Non-CpG methylation of the PGC-1alpha promoter through DNMT3B controls mitochondrial density.
By R. Barrès, M. Osler, Jie Yan, A. Rune, T. Fritz, K. Caidahl, A. Krook, J. Zierath. Cell Metabolism, 2009
632 citations recorded by the source corpus.
Subfields: Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/4a04e95dbe0297f0a51059b2ab7890362fad1e57
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Citations in the corpus
- Acute exercise remodels promoter methylation in human skeletal muscle. (2012, background): “Evidence is emerging that epigenetic modifications through DNA methylation contribute to the increased risk and development of metabolic disease by modifying the expression of genes controlling whole body energy and glucose homeostasis (Barrès et al., 2009; Klose and Bird, 2006).”
- A Six Months Exercise Intervention Influences the Genome-wide DNA Methylation Pattern in Human Adipose Tissue (2013, neutral): “Recent studies in human skeletal muscle and pancreatic islets point towards the involvement of epigenetic modifications in the regulation of genes important for glucose metabolism and the pathogenesis of T2D [11,12,16–21].”
- PGC-1α, Inflammation, and Oxidative Stress: An Integrative View in Metabolism (2020, background): “In muscle cells, PGC-1α promoter methylation by DNA methyltransferase 3B (DNMT3B) represses PGC-1α expression in response to high levels of fatty acids [25].”
- Epigenetics in Human Obesity and Type 2 Diabetes (2019, background): “Only a decade ago, the first epigenetics studies were performed in pancreatic islets and skeletal muscle from patients with T2D (Barrès et al., 2009; Ling et al., 2008).”
- Sex differences in human adipose tissues – the biology of pear shape (2012, background): “Recent studies showing that acute exercise, overfeeding, and type 2 diabetes can modulate gene expression in skeletal muscle through epigenetic mechanisms [71-73] open the exciting scenario that lifestyle factors can interact with developmental programming to regulate adipose tissue mass and distrib”