A cluster of genes, BAT1-BAT5, has been localized in the vicinity of the genes for TNF alpha and TNF beta. This gene is found near this cluster; it was mapped near the gene for C2 within a 120-kb region that included a HSP70 gene pair. These genes are all within the human major histocompatibility complex class III region. This gene was thought to be two different genes, NG36 and G9a, adjacent to each other but a recent publication shows that there is only a single gene. The protein encoded by this gene is thought to be involved in intracellular protein-protein interaction. There are three alternatively spliced transcript variants of this gene but only two are fully described.[7]
G9a andG9a-like protein, another histone-lysine N-methyltransferase, catalyze the synthesis ofH3K9me2, which is arepressive mark.[8][9][10] G9a is an important control mechanism forepigenetic regulation within thenucleus accumbens (NAcc);[11] reduced G9a expression in the NAcc plays a central role in mediating the development of anaddiction.[11] G9a opposes increases inΔFosB expression viaH3K9me2 and is suppressed by ΔFosB.[11][12] G9a exerts opposite effects to that of ΔFosB on drug-related behavior (e.g.,self-administration) and synaptic remodeling (e.g.,dendritic arborization – the development of additional tree-likedendritic branches andspines) in the nucleus accumbens, and therefore opposes ΔFosB's function as well as increases in its expression.[11] G9a and ΔFosB share many of the same gene targets.[13] In addition to its role in the nucleus accumbens, G9a play a critical role in the development and the maintenance of neuropathic pain.[14][15] Following peripheral nerve injury, G9a regulates the expression of +600 genes in thedorsal root ganglia. This transcriptomic change reprograms the sensory neurons to a hyperexcitable state leading to mechanical pain hypersensitivity.[14]
EHMT2 is known to drive process such as self-renewal andtumorigenicity, and its dysregulation can be associated with cancer. Abnormal EHMT2 expression is found both in haematological malignancies, as for exampleleukemia, and insolid tumors, ascolorectal cancer,lung cancer, head and neck tumours.[18]
^Rual JF, Venkatesan K, Hao T, Hirozane-Kishikawa T, Dricot A, Li N, Berriz GF, Gibbons FD, Dreze M, Ayivi-Guedehoussou N, Klitgord N, Simon C, Boxem M, Milstein S, Rosenberg J, Goldberg DS, Zhang LV, Wong SL, Franklin G, Li S, Albala JS, Lim J, Fraughton C, Llamosas E, Cevik S, Bex C, Lamesch P, Sikorski RS, Vandenhaute J,Zoghbi HY, Smolyar A, Bosak S, Sequerra R, Doucette-Stamm L, Cusick ME, Hill DE, Roth FP, Vidal M (October 2005). "Towards a proteome-scale map of the human protein-protein interaction network".Nature.437 (7062):1173–8.Bibcode:2005Natur.437.1173R.doi:10.1038/nature04209.PMID16189514.S2CID4427026.
Brown SE, Campbell RD, Sanderson CM (December 2001). "Novel NG36/G9a gene products encoded within the human and mouse MHC class III regions".Mammalian Genome.12 (12):916–24.doi:10.1007/s00335-001-3029-3.PMID11707778.S2CID9510386.
Rual JF, Venkatesan K, Hao T, Hirozane-Kishikawa T, Dricot A, Li N, Berriz GF, Gibbons FD, Dreze M, Ayivi-Guedehoussou N, Klitgord N, Simon C, Boxem M, Milstein S, Rosenberg J, Goldberg DS, Zhang LV, Wong SL, Franklin G, Li S, Albala JS, Lim J, Fraughton C, Llamosas E, Cevik S, Bex C, Lamesch P, Sikorski RS, Vandenhaute J, Zoghbi HY, Smolyar A, Bosak S, Sequerra R, Doucette-Stamm L, Cusick ME, Hill DE, Roth FP, Vidal M (October 2005). "Towards a proteome-scale map of the human protein-protein interaction network".Nature.437 (7062):1173–8.Bibcode:2005Natur.437.1173R.doi:10.1038/nature04209.PMID16189514.S2CID4427026.
Beausoleil SA, Villén J, Gerber SA, Rush J, Gygi SP (October 2006). "A probability-based approach for high-throughput protein phosphorylation analysis and site localization".Nature Biotechnology.24 (10):1285–92.doi:10.1038/nbt1240.PMID16964243.S2CID14294292.
