Report

Defective Lymphotoxin-β Receptor-Induced NF-κB Transcriptional Activity in NIK-Deficient Mice

See allHide authors and affiliations

Science  16 Mar 2001:
Vol. 291, Issue 5511, pp. 2162-2165
DOI: 10.1126/science.1058453

You are currently viewing the abstract.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

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.

  • * To whom correspondence should be addressed. E-mail: schreiber{at}immunology.wustl.edu

View Full Text