Home
Deutsch
Advanced Search
Browse by ...
Publication overview
Contact persons
Help
Publ. Version/Full Text Volltext
DOI
PMC
 |
Free by publisher |
Open Access Green as soon as Postprint is submitted to ZB.
Essential role for I kappa B kinase beta in remodeling Carma1-Bcl10-Malt1 complexes upon T cell activation
Mol. Cell 23, 13-23 (2006)
Publ. Version/Full Text Volltext
DOI
PMC
T cell receptor (TCR) signaling to IKB kinase (IKK)/NFKB is controlled by PKC theta-dependent activation of the Carma1, Bcl10, and Malt1 (CBM) complex. Antigen-induced phosphorylation of BcI10 has been reported, but its physiological function is unknown. Here we show that the putative downstream kinase IKK beta is required for initial CBM complex formation. Further, upon engagement of IKK beta/Malt1/Bcl10 with Carma1, IKK beta phosphorylates Bcl10 in the C terminus and thereby interferes with Bcl10/Malt1 association and Bcl10-mediated IKK gamma ubiquitination. Mutation of the IKK beta phosphorylation sites on Bcl10 enhances expression of NF-kappa B target genes IL-2 and TNF alpha after activation of primary T cells. Thus, our data provide evidence that IKK beta serves a dual role upstream of its classical substrates, the I kappa B proteins. While being essential for triggering initial CBM complex formation, IKK beta-dependent phosphorylation of Bcl10 exhibits a negative regulatory role in T cell activation.
Altmetric
Additional Metrics?
Edit extra informations
Login
Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Molimmuno ; Signaling
ISSN (print) / ISBN
1097-2765
e-ISSN
1097-4164
Journal
Molecular Cell
Quellenangaben
Volume: 23,
Issue: 1,
Pages: 13-23
Publisher
Elsevier
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Molecular Immunology (IMI)
Research Unit Signaling and Translation (SAT)
Research Unit Molecular Immune Regulation (AMIR)
Research Unit Signaling and Translation (SAT)
Research Unit Molecular Immune Regulation (AMIR)