OPA1 requires mitofusin 1 to promote mitochondrial fusion.

By S. Cipolat, Olga Martins de Brito, Barbara Dal Zilio, L. Scorrano. Proceedings of the National Academy of Sciences of the United States of America, 2004

1,318 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/73084b360d9c1b4246a7511dd1e12b97ec86e072

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In Clinical Biochemistry

1. L. Scorrano
2. D. C. Chan
3. R. Youle
4. Lígia C. Gomes
5. Orian Shirihai
6. D. Seol
7. Seon-Yong Jeong
8. K. Mihara

In Molecular Biology

1. D. C. Chan
2. R. Youle
3. Orian Shirihai
4. L. Scorrano
5. M. Liesa
6. D. Seol
7. Seon-Yong Jeong
8. K. Mihara

Citations in the corpus

• Regulation of mitochondrial morphology through proteolytic cleavage of OPA1 (2006, background): “Similarly, OPA1 requires Mfn1 of the outer membrane to promote mitochondrial fusion in mammalian cells (Cipolat et al, 2004), although the functional homologue of yeast Ugo1 is not known.”
• Mitochondrial Fusion Protects against Neurodegeneration in the Cerebellum (2007, neutral): “In mammals, three GTPases are required for mitochondrial fusion: Mfn1, Mfn2, and OPA1 (Chen et al., 2005, 2003; Cipolat et al., 2004).”
• Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease (2012, background): “As an inner membrane protein, OPA-1 faces the intermembrane space and corresponds with Mfn to enable inner-membrane fusion [39,41].”
• SLP‐2 is required for stress‐induced mitochondrial hyperfusion (2009, neutral): “OPA1 is responsible for fusion of the inner mitochondrial membrane, and exerts an effect in concert with MFN1 to coordinate fusion of the two membranes (Cipolat et al , 2004).”
• OPA1 controls apoptotic cristae remodeling independently from mitochondrial fusion. (2006, positive): “MFN2 is presumed to have mostly a regulatory role (Ishihara et al., 2004), while MFN1 tethers two juxtaposed organelles (Koshiba et al., 2004) and cooperates with Optic Atrophy 1 (OPA1) in the fusion process (Cipolat et al., 2004).”
• Mitochondrial dynamics and apoptosis. (2008, background): “These domains are required for the OPA1 mitochondrial fusion activity (Cipolat et al. 2004), suggesting these two functions, protection against apoptosis and mitochondrial fusion, could be linked.”
• Fission and selective fusion govern mitochondrial segregation and elimination by autophagy (2008, background): “As previously reported, OPA1 overexpression can result in either a decrease or an increase in mitochondrial size (Cipolat et al, 2004; Griparic et al, 2004; Chen et al, 2005).”