Sandbox Reserved 1644: Difference between revisions
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<p align="justify">The mitochondrial Lon protease is an '''important regulator of mitochondrial [https://en.wikipedia.org/wiki/Metabolism metabolism]''' including the maintenance and repair of mitochondrial [https://en.wikipedia.org/wiki/DNA DNA]. This protein is also essential for '''homeostasis of mitochondria''', and by regulating some regulatory proteins which have '''a short life or damaged proteins'''. | <p align="justify">The mitochondrial Lon protease is an '''important regulator of mitochondrial [https://en.wikipedia.org/wiki/Metabolism metabolism]''' including the maintenance and repair of mitochondrial [https://en.wikipedia.org/wiki/DNA DNA]. This protein is also essential for '''homeostasis of mitochondria''', and by regulating some regulatory proteins which have '''a short life or damaged proteins'''. | ||
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Lon protease has three main roles. | Lon protease has three main roles<ref>Bota, Daniela A., and Kelvin J. A. Davies. “Mitochondrial Lon Protease in Human Disease and Aging: Including an Etiologic Classification of Lon-Related Diseases and Disorders.” Free Radical Biology & Medicine 100 (November 2016): 188–98. https://doi.org/10.1016/j.freeradbiomed.2016.06.031. | ||
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This protein is able to do a '''[https://en.wikipedia.org/wiki/Proteolysis proteolytic] digestion''' of oxidized proteins which allows the renewal of essential mitochondrial enzymes such as [https://en.wikipedia.org/wiki/Aconitase aconitase] or [https://en.wikipedia.org/wiki/TFAM Mitochondrial transcription factor A]. | This protein is able to do a '''[https://en.wikipedia.org/wiki/Proteolysis proteolytic] digestion''' of oxidized proteins which allows the renewal of essential mitochondrial enzymes such as [https://en.wikipedia.org/wiki/Aconitase aconitase] or [https://en.wikipedia.org/wiki/TFAM Mitochondrial transcription factor A]. | ||
Lon protease is involved in [https://en.wikipedia.org/wiki/Mitochondrial_DNA mtDNA] [https://en.wikipedia.org/wiki/DNA_replication replication] and [https://en.wikipedia.org/w/index.php?title=Mitogenesis&redirect=no mitogenesis] by being a '''mitochondrial [https://en.wikipedia.org/wiki/DNA-binding_protein DNA-bing protein]'''. Human Lon and mtDNA associate at the level of their at least 4 contiguous [https://en.wikipedia.org/wiki/Guanine guanine] sequence and form '''a [https://en.wikipedia.org/wiki/G-quadruplex G-quadruplex]'''<ref>Bota, Daniela A., and Kelvin J. A. Davies. “Mitochondrial Lon Protease in Human Disease and Aging: Including an Etiologic Classification of Lon-Related Diseases and Disorders.” Free Radical Biology & Medicine 100 (November 2016): 188–98. https://doi.org/10.1016/j.freeradbiomed.2016.06.031.</ref>. This '''G-rich region''' is the control region for mtDNA replication and transcription<ref>Lu, Bin. “Mitochondrial Lon Protease and Cancer.” Advances in Experimental Medicine and Biology 1038 (2017): 173–82. https://doi.org/10.1007/978-981-10-6674-0_12.</ref>. | Lon protease is involved in [https://en.wikipedia.org/wiki/Mitochondrial_DNA mtDNA] [https://en.wikipedia.org/wiki/DNA_replication replication] and [https://en.wikipedia.org/w/index.php?title=Mitogenesis&redirect=no mitogenesis] by being a '''mitochondrial [https://en.wikipedia.org/wiki/DNA-binding_protein DNA-bing protein]'''. Human Lon and mtDNA associate at the level of their at least 4 contiguous [https://en.wikipedia.org/wiki/Guanine guanine] sequence and form '''a [https://en.wikipedia.org/wiki/G-quadruplex G-quadruplex]'''<ref>Bota, Daniela A., and Kelvin J. A. Davies. “Mitochondrial Lon Protease in Human Disease and Aging: Including an Etiologic Classification of Lon-Related Diseases and Disorders.” Free Radical Biology & Medicine 100 (November 2016): 188–98. https://doi.org/10.1016/j.freeradbiomed.2016.06.031.</ref>. This '''G-rich region''' is the control region for mtDNA replication and transcription<ref>Lu, Bin. “Mitochondrial Lon Protease and Cancer.” Advances in Experimental Medicine and Biology 1038 (2017): 173–82. https://doi.org/10.1007/978-981-10-6674-0_12.</ref>. | ||