Mitochondrial Fusion Protects against Neurodegeneration in the Cerebellum
By Hsiuchen Chen, J. McCaffery, D. C. Chan. Cell, 2007
910 citations recorded by the source corpus.
Subfields: Clinical Biochemistry, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/902bfaa5884b97f33bed4ed4e712e1aff8ab17ac
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Clinical Biochemistry
In Molecular Biology
Citations in the corpus
- Mitochondria: In Sickness and in Health (2012, neutral): “…results in OXPHOS deficiencies, mtDNA loss, and mitochondrial motility defects, and division defects also cause OXPHOS deficiencies and significant increases in ROS production (Chen et al., 2003, 2007; Hermann et al., 1998; Ishihara et al., 2009; Parone et al., 2008; Wakabayashi et al., 2009).”
- Mitochondrial transport in neurons: impact on synaptic homeostasis and neurodegeneration (2012, neutral): “Mitochondria in conditional Mfn2 -knockout mice are fragmented and are not found in long or branched neurites, indicating that fusion also influences mitochondrial transport and distributio”
- Mitochondrial dynamics in mammalian health and disease. (2009, neutral): “out nucleoids but without significant loss of mtDNA as measured by Southern blot (51, 52).”
- Mitochondrial fragmentation in neurodegeneration (2008, positive): “, the competing process, mitochondrial fusion, allows mitochondria to interact and communicate with each other, facilitating mitochondrial movement and distribution across long distances and to the synapse”
- Mitochondrial fusion and fission in cell life and death (2010, neutral): “Disruption of fusion in mammalian cells also leads to mitochondrial heterogeneity and dysfunction, possibly as a consequence of nucleoid loss in individual mitochondri”
- Functions and dysfunctions of mitochondrial dynamics (2007, neutral): “When mitochondrial fusion is abolished, a large fraction of the mitochondrial population loses mtDNA nucleoid”
- Mitofusins and OPA1 mediate sequential steps in mitochondrial membrane fusion. (2009, neutral): “At a cellular level, loss of mitofusins or OPA1 results in severe consequences for mitochondrial function, including heterogeneity in membrane potential, heterogeneity in mtDNA nucleoids, and greatly reduced respiratory capacity (Chen et al., 2005; Chen et al., 2007).”
- Mitochondrial fission factor Drp1 is essential for embryonic development and synapse formation in mice (2009, positive): “, and cerebellum-specific Mfn2-knockout mice revealed the importance of mitochondrial fusion in protecting cerebellar neurodegeneratio”
- Mitochondrial fusion is required for mtDNA stability in skeletal muscle and tolerance of mtDNA mutations (2010, neutral): “In contrast, deletion of mammalian mitofusins or OPA1 results in loss of mtDNA nucleoids from only a subpopulation of mitochondria (Chen et al., 2007).”