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Cited by 7 publications
(4 citation statements)
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References 7 publications
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“…Sirt have been linked to aging as they modulate genomic stability, stress resistance and energy metabolism. Activation of Sirt1 enables the deacetylation of a variety of proteins, resulting in a robust, protective cellular response, as it regulates processes such as cell death, metabolism or neurodegeneration [30]; while Sirt2 has been reported to regulate oxidative stress, genome integrity and myelination and its dysfunction is found in most age-related neurodegenerative disorders such as AD, Parkinson's disease and Amyotrophic Lateral Sclerosis, as well as in physiological aging [31]. Accumulated evidence indicates that Sirt6 gene expression is lower in the hippocampus and cerebral cortex of aged mice [32,33] and that it is concerned with H3K9 acetylation [32].…”
Section: Discussionmentioning
confidence: 99%
“…Sirt have been linked to aging as they modulate genomic stability, stress resistance and energy metabolism. Activation of Sirt1 enables the deacetylation of a variety of proteins, resulting in a robust, protective cellular response, as it regulates processes such as cell death, metabolism or neurodegeneration [30]; while Sirt2 has been reported to regulate oxidative stress, genome integrity and myelination and its dysfunction is found in most age-related neurodegenerative disorders such as AD, Parkinson's disease and Amyotrophic Lateral Sclerosis, as well as in physiological aging [31]. Accumulated evidence indicates that Sirt6 gene expression is lower in the hippocampus and cerebral cortex of aged mice [32,33] and that it is concerned with H3K9 acetylation [32].…”
Section: Discussionmentioning
confidence: 99%
“…It has been reported that SIRT2, as a strong deacetylase [23][24][25][26], is highly expressed in the brain and is markedly associated with aging [27,28]; additionally, SIRT2 was evaluated in the brains of PD patients, suggesting a potential role in PD development [29]. It has been confirmed that selective inhibitors of SIRT2 can protect against α-syn-mediated toxicity and dopaminergic cell death, both in vitro and in a Drosophila model of PD [19].…”
Section: Discussionmentioning
confidence: 94%
“…The luciferase reporter assay further confirmed that this mutation significantly influenced binding affinity, suggesting that the rs2241703 SNP influences SIRT2 levels by affecting the binding efficiency of miR-486-3p to SIRT2 due to mutation from the G allele to the A allele, resulting in weakening of the inhibitory effect and high levels of SIRT2, which may contribute to a high risk of PD or accelerate the development of this disease. Furthermore, SIRT2 increased with aging [17,28,40], which may explain why AA+GA genotype or A allele Cellular Physiology and Biochemistry Cellular Physiology and Biochemistry carriers of rs2241703 showed a higher risk of LOPD than PD. However, more evidence is needed be verify this speculation.…”
Section: Discussionmentioning
confidence: 99%
“…Sirt have been linked to aging as they modulate genomic stability, stress resistance and energy metabolism. Activation of Sirt1 enables the deacetylation of a variety of proteins, resulting in a robust, protective cellular response, as it regulates processes such as cell death, metabolism or neurodegeneration [33]; while Sirt2 has been reported to regulate oxidative stress, genome integrity and myelination and its dysfunction is found in most of age-related neurodegenerative disorders such as AD, Parkinson's disease or Amyotrophic Lateral Sclerosis, as well as in physiological aging [34]. Accumulated evidence indicates that Sirt6 gene expression is lower in the hippocampus and cerebral cortex of aged mice [35,36] and that it is concerned with H3K9 acetylation [35].…”
Section: Discussionmentioning
confidence: 99%