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Fig. 1 | Clinical Epigenetics

Fig. 1

From: Translating epigenetics into clinic: focus on lupus

Fig. 1

A description of the three main epigenetic mechanisms involved in SLE pathogenesis: DNA methylation, histone modification, and RNA-based mechanisms, which can alter genome and generate various gene expression profiles. DNA methylation is catalyzed by transferring a methyl group to the five positions of cytosine in DNA. Histone modifications refer to covalent posttranslational modifications of the nucleosomal histones H2A, H2B, H3, and H4, with one H3–H4 tetramer and two H2A–H2B dimers. The lysine and arginine residues of histone proteins that extrude from the nucleosome can be modified via methylation, acetylation, phosphorylation, or ubiquitylation, which can be altered with variants or chemical modifications on their histone tails. The most recent mechanism of epigenetic inheritance involves some RNAs, which may play a significant role in producing higher-order chromatin structures in nucleosomal chains. Several methylation-sensitive genes (CD11a, CD70, perforin, CD40L IFN-related genes, and CD5), histone modifications (histone deacetylation, H3k4me2, and H3K4me3), and microRNAs (miR-21, miR-126, miR-148a, miR-125a, miR-142, miR-29, miR-101, miR-17–miR-92) have been noted to illustrate their involvement in lupus pathogenesis

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