The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
The dynamin-related GTPase Opa1 is required for glucose-stimulated ATP production in pancreatic beta cells
Open accessAbstract
Previous studies using in vitro cell culture systems have shown the role of the dynamin-related GTPase Opa1 in apoptosis prevention and mitochondrial DNA (mtDNA) maintenance. However, it remains to be tested whether these functions of Opa1 are physiologically important in vivo in mammals. Here, using the Cre-loxP system, we deleted mouse Opa1 in pancreatic beta cells, in which glucose-stimulated ATP production in mitochondria plays a key role in insulin secretion. Beta cells lacking Opa1 maintained normal copy numbers of mtDNA; however, the amount and activity of electron transport chain complex IV were significantly decreased, leading to impaired glucose-stimulated ATP production and insulin secretion. In addition, in Opa1-null beta cells, cell proliferation was impaired, whereas apoptosis was not promoted. Consequently, mice lacking Opa1 in beta cells develop hyperglycemia. The data suggest that the function of Opa1 in the maintenance of the electron transport chain is physiologically relevant in beta cells.
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Cites
Fission and selective fusion govern mitochondrial segregation and elimination by autophagy
Twig, G., Elorza, A., Molina, A. J. A., Mohamed, H., Wikstrom, J. D., Walzer, G., Stiles, L., Haigh, S. E., Katz, S., Las, G., et al. (2008) · The EMBO Journal · doi:10.1038/sj.emboj.7601963 · Cited by 3,082 · cited 1×
“Supporting this idea, cytochrome c binds to complex IV and is required for the stability and activity of this complex (Vempati et al., 2009).”
BackgroundSelf-citationMitochondrial dysfunction and type 2 diabetes
Lowell, B. B., & Shulman, G. I. (2005) · Science · doi:10.1126/science.1104343 · Cited by 2,070
Islet cell failure in type 2 diabetes
Prentki, M. (2006) · Journal of Clinical Investigation · doi:10.1172/jci29103 · Cited by 1,690
OPA1 Controls Apoptotic Cristae Remodeling Independently from Mitochondrial Fusion
Frezza, C., Cipolat, S., Martins de Brito, O., Micaroni, M., Beznoussenko, G. V., Rudka, T., Bartoli, D., Polishuck, R. S., Danial, N. N., De Strooper, B., et al. (2006) · Cell · doi:10.1016/j.cell.2006.06.025 · Cited by 1,673
Disruption of Fusion Results in Mitochondrial Heterogeneity and Dysfunction
Chen, H., Chomyn, A., & Chan, D. C. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m503062200 · Cited by 1,376 · cited 2×
“Reduced mitochondrial fusion decreases oxidative phosphorylation (Chen et al., 2005, 2010).”
BackgroundResultOPA1 requires mitofusin 1 to promote mitochondrial fusion
Cipolat, S., de Brito, O. M., Dal Zilio, B., & Scorrano, L. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0407043101 · Cited by 1,300
Olichon, A., Baricault, L., Gas, N., Guillou, E., Valette, A., Belenguer, P., & Lenaers, G. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.c200677200 · Cited by 1,168
Diabetes and mitochondrial function: Role of hyperglycemia and oxidative stress
Rolo, A. P., & Palmeira, C. M. (2006) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2006.01.003 · Cited by 1,007
The Machines that Divide and Fuse Mitochondria
Hoppins, S., Lackner, L., & Nunnari, J. (2007) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.76.071905.090048 · Cited by 790
The dynamin-related GTPase Drp1 is required for embryonic and brain development in mice
Wakabayashi, J., Zhang, Z., Wakabayashi, N., Tamura, Y., Fukaya, M., Kensler, T. W., Iijima, M., & Sesaki, H. (2009) · Journal of Cell Biology · doi:10.1083/jcb.200903065 · Cited by 667
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Self-citationMitochondrial Dynamics in the Regulation of Nutrient Utilization and Energy Expenditure
Liesa, M., & Shirihai, O. S. (2013) · Cell Metabolism · doi:10.1016/j.cmet.2013.03.002 · Cited by 1,341
Self-citationMitochondrial Dynamics and Metabolic Regulation
Wai, T., & Langer, T. (2016) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2015.12.001 · Cited by 1,300
Mitochondrial dynamics in adaptive and maladaptive cellular stress responses
Eisner, V., Picard, M., & Hajnóczky, G. (2018) · Nature Cell Biology · doi:10.1038/s41556-018-0133-0 · Cited by 622
Mitochondrial dynamics, mitophagy and cardiovascular disease
Vásquez‐Trincado, C., García‐Carvajal, I., Pennanen, C., Parra, V., Hill, J. A., Rothermel, B. A., & Lavandero, S. (2016) · The Journal of Physiology · doi:10.1113/jp271301 · Cited by 629
Metadata
- Authors
- Zhang, Z., Wakabayashi, N., Wakabayashi, J., Tamura, Y., Song, W.-J., Sereda, S., Clerc, P., Polster, B. M., Aja, S. M., Pletnikov, M. V., Kensler, T. W., Shirihai, O. S., Iijima, M., Hussain, M. A., & Sesaki, H.
- Venue
- Molecular Biology of the Cell
- Published
- 2011-07
- Volume
- 22
- Issue
- 13
- Pages
- 2235-2245
- ISSN
- 1059-1524 (ISSN-L)
- 1939-4586
- OpenAlex
- W2154606893
- Cited by
- 171
- References
- 15
- FWCI
- 13.26
- Type
- journal article
- Language
- en
- Open access
- green
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- Zhang, Z., Wakabayashi, N., Wakabayashi, J., Tamura, Y., Song, W.-J., Sereda, S., Clerc, P., Polster, B. M., Aja, S. M., Pletnikov, M. V., Kensler, T. W., Shirihai, O. S., Iijima, M., Hussain, M. A., & Sesaki, H. (2011). The dynamin-related GTPase Opa1 is required for glucose-stimulated ATP production in pancreatic beta cells. Molecular Biology of the Cell. https://doi.org/10.1091/mbc.e10-12-0933
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