Biochemical and Biophysical Research Communications
Regular ArticleEts-2 Is Induced by Oxidative Stress and Sensitizes Cells to H2O2-Induced Apoptosis: Implications for Down's Syndrome
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Cited by (41)
HNE-modified proteins in Down syndrome: Involvement in development of Alzheimer disease neuropathology
2017, Free Radical Biology and MedicineCitation Excerpt :The overexpression of Ets-2 could play a role in the increased susceptibility of DS cells to undergo apoptosis given common pathophysiological features shared between Ets-2 overexpressing transgenic mice and individuals with DS [49]. Intriguingly, although Ets-2 overexpression is involved in neuronal apoptotic cell death it is conceivable that it may also play a role in the reduced incidence of solid tumors in people with DS [50]. Taken together, this “genetic fingerprint” suggests that DS individuals are exposed to chronic doses of free radicals from embryonic development until adult life as discussed below.
Trisomy 21 and cancers
2012, MorphologieLoss of dicer in sertoli cells has a major impact on the testicular proteome of mice
2011, Molecular and Cellular ProteomicsCitation Excerpt :Sod-1 was selected because of its potential biological interest: SOD-1 is a Cu-Zn superoxide dismutase that catalyzes the reaction 2O2− + 2H+ → O2 + H2O2, thus protecting cells from oxidative damage (reviewed in (35)). Perturbation of this reaction's equilibrium may lead to oxidative damage; indeed, it has been shown that overproduction of SOD-1 can cause increased oxidative damage resulting in enhanced cell death by apoptosis (for example see (36, 37)). We thus reckoned that Sod-1 would be an interesting candidate gene for the explanation of the testicular degeneration phenotype we observed.
DNA damage and repair in children with Down's syndrome
2008, Mutation Research - Fundamental and Molecular Mechanisms of MutagenesisOxidative stress: A bridge between Down's syndrome and Alzheimer's disease
2007, Neurobiology of AgingCitation Excerpt :An elevated level of 8-OH-dG in the intact DNA and a decreased concentration of its free repair product were demonstrated in the CSF [193] and lymphocytes [215,216] of AD individuals. In line with these observations, enhanced amounts of oxidized purines were described in AD lymphocytes [164,231] and leukocytes [222], and in our recent study on DS lymphocytes, supporting the existence of a heightened OS in vivo and the earlier results that trisomic cells are more prone to OS and apoptotic cell death [236,292,384]. The higher level of urine 8-OH-dG found in DS [142] (Table 2) may also be in agreement with the observed premature aging and the enhanced incidence of dysfunctions (e.g. infections, cancer and cataracts) and early AD-like changes in DS.
Down syndrome, antioxidant balance and the “gene dosage effect” hypothesis
2007, Oxidative Stress and Neurodegenerative Disorders
- 1
Present address: Pharmacia Upjohn Monsanto, 301 Henrietta Street, Kalamazoo, MI 49007.
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To whom correspondence should be addressed. Fax: 61-3-9594 7211. E-mail: [email protected].