Lineage-Restricted Function of Nuclear Factor κB–Inducing Kinase (Nik) in Transducing Signals via Cd40

CD40 signaling in B cells and dendritic cells (DCs) is critical for the development of humoral and cell-mediated immunity, respectively. Nuclear factor κB (NF-κB)–inducing kinase (NIK) has been implicated as a central transducing kinase in CD40-dependent activation. Here, we show that although NIK i...

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Main Authors: Garceau, Norman, Kosaka, Yoko, Masters, Sally, Hambor, John, Shinkura, Reiko, Honjo, Tasuku, Noelle, Randolph J.
Format: Online
Language:English
Published: The Rockefeller University Press 2000
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2195761/
id pubmed-2195761
recordtype oai_dc
spelling pubmed-21957612008-04-16 Lineage-Restricted Function of Nuclear Factor κB–Inducing Kinase (Nik) in Transducing Signals via Cd40 Garceau, Norman Kosaka, Yoko Masters, Sally Hambor, John Shinkura, Reiko Honjo, Tasuku Noelle, Randolph J. Brief Definitive Report CD40 signaling in B cells and dendritic cells (DCs) is critical for the development of humoral and cell-mediated immunity, respectively. Nuclear factor κB (NF-κB)–inducing kinase (NIK) has been implicated as a central transducing kinase in CD40-dependent activation. Here, we show that although NIK is essential for B cell activation, it is dispensable for activation of DCs. Such data provide compelling evidence that different intermediary kinases are used by different cellular lineages to trigger NF-κB activation via CD40. The Rockefeller University Press 2000-01-17 /pmc/articles/PMC2195761/ /pubmed/10637282 Text en © 2000 The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Garceau, Norman
Kosaka, Yoko
Masters, Sally
Hambor, John
Shinkura, Reiko
Honjo, Tasuku
Noelle, Randolph J.
spellingShingle Garceau, Norman
Kosaka, Yoko
Masters, Sally
Hambor, John
Shinkura, Reiko
Honjo, Tasuku
Noelle, Randolph J.
Lineage-Restricted Function of Nuclear Factor κB–Inducing Kinase (Nik) in Transducing Signals via Cd40
author_facet Garceau, Norman
Kosaka, Yoko
Masters, Sally
Hambor, John
Shinkura, Reiko
Honjo, Tasuku
Noelle, Randolph J.
author_sort Garceau, Norman
title Lineage-Restricted Function of Nuclear Factor κB–Inducing Kinase (Nik) in Transducing Signals via Cd40
title_short Lineage-Restricted Function of Nuclear Factor κB–Inducing Kinase (Nik) in Transducing Signals via Cd40
title_full Lineage-Restricted Function of Nuclear Factor κB–Inducing Kinase (Nik) in Transducing Signals via Cd40
title_fullStr Lineage-Restricted Function of Nuclear Factor κB–Inducing Kinase (Nik) in Transducing Signals via Cd40
title_full_unstemmed Lineage-Restricted Function of Nuclear Factor κB–Inducing Kinase (Nik) in Transducing Signals via Cd40
title_sort lineage-restricted function of nuclear factor κb–inducing kinase (nik) in transducing signals via cd40
description CD40 signaling in B cells and dendritic cells (DCs) is critical for the development of humoral and cell-mediated immunity, respectively. Nuclear factor κB (NF-κB)–inducing kinase (NIK) has been implicated as a central transducing kinase in CD40-dependent activation. Here, we show that although NIK is essential for B cell activation, it is dispensable for activation of DCs. Such data provide compelling evidence that different intermediary kinases are used by different cellular lineages to trigger NF-κB activation via CD40.
publisher The Rockefeller University Press
publishDate 2000
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2195761/
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