Acetylation of MnSOD directs enzymatic activity responding to cellular nutrient status or oxidative stress
    
Yazarlar (7)
Seong-Hoon Park Türkiye
Hyun-Seok Kim Türkiye
Haiyan Jiang Türkiye
Mitchell C Coleman Türkiye
Douglas R Spitz Türkiye
David Gius Türkiye
Makale Türü Açık Erişim Diğer (Teknik, not, yorum, vaka takdimi, editöre mektup, özet, kitap krıtiği, araştırma notu, bilirkişi raporu ve benzeri) (SCI, SSCI, AHCI, SCI-Exp dergilerinde yayınlanan teknik not, editöre mektup, tartışma, vaka takdimi ve özet türünden makale)
Dergi Adı AGING-US
Dergi ISSN 1945-4589 Wos Dergi Scopus Dergi
Dergi Tarandığı Indeksler SCI
Makale Dili İngilizce Basım Tarihi 02-2011
Cilt / Sayı / Sayfa 3 / 2 / 102–107 DOI 10.18632/aging.100291
Özet
A fundamental observation in biology is that mitochondrial function, as measured by increased reactive oxygen species (ROS), changes significantly with age, suggesting a potential mechanistic link between the cellular processes governing longevity and mitochondrial metabolism homeostasis. In addition, it is well established that altered ROS levels are observed in multiple age-related illnesses including carcinogenesis, neurodegenerative, fatty liver, insulin resistance, and cardiac disease, to name just a few. Manganese superoxide dismutase (MnSOD) is the primary mitochondrial ROS scavenging enzyme that converts superoxide to hydrogen peroxide, which is subsequently converted to water by catalase and other peroxidases. It has recently been shown that MnSOD enzymatic activity is regulated by the reversible acetylation of specific, evolutionarily conserved lysine(s) in the protein. These results, suggest for the first time, that the mitochondria contain bidirectional post-translational signaling networks, similar to that observed in the cytoplasm and nucleus, and that changes in lysine acetylation alter MnSOD enzymatic activity. In addition, these new results demonstrate that the mitochondrial anti-aging or fidelity / sensing protein, SIRT3, responds to changes in mitochondrial nutrient and/or redox status to alter the enzymatic activity of specific downstream targets, including MnSOD that adjusts and/or maintains ROS levels as well as metabolic homeostatic poise.
Anahtar Kelimeler
MnSOD | Sirt3 | mitochondria | acetylation