IFNG-AS1

IFNG antisense RNA 1 is a long non-coding RNA that in humans is encoded by the IFNG-AS1 gene.^[3] It is a positive regulator of interferon gamma in T and NK cells.^[4]

IFNG-AS1
Identifiers
Aliases	IFNG-AS1, GS1-410F4.2, Tmevpg1, NEST, IFNG antisense RNA 1
External IDs	GeneCards: IFNG-AS1; OMA:IFNG-AS1 - orthologs
Gene location (Human) Chr. Chromosome 12 (human)[1] Band 12q15 Start 67,989,445 bp[1] End 68,234,686 bp[1]
RNA expression pattern Bgee Human Mouse (ortholog) Top expressed in bone marrow cells testicle lymph node epithelium of colon tonsil appendix sural nerve granulocyte urinary bladder skeletal muscle tissue n/a More reference expression data BioGPS n/a
Orthologs Species Human Mouse Entrez 100885789 n/a Ensembl ENSG00000255733 n/a UniProt n a n/a RefSeq (mRNA) n/a n/a RefSeq (protein) n/a n/a Location (UCSC) Chr 12: 67.99 – 68.23 Mb n/a PubMed search [2] n/a
Wikidata
View/Edit Human

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]