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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Innate immune responses in NF-kappaB-repressing factor-deficient mice.

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.[1]

References

  1. Innate immune responses in NF-kappaB-repressing factor-deficient mice. Froese, N., Schwarzer, M., Niedick, I., Frischmann, U., Köster, M., Kröger, A., Mueller, P.P., Nourbakhsh, M., Pasche, B., Reimann, J., Staeheli, P., Hauser, H. Mol. Cell. Biol. (2006) [Pubmed]
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