Literature DB >> 11251123

Defective lymphotoxin-beta receptor-induced NF-kappaB transcriptional activity in NIK-deficient mice.

L Yin1, L Wu, H Wesche, C D Arthur, J M White, D V Goeddel, R D Schreiber.   

Abstract

The role of NF-kappaB-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-kappaB DNA binding activity when treated with a variety of cytokines, including tumor necrosis factor (TNF), interleukin-1 (IL-1), and lymphotoxin-beta (LTbeta). However, NIK was selectively required for gene transcription induced through ligation of LTbeta receptor but not TNF receptors. These results reveal that NIK regulates the transcriptional activity of NF-kappaB in a receptor-restricted manner.

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Year:  2001        PMID: 11251123     DOI: 10.1126/science.1058453

Source DB:  PubMed          Journal:  Science        ISSN: 0036-8075            Impact factor:   47.728


  136 in total

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