NFIL3

NFIL3

A gene on chromosome 9q22 that encodes a transcription regulator that binds to regulatory regions of genes, usually upstream of a transcription start site, primarily downregulating transcription from promoters with activating transcription factor (ATF) sites. NFIL3 is thought to repress promoter activity in osteoblasts, transcription of PER1, and of PER2 via the promoter’s B-site. It activates transcription from the interleukin-3 promoter in T-cells, competes with PAR DNA-binding factors (DBP) HLF and TEF for the consensus-binding site, acts as a negative regulator for the circadian expression of PER2 oscillation in the cell-autonomous clock and protects pro-B cells from apoptosis.
References in periodicals archive ?
Specifically, E2 treatment upregulated interleukin 3-regulated nuclear factor (NFIL3, GeneID 4783), nuclear receptor subfamily 1 group D member 1 (NR1D1, GeneID 9572), nuclear receptor subfamily 4 group A member 1 (NR4A1, GeneID 3164), while downregulated nuclear receptor subfamily 1 group I member 2 (NR1I2, GeneID 8856).
Moreover, MEL directly interferes with the differentiation of T cells, inducing the expression of the repressor transcription factor Nfil3, blocking the differentiation of pathogenic Th17 cells and boosting the generation of protective Tr1 cells via Erk1/2 and the transactivation of the IL-10 promoter by ROR-[alpha] [33]; MEL inhibits also demyelination and increases remyelination [34].
The three genes with the largest change in expression were peroxisome proliferator activator receptor delta (Ppard), interleukin-3 regulated nuclear factor (Nfil3), and nuclear receptor subfamily 1, group D, member 2 (Nr1d2); all of them are also linked with circadian rhythms [42].
Using a mouse model, the researchers identified a gene called Nfil3, which guides the development of the TH17 cells that patrol mucosal surfaces like the intestinal lining and protect against bacterial and fungal infections.
Recently, E4BP4 (NFIL3), a basic leucine zipper transcription factor, which was first recognized for its importance in NK cell development [116, 117], has been implicated in [CD8.sup.+] DC development.
This effect requires the IL-27-mediated induction of the nuclear factor, interleukin 3 regulated (NFIL3), which mediates Tim-3 expression in vivo.
Markey et al., "CD8[[alpha].sup.+] DCs can be induced in the absence of transcription factors Id2, Nfil3, and Batf3," Blood, vol.
In particular, studies in mice demonstrated the requirement of NFIL3 and Tbx21 (the gene encoding T-bet) for their development, while RORc (the gene encoding ROR[gamma]t) and aryl hydrocarbon receptor (AhR) were dispensable [17].