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Fig. 1 | Cell Communication and Signaling

Fig. 1

From: DNA methylation and histone post-translational modifications in atherosclerosis and a novel perspective for epigenetic therapy

Fig. 1

Association with epigenetic modifications and the TLR, NF-κB, and JAK/STAT signaling pathway. TLRs can be regulated by DNA methylation, and histone modifications, which will eventually result in changed TLRs expression. DNA methylation that occurs on the promoter region of TLR genes, such as TLR1, 2, 3, 4, 5, 6, and 8, can reduce the expression of TLR on the membranes. Depending on the type of modification, the histone modifications that occurs on the nucleosome near the promoter of TLR genes, such as TLR2, 3, 4, and 5, can also positively or negatively regulate the expression of TLRs on the membranes; HATs interacts directly with NF-κB or induces its acetylation, and recruits NF-κB to the promoters of proinflammatory genes such as IL-6, IL-8 and cyclooxygenase-2 (COX-2) to regulate inflammatory signaling pathway activation; JAK kinases are activated in response to stimulation, which causes Stat3 activation, resulting in Stat3 nuclear transfer. Stat3 can also be activated by HDAC or DNMT. Activation of Stat3 leading to the DNA methylation of Stat3

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