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Open Access Green as soon as Postprint is submitted to ZB.
The IkappaB kinase complex and NF-kappaB act as master regulators of lipopolysaccharide-induced gene expression and control subordinate activation of AP-1.
Mol. Cell. Biol. 24, 6488-6500 (2004)
Toll-like receptors (TLRs) recognize conserved products of microbial pathogens to initiate the innate immune response. TLR4 signaling is triggered upon binding of lipopolysaccharides (LPS) from gram-negative bacteria. Using comparative gene expression profiling, we demonstrate a master regulatory role of IkappaB kinase (IKK)/NF-kappaB signaling for immediate-early gene induction after LPS engagement in precursor B cells. IKK/NF-kappaB signaling controls a large panel of gene products associated with signaling and transcriptional activation and repression. Intriguingly, the induction of AP-1 activity by LPS in precursor B cells and primary dendritic cells fully depends on the IKK/NF-kappaB pathway, which promotes expression of several AP-1 family members, including JunB, JunD, and B-ATF. In pre-B cells, AP-1 augments induction of a subset of primary NF-kappaB targets, as shown for chemokine receptor 7 (CCR7) and immunoglobulin kappa light chain. Thus, our data illustrate that NF-kappaB orchestrates immediate-early effects of LPS signaling and controls secondary AP-1 activation to mount an appropriate biological response.
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Publication type
Article: Journal article
Document type
Scientific Article
ISSN (print) / ISBN
0270-7306
e-ISSN
1098-5549
Journal
Molecular and Cellular Biology
Quellenangaben
Volume: 24,
Issue: 14,
Pages: 6488-6500
Publisher
American Society for Microbiology (ASM)
Reviewing status
Peer reviewed
Institute(s)
Research Unit Cellular Signal Integration (TOX-AZS)