SOD2 acetylation and deacetylation: Another tale of Jekyll and Hyde in cancer

Hjelmeland, Anita B.; Patel, Rakesh P.

doi:10.1073/pnas.1916214116

Cited by 17 publications

(14 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Protein levels of the oxidative stress marker manganese superoxide dismutase (MnSOD) were increased by 21% (P < 0.05) in WSD-exposed livers compared with CD-exposed livers (Figure 7, A and B). Expression of acetylated MnSOD (Ac-MnSOD), the prooxidant form of MnSOD (40,41), was also increased (P = 0.05; Figure 7, A and B). The ratio of acetylated/total MnSOD was not different between CD-and WSD-exposed livers (Figure 7A).…”

Section: Resultsmentioning

confidence: 97%

Maternal Western diet exposure increases periportal fibrosis beginning in utero in nonhuman primate offspring

Nash¹,

Dobrinskikh²,

Newsom³

et al. 2021

JCI Insight

View full text Add to dashboard Cite

Section: Resultsmentioning

confidence: 97%

Maternal Western diet exposure increases periportal fibrosis beginning in utero in nonhuman primate offspring

Nash¹,

Dobrinskikh²,

Newsom³

et al. 2021

JCI Insight

View full text Add to dashboard Cite

“…Moreover, low levels of ROS are able to promote health and lifespan by boosting cellular defense mechanisms via an adaptive up-regulation of antioxidant enzymes [ 26 ]. However, overwhelming ROS levels results in damage of proteins, lipids and DNA, causing massive oxidative stress and triggering the development of pathological states such as neurodegenerative disorders [ 27 ] and cancer [ 28 ]. Mitochondrial DNA (mtDNA) is especially vulnerable to ROS-induced damage due to the lack of repair mechanisms and histones, which pack and order nuclear DNA [ 29 ].…”

Section: Ros Homeostasismentioning

confidence: 99%

Interrelation between ROS and Ca2+ in aging and age-related diseases

2020

View full text Add to dashboard Cite

Calcium (Ca 2+ ) and reactive oxygen species (ROS) are versatile signaling molecules coordinating physiological and pathophysiological processes. While channels and pumps shuttle Ca 2+ ions between extracellular space, cytosol and cellular compartments, short-lived and highly reactive ROS are constantly generated by various production sites within the cell. Ca 2+ controls membrane potential, modulates mitochondrial adenosine triphosphate (ATP) production and affects proteins like calcineurin (CaN) or calmodulin (CaM), which, in turn, have a wide area of action. Overwhelming Ca 2+ levels within mitochondria efficiently induce and trigger cell death. In contrast, ROS comprise a diverse group of relatively unstable molecules with an odd number of electrons that abstract electrons from other molecules to gain stability. Depending on the type and produced amount, ROS act either as signaling molecules by affecting target proteins or as harmful oxidative stressors by damaging cellular components. Due to their wide range of actions, it is little wonder that Ca 2+ and ROS signaling pathways overlap and impact one another. Growing evidence suggests a crucial implication of this mutual interplay on the development and enhancement of age-related disorders, including cardiovascular and neurodegenerative diseases as well as cancer.

show abstract

“…In human cancer progression, it has been proposed that acetylation of SOD2 results in loss of dismutase activity (i.e. the ability to make H 2 O 2 ; antioxidant form) and gain of peroxidase activity (prooxidant form) (Ganini et al., 2018; Hjelmeland & Patel, 2019). Taken together, we speculate that the cetacean‐specific loss of an acetylation site facilitates the generation of the antioxidant form of SOD2.…”

Section: Resultsmentioning

confidence: 99%

Comparative analysis of the superoxide dismutase gene family in Cetartiodactyla

Tian

Geng

Guo

et al. 2021

J of Evolutionary Biology

View full text Add to dashboard Cite

Cetacea, whales, dolphins and porpoises form an order of mammals adapted to aquatic life. Their transition to an aquatic habitat resulted in exceptional protection against cellular insults, including oxidative and osmotic stress. Here, we considered the structure and molecular evolution of the superoxide dismutase (SOD) gene family, which encodes essential enzymes in the mammalian antioxidant system, in the superorder Cetartiodactyla. To this end, we juxtaposed cetaceans and their closest extant relatives (order Artiodactyla). We identified 94 genes in 23 species, of which 70 are bona fide intact genes. Although the SOD gene family is conserved in Cetartiodactyla, lineage‐specific gene duplications and deletions were observed. Phylogenetic analyses show that the SOD2 subfamily diverged from a clade containing SOD1 and SOD3, suggesting that cytoplasmic, extracellular and mitochondrial SODs have started down independent evolutionary paths. Specific‐amino acid changes (e.g. K130N in SOD2) that may enhance ROS elimination were identified in cetaceans. In silico analysis suggests that the core transcription factor repertoire of cetartiodactyl SOD genes may include Sp1, NF‐κB, Nrf2 and AHR. Putative transcription factors binding sites responding to hypoxia were (e.g. Suppressor of Hairless; Su(H)) found in the cetacean SOD1 gene. We found significant evidence for positive selection in cetaceans using codon models. Cetaceans with different diving abilities also show divergent evolution of SOD1 and SOD2. Our genome‐wide analysis of SOD genes helps clarify their relationship and evolutionary trajectory and identify putative functional changes in cetaceans.

show abstract

SOD2 acetylation and deacetylation: Another tale of Jekyll and Hyde in cancer

Cited by 17 publications

References 30 publications

Maternal Western diet exposure increases periportal fibrosis beginning in utero in nonhuman primate offspring

Maternal Western diet exposure increases periportal fibrosis beginning in utero in nonhuman primate offspring

Interrelation between ROS and Ca2+ in aging and age-related diseases

Comparative analysis of the superoxide dismutase gene family in Cetartiodactyla

Contact Info

Product

Resources

About