Abstract |
The lymphotoxin-beta receptor (LTbetaR) plays critical roles in inflammation and lymphoid organogenesis through activation of NF-kappaB. In addition to activation of the classical NF-kappaB, ligation of this receptor induces the processing of the cytosolic NF-kappaB2/p100 precursor to yield the mature p52 subunit, followed by translocation of p52 to the nucleus. This activation of NF-kappaB2 requires NIK and IKKalpha, while NEMO/IKKgamma is dispensable for p100 processing. IKKbeta-dependent activation of canonical NF-kappaB is required for the expression but not processing of p100 and for the expression of proinflammatory molecules including VCAM-1, MIP-1beta, and MIP-2 in response to LTbetaR ligation. In contrast, IKKalpha controls the induction by LTbetaR ligation of chemokines and cytokines involved in lymphoid organogenesis, including SLC, BLC, ELC, SDF1, and BAFF.
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Authors | Emmanuel Dejardin, Nathalie M Droin, Mireille Delhase, Elvira Haas, Yixue Cao, Constantin Makris, Zhi-Wei Li, Michael Karin, Carl F Ware, Douglas R Green |
Journal | Immunity
(Immunity)
Vol. 17
Issue 4
Pg. 525-35
(Oct 2002)
ISSN: 1074-7613 [Print] United States |
PMID | 12387745
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- LTBR protein, human
- Ltbr protein, mouse
- Lymphotoxin beta Receptor
- NF-kappa B
- NF-kappa B p52 Subunit
- Receptors, Tumor Necrosis Factor
- Protein Serine-Threonine Kinases
- CHUK protein, human
- Chuk protein, mouse
- I-kappa B Kinase
- IKBKB protein, human
- IKBKE protein, human
- Ikbkb protein, mouse
- Ikbke protein, mouse
- NF-kappa B kinase
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Topics |
- Active Transport, Cell Nucleus
- Animals
- Cell Line
- Gene Expression Regulation
- Humans
- I-kappa B Kinase
- Lymphotoxin beta Receptor
- Mice
- Mice, Knockout
- Mice, Transgenic
- Models, Biological
- NF-kappa B
(metabolism)
- NF-kappa B p52 Subunit
- Phosphorylation
- Protein Processing, Post-Translational
- Protein Serine-Threonine Kinases
(deficiency, genetics, metabolism)
- Receptors, Tumor Necrosis Factor
(deficiency, genetics, metabolism)
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