PuSH - Publikationsserver des Helmholtz Zentrums München

Export: TXT Text RIS Endnote (RIS) BIB BibTeX
Wegener, E. ; Oeckinghaus, A.* ; Papadopoulou, N. ; Lavitas, L.* ; Schmidt-Supprian, M.* ; Ferch, U.* ; Mak, T.W.* ; Ruland, J.* ; Heissmeyer, V. ; Krappmann, D.

Essential role for I kappa B kinase beta in remodeling Carma1-Bcl10-Malt1 complexes upon T cell activation

Mol. Cell 23, 13-23 (2006)
Verlagsversion Volltext DOI PMC
Closed
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Scopus
Cited By
Altmetric
14.971
3.041
108
105
Tags
Anmerkungen
Besondere Publikation
Auf Hompepage verbergern

Zusatzinfos bearbeiten
Eigene Tags bearbeiten
Privat
Eigene Anmerkung bearbeiten
Privat
Auf Publikationslisten für
Homepage nicht anzeigen
Als besondere Publikation
markieren
Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Molimmuno ; Signaling
Sprache englisch
Veröffentlichungsjahr 2006
HGF-Berichtsjahr 2006
ISSN (print) / ISBN 1097-2765
e-ISSN 1097-4164
Zeitschrift Molecular Cell
Quellenangaben Band: 23, Heft: 1, Seiten: 13-23 Artikelnummer: , Supplement: ,
Verlag Elsevier
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Immunology (IMI)
Research Unit Signaling and Translation (SAT)
Research Unit Molecular Immune Regulation (AMIR)
POF Topic(s)
30203 - Molecular Targets and Therapies
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Forschungsfeld(er)
Enabling and Novel Technologies
Immune Response and Infection
PSP-Element(e) G-551000-001
G-509800-002
G-501792-001
PubMed ID 16818229
DOI 10.1016/j.molcel.2006.05.027
WOS ID 000239215700002
Scopus ID 33745494351
Erfassungsdatum 2006-07-07
[➜Korrektur melden]