Mitochondrial fission factor Drp1 is essential for embryonic development and synapse formation in mice

By Naotada Ishihara, M. Nomura, A. Jofuku, H. Kato, Satoshi O. Suzuki, K. Masuda, Hidenori Otera, Yae Nakanishi, I. Nonaka, Yu-ichi Goto and 6 more. Nature Cell Biology, 2009

1,052 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/06af7292499138c6eb23fd78a21c68867e1d653a

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In Molecular Biology

1. R. Youle
2. D. C. Chan
3. B. Westermann
4. J. Nunnari
5. Orian Shirihai
6. Hsiuchen Chen
7. L. Scorrano
8. M. Liesa

Citations in the corpus

• The Interplay Between Mitochondrial Dynamics and Mitophagy (2011, background): “Drp1, a profission protein, is essential for dendritic spine formation during the embryonic period (42).”
• During autophagy mitochondria elongate, are spared from degradation and sustain cell viability (2011, background): “) MEFs, which lack the core components of the mitochondrial fusion machinery, and mitochondria remained elongated in Drp1 −/− cells, in which fission is genetically impaire”
• Mitochondrial dynamics–fusion, fission, movement, and mitophagy–in neurodegenerative diseases (2009, background): “Mihara (80) and colleagues have recently disrupted Drp1 in mice and have provided additional evidence for the role of mitochondrial fission in neuronal development.”
• Mitochondrial Dynamics in the Regulation of Nutrient Utilization and Energy Expenditure (2013, background): “…cycle, extended exposure to excess nutrient environment is expected to impact quality control, a condition that will contribute to reduced longevity. lethality with brain developmental defects and severe neurodegeneration (Ishihara et al., 2009; Wakabayashi et al., 2009; Waterham et al., 2007).”
• BAK/BAX macropores facilitate mitochondrial herniation and mtDNA efflux during apoptosis (2018, result): “In contrast, and as previously reported (51, 52), fission-deficient Drp1 cells at steady state exhibited a hyperfused mitochondrial network (fig.”
• Mitochondria: In Sickness and in Health (2012, background): “…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).”
• Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer's disease: implications for neuronal damage. (2011, background): “Further, recent studies of Drp1 knockout in mice revealed that double knockouts are embryonic lethal (37,38).”
• Bax, Bak and beyond — mitochondrial performance in apoptosis (2018, background): “Although the role of mitochondrial fission in apoptosis still remains controversial, it is accepted that Drp1 is not required for Bax and Bak activation and foci formation at the mitochondria [99, 106] but that the absence of Drp1 delays cytochrome c release [57, 103, 104, 107].”