Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. STKE, 20 March 2001
Vol. 2001, Issue 74, p. tw7
[DOI: 10.1126/stke.2001.74.tw7]

EDITORS' CHOICE

Immunology Mixed Signals

Multiple signaling pathways converge on the transcription factor NF-{kappa}B, which results in the expression of a range of genes. One of the upstream kinases that can activate NF-{kappa}B is NF-{kappa}B-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-{kappa}B in mice carrying a targeted disruption of the NIK locus and observed the selective loss of transcription, but not NF-{kappa}B-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-{kappa}B transcriptional activity in NIK-deficient mice. Science 291, 2162-2165 (2001). [Abstract] [Full Text]

Citation: Mixed Signals. Sci. STKE 2001, tw7 (2001).


To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882