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The lymphotoxin-beta receptor induces different patterns of gene expression via two NF-kappaB pathways.

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.
AuthorsEmmanuel Dejardin, Nathalie M Droin, Mireille Delhase, Elvira Haas, Yixue Cao, Constantin Makris, Zhi-Wei Li, Michael Karin, Carl F Ware, Douglas R Green
JournalImmunity (Immunity) Vol. 17 Issue 4 Pg. 525-35 (Oct 2002) ISSN: 1074-7613 [Print] United States
PMID12387745 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
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
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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