Skip to main content
Fig. 1 | Clinical Epigenetics

Fig. 1

From: Epigenetic regulation of inflammation in periodontitis: cellular mechanisms and therapeutic potential

Fig. 1

Schematic representation of the biochemical processes involved in DNA methylation and histone acetylation. a Unmethylated cytosine at the CpG site can be methylated de novo by DNMT3A or DNMT3B in complex with DNMT3L, the latter lacking methyltransferase activity. The DNMT1:UHRF1 complex is responsible for the conservation of the CpG methylation pattern on the complementary DNA strand after replication. TET enzymes catalyze the formation of oxidized 5mC derivatives, which are no longer recognized by the DNMT1:UHRF1 complex (passive demethylation). Additionally, 5fC and 5caC can be recognized and excised by TDG, leading to replacement with unmodified cytosine through BER (active demethylation). b N-terminal lysine residues on histone tails are acetylated by HATs, which leads to neutralization of their positive charge, relaxation of chromatin structure, and increased transcriptional accessibility of gene promoters. Bromodomain-containing proteins recognize specific acetyl-lysine containing sequences within the histone, promoting the formation of acetylation-dependent transcriptional complexes. Acetylated lysine residues can be deacetylated by HDACs. BER base-excision repair, DNMT DNA methyltransferase, HAT histone acetyltransferase, HDAC histone deacetylase, TET ten-eleven translocation, TDG thymine DNA glycosylase, UHRF1 Ubiquitin-like, containing PHD and RING finger domains-1

Back to article page