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SIRT3 could be a target for colon cancer.
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these results identified a tumor-suppressive role for Sirt3 deficiency in tongue cancer via activation of the JNK-Fis1 axis and subsequent initiation of fatal mitochondrial fission.
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SIRT3 promoted mitochondrial biogenesis by increasing both the expression and deacetylation of TFAM in clear cell renal cell carcinoma.
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that SIRT3 dysfunction leads to p53-mediated mitochondrial and neuronal damage in Alzheimer's disease
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Myricetin nanoliposomes induced SIRT3-mediated glycolytic metabolism leading to glioblastoma cell death.
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High SIRT3 expression is associated with diabetes and hypothyroidism.
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SIRT3 knockout cells upregulated the diversion of glutamine into de novo nucleotide synthesis through hyperactive mTORC1 signaling.
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Increased levels of miR-195 in failing myocardium regulate a novel pathway that involves direct SIRT3 suppression and enzymatic inhibition via increased acetylation of pyruvate dehydrogenase and ATP synthase that are essential for cardiac energy metabolism.
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The Sirt3-mediated protein deacetylation plays an important role in regulating oxidative metabolism and antioxidant defence in stem cell differentiation, and that Sirt3 deficiency may be related to insulin resistance.
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SIRT3 gene expression is altered in adipose tissue from overweight and obese subjects compared to normal weight subjects.
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MiR-494-3p inhibition exerted a neuroprotective role in 1-Methyl-4-phenylpyridinium induced Parkinson's disease by targeting SIRT3, providing a possible therapeutic strategy for Parkinson's disease patients.
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ZEB1 silenced SIRT3 expression via interaction with MBD1 to promote aerobic glycolysis in pancreatic cancer.
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The SIRT3 promoted FOXO3A expression by attenuating Wnt/beta-catenin pathway, thereby inhibiting EMT and migration of prostate cancer cells.
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Sirtuin-3 mitochondrial NAD-dependent deacetylase (SIRT3) is responsible for serine hydroxymethyltransferase 2 (SHMT2)deacetylation in colorectal cancer (CRC) cells. The increased expression of SIRT3 in human CRC samples is correlated with poorer postoperative overall survival.
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genetic manipulation of Sirt3 revealed that amyloid-beta increased levels of total tau acetylated tau through its modulation of Sirt3.
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The SIRT3 protein level negatively correlated with advanced glycation end products accumulation and the grade of intervertebral disc degeneration degeneration.
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Melatonin's functions in the mitochondria are highly diverse, not unlike those of sirtuin 3 (SIRT3). SIRT3 is an NAD+-dependent deacetylase which regulates, among many functions, the redox state of the mitochondria. Recent data proves that melatonin and SIRT3 post-translationally collaborate in regulating free radical generation and removal from mitochondria. [review]
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Master athletes had lower levels of miR-7, while mRNA or protein levels of SIRT3, SIRT1, SOD2, and FOXO1 levels were significantly higher in the vastus lateralis muscle of master athletes compared to muscles of age-matched controls.
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BER modulated autophagy in DOX-treated H9c2 cardiomyoblasts. Interestingly, mitochondrial biogenesis markers were upregulated in in BER/DOX-treated cells. Sirt3 over-expression contributes to decrease DOX cytotoxicity on H9c2 cardiomyoblasts, while BER can be used as a modulator of Sirtuin function and cell quality control pathways to decrease DOX toxicity.
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The loss of Sirt3 triggered fatal mitochondrial fission by suppressing the Akt/PTEN pathway.