K38A) or down-regulation of Drp1 by RNAi delays mitochondrial fragmentation, cytochrome c release, caspase activation, and cell death (Frank et al. 2001; Breckenridge et al. 2003; Lee et a”
• Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease. (2008, background): “In another study, Aβ was found to increase ROS production, to activate mitochondrial fission proteins Drp1 and Fis1, and to cause mitochondrial fragmentation [70].”
• Fission and selective fusion govern mitochondrial segregation and elimination by autophagy (2008, background): “…of cells treated with agents that impose immediate and extensive mitochondrial fragmentation observed neighboring fragments with disparate cristae structures, suggesting the possibility that fission of mitochondria might yield daughters with unequal membranous structures (Barsoum et al, 2006).”
• Mitochondrial fragmentation in neurodegeneration (2008, background): “However, recent studies suggest that mitochondrial fission could also have a protective role as the segregation of damaged and inactive mitochondria facilitates autophagic clearanc”
• Impaired mitochondrial biogenesis, defective axonal transport of mitochondria, abnormal mitochondrial dynamics and synaptic degeneration in a mouse model of Alzheimer's disease. (2011, background): “AD is also associated with inflammatory responses, synaptic damage and mitochondrial structural and functional abnormalities (3-10).”
• The Interplay Between Mitochondrial Dynamics and Mitophagy (2011, background): “In these models, inhibition of fission is associated with neural protection (5, 74).”
• Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease (2012, background): “Earlier studies also found that rotenone and 6-OHDA induce a rapid DLP1-dependent mitochondrial fragmentation before cell death in various cells [107,141,142].”