[1][2][3] H3K9me2 levels are higher at silent compared to active genes in a 10kb region surrounding the transcriptional start site.
[4] H3K9me2 represses gene expression both passively, by prohibiting acetylation[5] as therefore binding of RNA polymerase or its regulatory factors, and actively, by recruiting transcriptional repressors.
[6][7] H3K9me2 has also been found in megabase blocks, termed Large Organised Chromatin K9 domains (LOCKS), which are primarily located within gene-sparse regions but also encompass genic and intergenic intervals.
[1][3][12] H3K9me2 can be removed by a wide range of histone lysine demethylases (KDMs) including KDM1, KDM3, KDM4 and KDM7 family members.
[24] The current understanding and interpretation of histones comes from two large scale projects: ENCODE and the Epigenomic roadmap.
This led to chromatin states which define genomic regions by grouping the interactions of different proteins and/or histone modifications together.
[32] H3K9me2 is present at a subset of cardiovascular disease-associated gene promoters in vascular smooth muscle cells[16] to block binding of NFκB and AP-1 (activator protein-1) transcription factors.
[16] Reduced levels of H3K9me2 have been observed in vascular smooth muscle cells from human atherosclerotic lesions compared to healthy aortic tissue in patients.