| First Author | Froese N | Year | 2006 |
| Journal | Mol Cell Biol | Volume | 26 |
| Issue | 1 | Pages | 293-302 |
| PubMed ID | 16354699 | Mgi Jnum | J:104192 |
| Mgi Id | MGI:3611500 | Doi | 10.1128/MCB.26.1.293-302.2006 |
| Citation | Froese N, et al. (2006) Innate Immune Responses in NF-{kappa}B-Repressing Factor-Deficient Mice. Mol Cell Biol 26(1):293-302 |
| abstractText | NF-kappaB-repressing factor (NRF) is a transcriptional silencer protein that specifically counteracts the basal activity of several NF-kappaB-dependent promoters by direct binding to specific neighboring DNA sequences. In cell culture experiments, the reduction of NRF mRNA leads to a derepression of beta interferon, interleukin-8, and inducible nitric oxide synthase transcription. The X chromosome-located single-copy NRF gene is ubiquitously expressed and encodes a protein of 690 amino acids. The N-terminal part contains a nuclear localization signal, the DNA-binding domain, and the NF-kappaB-repressing domain, while the C-terminal part is responsible for double-stranded RNA binding and nucleolar localization. To study the function of NRF in a systemic context, transgenic mice lacking the NRF gene were created. Against predictions from in vitro experiments, mice with a deletion of the NRF gene are viable and have a phenotype that is indistinguishable from wild-type mice, even after challenge with different pathogens. The data hint towards an unexpected functional redundancy of NRF. |
