Addiction Chronic addictive drug exposure results in ΔFosB-mediated repression of G9a and reduced H3K9 dimethylation in the nucleus accumbens, which in turn causes dendritic arborization, altered synaptic protein expression, and increased drug seeking behavior. In contrast, accumbal G9a hyperexpression results in markedly increased H3K9 dimethylation and blocks the induction of this neural and behavioral plasticity by chronic drug use, which occurs via<unk> -mediated repression of transcription factors for ΔFosB and<unk> -mediated repression of various ΔFosB transcriptional targets (e.g., CDK5). Figure 4: Epigenetic basis of drug regulation of gene expression Due to the involvement of<unk>  in these feedback loops and the central pathophysiological role of ΔFosB overexpression as the mechanistic trigger for addiction, the reduction of accumbal<unk>  following repeated drug exposure directly mediates the development of drug addictions. Friedreich's ataxia R-loop's are found with<unk>  mark at FXN in Friedreich's ataxia cells. Cardiovascular disease<unk>  is present at a subset of cardiovascular disease-associated gene promoters in vascular smooth muscle cells to block binding of NFκB and AP-1 (activator protein-1) transcription factors. Reduced levels of<unk>  have been observed in vascular smooth muscle cells from human atherosclerotic lesions compared to healthy aortic tissue in patients. Vascular smooth muscle cells from diabetic patients display reduced levels of<unk>  compared to non-diabetic controls; it has therefore been suggested that dysregulation of<unk>  might underlie the vascular complications associated with diabetes. Loss of<unk>  in vascular smooth muscle cells exacerbates upregulation of a subset of cardiovascular disease-associated genes in vascular disease models.
H3K9me2
H3K9me3
H3K36me
H3K14ac
H4K8ac
H4K12ac
H4K5ac
H3K9ac