Abstract
Multiple signaling pathways converge on the transcription factor NF-κB, which results in the expression of a range of genes. One of the upstream kinases that can activate NF-κB is NF-κB-inducing kinase (NIK), an enzyme that has been implicated in the selective gene expression in response to discrete signals received at the cell surface. Yin et al. (p. 2162) studied cytokine-induced transcriptional activity of NF-κB in mice carrying a targeted disruption of the NIK locus and observed the selective loss of transcription, but not NF-κB-DNA binding, in response to signals delivered through the lymphotoxin-β receptor (LTβR). This effect, which was not seen in response to related cytokines, namely tumor necrosis factor and interleukin-1, correlated directly with disruption to the development of lymphoid tissue already reported in mice deficient in LTβR. L. Yin, L. Wu, H. Wesche, C. D. Arthur, J. M. White, D. V. Goeddel, R. D. Schreiber, Defective lymphotoxin-β receptor-induced NF-κB transcriptional activity in NIK-deficient mice. Science 291 , 2162-2165 (2001). [Abstract] [Full Text]
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