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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
MALT1 directs B cell receptor–induced canonical nuclear factor-kappaB signaling selectively to the c-Rel subunit.
Nat. Immunol. 8, 984-991 (2007)
NF-kappaB (Rel) transcription factors control physiological and pathological immune cell function. The scaffold proteins Bcl-10 and MALT1 couple antigen-receptor signals to the canonical NF-kappaB pathway and are pivotal in lymphomagenesis. Here we found that Bcl-10 and MALT1 differentially regulated B cell receptor–induced activation of RelA and c-Rel. Bcl-10 was essential for recruitment of the kinase IKK into lipid rafts for the activation of RelA and c-Rel, for blocking apoptosis and for inducing division after B cell receptor ligation. In contrast, MALT1 participated in survival signaling but was not involved in IKK recruitment or activation and was dispensable for RelA induction and proliferation. MALT1 selectively activated c-Rel to control a distinct subprogram. Our results provide mechanistic insights into B cell receptor–induced survival and proliferation signals and demonstrate the selective control of c-Rel in the canonical NF-kappaB pathway.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Times Cited
Scopus
Cited By
Cited By
Altmetric
27.596
0.000
68
63
Anmerkungen
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Sprache
englisch
Veröffentlichungsjahr
2007
HGF-Berichtsjahr
2007
ISSN (print) / ISBN
1529-2908
e-ISSN
1529-2916
Zeitschrift
Nature Immunology
Quellenangaben
Band: 8,
Heft: 9,
Seiten: 984-991
Verlag
Nature Publishing Group
Begutachtungsstatus
Peer reviewed
Institut(e)
Research Unit Signaling and Translation (SAT)
Institute of Pathology (PATH)
Institute of Pathology (PATH)
POF Topic(s)
30203 - Molecular Targets and Therapies
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Forschungsfeld(er)
Enabling and Novel Technologies
PSP-Element(e)
G-509800-002
G-500300-001
G-500300-001
PubMed ID
17660823
DOI
10.1038/ni1493
WOS ID
000248918200022
Scopus ID
34548136086
Erfassungsdatum
2007-07-29