Acetylation of MnSOD directs enzymatic activity responding to cellular nutrient status or oxidative stress

Özden, Özkan; Park, Seong Hoon; Kim, Hyun‐Seok; Jiang, Haiyan; Coleman, Mitchell C.; Spitz, Douglas R.; Gius, David

doi:10.18632/aging.100291

Cited by 134 publications

(110 citation statements)

References 44 publications

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“…In this study, we identified NCF2 gene as a novel p53 target. [76][77][78][79] Expression of NCF2/p67phox, by activating the Nox2 complex, 4 generates ROS that have protective functions against apoptosis in HCT116 and HaCat cell lines, confirming previous results obtained for Nox4 in pancreatic cancer cells.…”

Section: Discussionsupporting

confidence: 84%

Identification of NCF2/p67phox as a novel p53 target gene

et al. 2012

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Analysis of microarrays performed in p53-, TAp63α- and ΔNp63α-inducible SaOs-2 cell lines allowed the identification of NCF2 mRNA upregulation in response to p53 induction. NCF2 gene encodes for p67phox, the cytosolic subunit of the NADPH oxidase enzyme complex. The recruitment of p67phox to the cell membrane causes the activation of the NADPH oxidase complex followed by the generation of NADP+ and superoxide from molecular oxygen. The presence of three putative p53 binding sites on the NCF2 promoter was predicted, and the subsequent luciferase and chromatin immunoprecipitation assays showed the activation of NCF2 promoter by p53 and its direct binding in vivo to at least one of the sites, thus confirming the hypothesis. NCF2 upregulation was also confirmed by real-time PCR in several cell lines after p53 activation. NCF2 knockdown by siRNA results in a significant reduction of ROS production and stimulates cell death, suggesting a protective function of Nox2-generated ROS in cells against apoptosis. These results provide insight into the redox-sensitive signaling mechanism that mediates cell survival involving p53 and its novel target NCF2/p67phox

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Section: Discussionsupporting

confidence: 84%

Identification of NCF2/p67phox as a novel p53 target gene

et al. 2012

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“…These enzymes have a variety of substrates within the cells and are not restricted only to histones. In mammals, there are 7 SIRTs which are located in different compartments of the cells [21] . SIRT2 removed mouse model suggests that these proteins have various antiaging, anti carcinogenic, and immune regulatory functions.…”

Section: Discussionmentioning

confidence: 99%

SIRT2 - JAK1 Etkileşimi Kanser Hücrelerindeki IL-6’in Neden Olduğu İnflamatuar Tepkiyi Azaltır

Özden¹

2015

Kafkas Univ Vet Fak Derg

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Interleukin-6 (IL-6) is a pro-inflammatory cytokine critical in immunoregulation. Aberrant IL-6 signaling has been implicated in various diseases including inflammation-associated cancer. Sirtuin-2 (SIRT2) is a cytoplasmic deacetylase and is generally considered a tumor suppressor. SIRT2 gene removed mouse develops tumors in many organs, primarily in the liver and breast tissues as the mouse ages. The purpose of the study was to investigate the roles of SIRT2 on IL-6 induced inflammatory response in mouse embryonic fibroblasts (MEFs) with SIRT2 gene removed and HeLa cervical cancer cell lines that overexpress SIRT2 gene. Immunoprecipitation and immunoblotting techniques were utilized in the study. SIRT2 interacts with JAK1, which is one of the downstream proteins of IL-6. We also found that overexpression of SIRT2 in HeLa cervical cancer cells decreases IL-6 induced inflammatory response by decreasing the activity of JAK1. These results suggest that SIRT2 has a protective role against chronic inflammatory diseases including inflammationassociated cancer.

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“…modified and was found decreased in abundance in Arabidopsis (212), and post-translational modifications, such as tyrosine nitration and lysine acetylation identified on MnSOD in human and mouse mitochondria, may additionally modulate superoxide signals (56,157). In plant and animal mitochondria, there are also several Fe-S cluster-containing enzymes, of which aconitase is particularly prone to inactivation by superoxide (143).…”

Section: Figmentioning

confidence: 99%

Mitochondrial Energy and Redox Signaling in Plants

Schwarzländer

Finkemeier

2013

Antioxidants & Redox Signaling

147

107

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Significance: For a plant to grow and develop, energy and appropriate building blocks are a fundamental requirement. Mitochondrial respiration is a vital source for both. The delicate redox processes that make up respiration are affected by the plant's changing environment. Therefore, mitochondrial regulation is critically important to maintain cellular homeostasis. This involves sensing signals from changes in mitochondrial physiology, transducing this information, and mounting tailored responses, by either adjusting mitochondrial and cellular functions directly or reprogramming gene expression. Recent Advances: Retrograde (RTG) signaling, by which mitochondrial signals control nuclear gene expression, has been a field of very active research in recent years. Nevertheless, no mitochondrial RTG-signaling pathway is yet understood in plants. This review summarizes recent advances toward elucidating redox processes and other bioenergetic factors as a part of RTG signaling of plant mitochondria. Critical Issues: Novel insights into mitochondrial physiology and redoxregulation provide a framework of upstream signaling. On the other end, downstream responses to modified mitochondrial function have become available, including transcriptomic data and mitochondrial phenotypes, revealing processes in the plant that are under mitochondrial control. Future Directions: Drawing parallels to chloroplast signaling and mitochondrial signaling in animal systems allows to bridge gaps in the current understanding and to deduce promising directions for future research. It is proposed that targeted usage of new technical approaches, such as quantitative in vivo imaging, will provide novel leverage to the dissection of plant mitochondrial signaling.

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Acetylation of MnSOD directs enzymatic activity responding to cellular nutrient status or oxidative stress

Cited by 134 publications

References 44 publications

Identification of NCF2/p67phox as a novel p53 target gene

Identification of NCF2/p67phox as a novel p53 target gene

SIRT2 - JAK1 Etkileşimi Kanser Hücrelerindeki IL-6’in Neden Olduğu İnflamatuar Tepkiyi Azaltır

Mitochondrial Energy and Redox Signaling in Plants

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