http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Yoo, Y,Park, J H,Weigel, C,Liesenfeld, D B,Weichenhan, D,Plass, C,Seo, D-G,Lindroth, A M,Park, Y J Nature Publishing Group 2017 International Journal of Obesity Vol.41 No.4
<P>CONCLUSIONS: TET proteins, particularly TET2, were required for adipogenesis by modulating DNA methylation at the Ppar. locus, subsequently by inducing Ppar. gene expression.</P>
Arab, K.,Park, Y.,Lindroth, Anders M.,Schafer, A.,Oakes, C.,Weichenhan, D.,Lukanova, A.,Lundin, E.,Risch, A.,Meister, M.,Dienemann, H.,Dyckhoff, G.,Herold-Mende, C.,Grummt, I.,Niehrs, C.,Plass, C. Cell Press 2014 Molecular cell Vol.55 No.4
DNA methylation is a dynamic and reversible process that governs gene expression during development and disease. Several examples of active DNA demethylation have been documented, involving genome-wide and gene-specific DNA demethylation. How demethylating enzymes are targeted to specific genomic loci remains largely unknown. We show that an antisense lncRNA, termed TARID (for TCF21 antisense RNA inducing demethylation), activates TCF21 expression by inducing promoter demethylation. TARID interacts with both the TCF21 promoter and GADD45A (growth arrest and DNA-damage-inducible, alpha), a regulator of DNA demethylation. GADD45A in turn recruits thymine-DNA glycosylase for base excision repair-mediated demethylation involving oxidation of 5-methylcytosine to 5-hydroxymethylcytosine in the TCF21 promoter by ten-eleven translocation methylcytosine dioxygenase proteins. The results reveal a function of lncRNAs, serving as a genomic address label for GADD45A-mediated demethylation of specific target genes.
Alterations in cardiac DNA methylation in human dilated cardiomyopathy
Haas, Jan,Frese, Karen S,Park, Yoon Jung,Keller, Andreas,Vogel, Britta,Lindroth, Anders M,Weichenhan, Dieter,Franke, Jennifer,Fischer, Simon,Bauer, Andrea,Marquart, Sabine,Sedaghat-Hamedani, Farbod,Ka WILEY-VCH Verlag 2013 EMBO molecular medicine Vol.5 No.3
<P>Dilated cardiomyopathies (DCM) show remarkable variability in their age of onset, phenotypic presentation, and clinical course. Hence, disease mechanisms must exist that modify the occurrence and progression of DCM, either by genetic or epigenetic factors that may interact with environmental stimuli. In the present study, we examined genome-wide cardiac DNA methylation in patients with idiopathic DCM and controls. We detected methylation differences in pathways related to heart disease, but also in genes with yet unknown function in DCM or heart failure, namely <I>Lymphocyte antigen 75</I> (<I>LY75</I>), <I>Tyrosine kinase-type cell surface receptor HER3</I> (<I>ERBB3</I>), <I>Homeobox B13</I> (<I>HOXB13</I>) and <I>Adenosine receptor A2A</I> (<I>ADORA2A</I>). Mass-spectrometric analysis and bisulphite-sequencing enabled confirmation of the observed DNA methylation changes in independent cohorts. Aberrant DNA methylation in DCM patients was associated with significant changes in <I>LY75</I> and <I>ADORA2A</I> mRNA expression, but not in <I>ERBB3</I> and <I>HOXB13</I>. <I>In vivo</I> studies of orthologous <I>ly75</I> and <I>adora2a</I> in zebrafish demonstrate a functional role of these genes in adaptive or maladaptive pathways in heart failure.</P>