Mitochondrial Acetylation and Genetic Models of Parkinson's Disease

Auburger, Georg; Gispert, Suzana; Jendrach, Marina

doi:10.1016/b978-0-12-394625-6.00006-4

Cited by 23 publications

(16 citation statements)

References 133 publications

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“…Mammalian Sirtuins include the mitochondrial deacetylase SIRT3 and recently mitochondrial lysine acetylation (AcLys) was found to initiate mitochondrial degradation by autophagy. This mitophagy process is closely regulated by PINK1 and Parkin (Ashrafi et al, 2014; Auberger et al, 2014), two interacting proteins that relocalize to mitochondria to stimulate deficient proton gradients. Deacetylation of mitochondrial proteins and altered SIRT3 levels occur in rodent models of PD before the onset of the toxic aggregate formation.…”

Section: Consequences Of Increased Nitroxidative Stressmentioning

confidence: 99%

Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress

et al. 2016

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Mitochondria are important for providing cellular energy ATP through the oxidative phosphorylation pathway. They are also critical in regulating many cellular functions including the fatty acid oxidation, the metabolism of glutamate and urea, the anti-oxidant defense, and the apoptosis pathway. Mitochondria are an important source of reactive oxygen species leaked from the electron transport chain while they are susceptible to oxidative damage, leading to mitochondrial dysfunction and tissue injury. In fact, impaired mitochondrial function is commonly observed in many types of neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, alcoholic dementia, brain ischemia-reperfusion related injury, and others, although many of these neurological disorders have unique etiological factors. Mitochondrial dysfunction under many pathological conditions is likely to be promoted by increased nitroxidative stress, which can stimulate post-translational modifications (PTMs) of mitochondrial proteins and/or oxidative damage to mitochondrial DNA and lipids. Furthermore, recent studies have demonstrated that various antioxidants, including naturally occurring flavonoids and polyphenols as well as synthetic compounds, can block the formation of reactive oxygen and/or nitrogen species, and thus ultimately prevent the PTMs of many proteins with improved disease conditions. Therefore, the present review is aimed to describe the recent research developments in the molecular mechanisms for mitochondrial dysfunction and tissue injury in neurodegenerative diseases and discuss translational research opportunities.

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Section: Consequences Of Increased Nitroxidative Stressmentioning

confidence: 99%

Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress

et al. 2016

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“…The class III HDACs, also termed sirtuins, possess NAD-dependent catalytic sites and traditional inhibitors of HDACs cannot inhibit sirtuin function (76). Mammals have seven sirtuins, with sirtuin (SIRT) 1-3 exhibiting strong NAD + -dependent deacetylation activity, whereas SIRT4-7 exhibit strong deacetylation and are more accurately described as NAD + -dependent deacylases (77). SIRT2 is predominantly localized in the cytoplasm, whereas SIRT3, SIRT4 and SIRT5 are predominantly in the mitochondria, and SIRT1, SIRT6, SIRT7 in the nucleus (78).…”

Section: Acetylation Of Foxo Proteinsmentioning

confidence: 99%

Post-translational modifications of FOXO family proteins

Wang

Huang

2016

Molecular Medicine Reports

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Abstract. The Forkhead box O (FOXO) protein family is predominantly involved in apoptosis, oxidative stress, DNA damage/repair, tumor angiogenesis, glycometabolism, regulating life span and other important biological processes. Its activity is affected by a variety of posttranslational modifications (PTMs), including phosphorylation, acetylation, ubiquitination, methylation and glycosylation. When cells are subjected to different environments, the corresponding PTMs act on the FOXO protein family, to change transcriptional activity or subcellular localization, and the expression of downstream target genes, will ultimately affect the biological behavior of the cells. In this review, we will discuss the biological characteristics of FOXO protein PTMs.

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“…tant factor in cancer [180]. Lower levels of SIRT3 and SIRT4 expression 929 occur in multiple cancers, and overexpression of SIRT3 has been found 930 in others [181,182]. One clue as to how differential SIRT3 expression 931 exerts these effects may lie in its regulation of SOD2, respiratory 932 complex I, and complex III and therefore ROS concentrations and 933 energy homeostasis [183][184][185].…”

mentioning

confidence: 99%

The role of mitochondrial dysfunction in age-related diseases

Lane¹,

Hilsabeck²,

Rea

2015

Biochimica et Biophysica Acta (BBA) - Bioenergetics

181

142

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The aging process is accompanied by the onset of disease and a general decline in wellness. Insights into the aging process have revealed a number of cellular hallmarks of aging, among these epigenetic alterations, loss of proteostasis, mitochondrial dysfunction, cellular senescence, and stem cell exhaustion. Mitochondrial dysfunction increasingly appears to be a common factor connecting several of these hallmarks, driving the aging process and afflicting tissues throughout the body. Recent research has uncovered a much more complex involvement of mitochondria in the cell than has previously been appreciated and revealed novel ways in which mitochondrial defects feed into disease pathology. In this review we evaluate ways in which problems in mitochondria contribute to disease beyond the well-known mechanisms of oxidative stress and bioenergetic deficits, and we predict the direction that mitochondrial disease research will take in years to come.

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Mitochondrial Acetylation and Genetic Models of Parkinson's Disease

Cited by 23 publications

References 133 publications

Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress

Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress

Post-translational modifications of FOXO family proteins

The role of mitochondrial dysfunction in age-related diseases

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