IFNG-AS1 (Tmevpg1, NeST) is encoded by a gene near the Ifng locus. Some studies have shown that IFNG-AS1 expression is dependent on T-bet. In fact, transcription of IFNG-AS1 is regulated by T-bet. The upregulation of this LncRNA could enhance the production of IFN-γ from Th1 cells by cooperation of T-bet. In the other hand, in human genomic region, there are some preserved DNase 1 hypersensitivity sites (HS) between Ifng and IFNG-AS1 which induce transcription factors such as NF-κB and ETS proto-oncogene 1 (Ets-1). T-bet could control chromatin remodeling through recruiting These HS. These hypersensitivity sites have transcriptional enhancer activity to enhance or repress transcription of either IFNG or IFNG-AS1. T-bet through this epigenetic mechanism could affect on expression of IFNG-AS1. Also IFNG-AS1 with binding to WD repeat domain 5 (WDR5), stimulates the formation of histone H3 lysine 4 (H3K4) methylation at the IFNG gene and affect on the enhancement of this gene expression. Also, the effective role of IFNG-AS1 in many protective actions, including enhancing the expression of IFN-γ in the immune response in brucellosis patients, suggest a new molecular interaction response to brucella infection.[5]
^Gheitasi R, Jourghasemi S, Pakzad I, Hosseinpour Sarmadi V, Samieipour Y, Sekawi Z, et al. (December 2019). "A potential marker in brucellosis, long non coding RNA IFNG-AS1". Molecular Biology Reports. 46 (6): 6495–6500. doi:10.1007/s11033-019-05095-w. PMID31595441.
Li H, Hao Y, Zhang D, Fu R, Liu W, Zhang X, et al. (November 2016). "Aberrant expression of long noncoding RNA TMEVPG1 in patients with primary immune thrombocytopenia". Autoimmunity. 49 (7): 496–502. doi:10.3109/08916934.2016.1167192. PMID27050808. S2CID23831262.
