The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

Nfil3  -  nuclear factor, interleukin 3, regulated

Mus musculus

Synonyms: AV225605, E4 promoter-binding protein 4, E4BP4, E4bp4, Embryo implantation-related NFIL3/E4BP4-like transcription factor, ...
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Nfil3


High impact information on Nfil3


Biological context of Nfil3


Anatomical context of Nfil3

  • Adenovirus E4 promoter-binding protein/nuclear factor regulated by IL-3 (E4BP4/NFIL3), a transcriptional repressor, is a PTH-induced primary response gene in primary mouse osteoblasts (MOBs) [5].

Regulatory relationships of Nfil3

  • One unknown gene (designated Fig1 for IL-Four Induced Gene 1) and one gene with homology to the human transcription factor E4BP4 were confirmed by Northern blot analysis to be induced 10-20-fold by IL-4 treatment [6].

Other interactions of Nfil3

  • Further analysis of the cis-regulatory regions of downregulated genes revealed that transcription suppressors, BCL6 and E4BP4, were probable candidates that mediated the inhibitory effect of NHE1 null mutation [7].

Analytical, diagnostic and therapeutic context of Nfil3

  • Northern blot analysis showed that Nfil3/E4bp4 is regulated as a "delayed-early" IL-3-responsive gene, requiring de novo protein synthesis [8].


  1. Inducibility of E4BP4 suggests a novel mechanism of negative gene regulation by glucocorticoids. Wallace, A.D., Wheeler, T.T., Young, D.A. Biochem. Biophys. Res. Commun. (1997) [Pubmed]
  2. Antagonistic role of E4BP4 and PAR proteins in the circadian oscillatory mechanism. Mitsui, S., Yamaguchi, S., Matsuo, T., Ishida, Y., Okamura, H. Genes Dev. (2001) [Pubmed]
  3. Two distinct interleukin-3-mediated signal pathways, Ras-NFIL3 (E4BP4) and Bcl-xL, regulate the survival of murine pro-B lymphocytes. Kuribara, R., Kinoshita, T., Miyajima, A., Shinjyo, T., Yoshihara, T., Inukai, T., Ozawa, K., Look, A.T., Inaba, T. Mol. Cell. Biol. (1999) [Pubmed]
  4. Calcium-dependent activation of nuclear factor regulated by interleukin 3/adenovirus E4 promoter-binding protein gene expression by calcineurin/nuclear factor of activated T cells and calcium/calmodulin-dependent protein kinase signaling. Nishimura, Y., Tanaka, T. J. Biol. Chem. (2001) [Pubmed]
  5. Parathyroid hormone induces E4bp4 messenger ribonucleic acid expression primarily through cyclic adenosine 3',5'-monophosphate signaling in osteoblasts. Ozkurt, I.C., Pirih, F.Q., Tetradis, S. Endocrinology (2004) [Pubmed]
  6. Expressed genes in interleukin-4 treated B cells identified by cDNA representational difference analysis. Chu, C.C., Paul, W.E. Mol. Immunol. (1998) [Pubmed]
  7. Na+/H+ exchanger 1 deficiency alters gene expression in mouse brain. Zhou, D., Xue, J., Gavrialov, O., Haddad, G.G. Physiol. Genomics (2004) [Pubmed]
  8. Pivotal role for the NFIL3/E4BP4 transcription factor in interleukin 3-mediated survival of pro-B lymphocytes. Ikushima, S., Inukai, T., Inaba, T., Nimer, S.D., Cleveland, J.L., Look, A.T. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
WikiGenes - Universities