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Role of Epigenetic Mechanisms in Plant Response to Low Temperature

100%
Achrem M., Skuza L., Kalinka A., Szućko I., Filip E., Słomińska-Walkowiak R., Rogalska S. M.
Acta Biologica Cracoviensia s. Botanica
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2012
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vol. 54
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issue 1
2
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The catalytic activity of sirtuins in physiology and disease from the epigenetic point of view

88%
Albani D., Forloni G.
Epigenetics of Degenerative Diseases
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2013
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vol. 1
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issue 1
EN
Sirtuins are a family of conserved enzymes that are involved in physiological and pathological pathways and have been investigated in relation to the ageing process. There are seven different sirtuins in mammals that are encoded by individual genes (SIRT1-7). Sirtuins share a highly conserved catalytic domain, and they have NAD+ dependent deacetylase activity and secondary ADPribosylase activity in different proportions and on different molecular targets. Sirtuins might be pharmacologically modulated by small molecules that might represent a novel class of “epigenetic” drugs. In fact, sirtuins’ deacetylase activity may impact the epigenetic regulation network acting on histones or affecting chromatin stability, while the mono-ADP-ribosylase catalysis is less explored to this respect. Here we review and discuss the potential impact of sirtuin catalytic activities from the epigenetic pointof- view, with a focus on age-related diseases (cancer,
3
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Exposure to Maternal Diabetes in Utero and DNA Methylation Patterns in the Offspring

88%
West N. A., Kechris K., Dabelea D.
Immunometabolism
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2013
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vol. 1
1-9
EN
Perturbations in early life environments, including intrauterine exposure to maternal gestational diabetes (GDM), are hypothesized to lead to metabolic imprinting resulting in increased risk of cardiometabolic outcomes later in life. We aimed to 1) identify candidate genes and biological pathways associated with differentially methylated regions (DMRs) in relation to exposure to GDM in utero and, 2) using mediation analysis, more definitively investigate the potential for mediation of the effect of exposure to maternal diabetes in utero on cardiometabolic traits in childhood risk through our identified DMRs. Genome-wide methylation analysis of peripheral blood mononuclear cell’s DNA was conducted in 21 healthy children, ages 8-12 years. P-values from multiple linear regression analyses for >27,000 CpG sites were ranked to identify DMRs between the exposure groups. Among the top 10 ranked DMRs, we identified several genes, including NPR1, PANK1, SCAND1, and GJA4, which are known to be associated with cardiometabolic traits. Gene enrichment analysis of the top 84 genes, each with p<=0.005, identified the ubiquitin proteasome system (UPS) as the most enriched biological pathway (p = 0.07). The UPS pathway reflects biological processes known to be associated with endothelial function, inflammation, lipid metabolism, insulin resistance and b-cell apoptosis, whose derangements are central to the pathogenesis of cardiometabolic diseases. Increased methylation of PYGO1 and CLN8 had the greatest relative mediation effect (RME = 87%, p=0.005 and RME=50%, p=0.01) on the impact of exposure to maternal diabetes in utero on VCAM-1 levels in the offspring. Multiple candidate genes and the UPS were identified for future study as possible links between exposure to maternal gestational diabetes in utero and adverse cardiometabolic traits in the offspring. In particular, increased methylation of PYGO1 and CLN8 may be biological links between intrauterine exposure to maternal diabetes and significantly increased VCAM-1 levels in the offspring.
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Advances in the Genetics and Epigenetics of Neurodegenerative Diseases

63%
Coppedè F.
Epigenetics of Degenerative Diseases
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2013
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vol. 1
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issue 1
EN
Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD) represent four of the major neurodegenerative diseases. AD, PD and ALS are complex disorders including both Mendelian and sporadic forms. Studies on families with these diseases led to the identification of several genes and pathways responsible for the familial forms. Those studies have been paralleled by hundreds of genetic association studies, including genome-wide screenings, in order to identify genes likely contributing to the sporadic forms. HD is a monogenic disorder caused by a trinucleotide repeat expansion in the causative gene. Increasing evidence points to an epigenetic contribution to neurodegeneration, suggesting that DNA methylation, histone tail modifications and RNA mediated mechanisms might contribute to the onset and progression of all the above diseases. In addition, epigenetic drugs are promising for the restoration of memory and motor impairments in animal models of the diseases. The aim of this review article is to provide an updated overview of the genetics and epigenetics of these major neurodegenerative disorders.
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