NFIL3

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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.
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References in periodicals archive ?
Ishida, "A novel E4BP4 element drives circadian expression of mPeriod2," Nucleic Acids Research, vol.
(1) In mammals, circadian rhythms are driven by interlocked transcriptional-translational feedback loops (TTFLs) that involve a set of clock proteins including PER1, PER2, PER3, CRY1, CRY2, CLOCK, BMAL1, ROR[alpha], REV-ERB[alpha], and E4BP4. (2,3) The TTFL-based core clock machinery resides not only in the mammalian central pacemaker, the suprachiasmatic nucleus (SCN) of hypothalamus, but also in almost all peripheral tissues in the body.
Given the expression profiles of clock genes and clock-controlled genes such as Per1, Per2, Dbp, Bmal1, and E4bp4 showing clear circadian rhythms in DD conditions (Fig.
E4BP4. 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.
In addition to Batf3, Id2, and E4BP4, [CD8.sup.+] cDCs also require IRF-8 (ICSBP; interferon consensus-binding protein) for their development [124, 125].
Interestingly, IRF-4 mRNA expression levels were greater in E4BP4-/pre-cDCs compared to the wildtype counterparts, suggesting that E4BP4 might act by restricting the IRF4-mediated development of other DC lineages [30].
The partial restoration of a wildtype phenotype by transducing [E4BP4.sup.-/-] cells with Batf3 suggests that either E4BP4 and Batf3 have similar transcriptional targets or Batf3 is upregulated by E4BP4.
Veiga-Fernandes et al., "The basic leucine zipper transcription factor E4BP4 is essential for natural killer cell development," Nature Immunology, vol.10, no.10, pp.
London, Sep 14 (ANI): British scientists have identified the master gene, called E4bp4, that causes blood stem cells to turn into disease-fighting 'Natural Killer' (NK) immune cells.
By 'knocking out' E4bp4 in a mouse model, the researchers created the world's first animal model entirely lacking NK cells, but with all other blood cells and immune cells intact.
The gene E4bp4 is the 'master gene' for NK cell production, which means it is the primary driver that causes blood stem cells in the bone marrow to differentiate into NK cells.
Led by Dr Hugh Brady, the researchers are hoping to progress with a drug treatment for cancer patients which reacts with the protein expressed by their E4bp4 gene, causing their bodies to produce a higher number of NK cells than normal, to increase the chances of successfully destroying tumours.