Defective lymphotoxin-β receptor-induced NF-κB transcriptional activity in NIK-deficient mice

L. Yin, L. Wu, H. Wesche, C. D. Arthur, J. M. White, D. V. Goeddel, R. D. Schreiber

Research output: Contribution to journalArticlepeer-review

346 Scopus citations

Abstract

The role of NF-κB-inducing kinase (NIK) in cytokine signaling remains controversial. To identify the physiologic functions of NIK, we disrupted the NIK locus by gene targeting. Although NIK-/- mice displayed abnormalities in both lymphoid tissue development and antibody responses, NIK-/- cells manifested normal NF-κB DNA binding activity when treated with a variety of cytokines, including tumor necrosis factor (TNF), interleukin-1 (IL-1), and lymphotoxin-β (LTβ). However, NIK was selectively required for gene transcription induced through ligation of LTβ receptor but not TNF receptors. These results reveal that NIK regulates the transcriptional activity of NF-κB in a receptor-restricted manner.

Original languageEnglish
Pages (from-to)2162-2165
Number of pages4
JournalScience
Volume291
Issue number5511
DOIs
StatePublished - Mar 16 2001

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