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Giehler, F. ; Ostertag, M.S. ; Sommermann, T.* ; Weidl, D.* ; Sterz, K. ; Kutz, H. ; Moosmann, A. ; Feller, S.M.* ; Geerlof, A. ; Biesinger, B.* ; Popowicz, G.M. ; Kirchmair, J.* ; Kieser, A.

Epstein-Barr virus-driven B cell lymphoma mediated by a direct LMP1-TRAF6 complex.

Nat. Commun. 15:414 (2024)
Verlagsversion Forschungsdaten DOI PMC
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Creative Commons Lizenzvertrag
Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) drives viral B cell transformation and oncogenesis. LMP1’s transforming activity depends on its C-terminal activation region 2 (CTAR2), which induces NF-κB and JNK by engaging TNF receptor-associated factor 6 (TRAF6). The mechanism of TRAF6 recruitment to LMP1 and its role in LMP1 signalling remains elusive. Here we demonstrate that TRAF6 interacts directly with a viral TRAF6 binding motif within CTAR2. Functional and NMR studies supported by molecular modeling provide insight into the architecture of the LMP1-TRAF6 complex, which differs from that of CD40-TRAF6. The direct recruitment of TRAF6 to LMP1 is essential for NF-κB activation by CTAR2 and the survival of LMP1-driven lymphoma. Disruption of the LMP1-TRAF6 complex by inhibitory peptides interferes with the survival of EBV-transformed B cells. In this work, we identify LMP1-TRAF6 as a critical virus-host interface and validate this interaction as a potential therapeutic target in EBV-associated cancer.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Nf-kappa-b; Membrane-protein 1; Receptor-associated Factor-3; Terminal Kinase Pathway; Latent Membrane-protein-1; Binding-site; Traf-binding; Growth Transformation; Signal-transduction; Critical Regulator
Sprache englisch
Veröffentlichungsjahr 2024
HGF-Berichtsjahr 2024
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 15, Heft: 1, Seiten: , Artikelnummer: 414 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Research Unit Signaling and Translation (SAT)
Institute of Structural Biology (STB)
Research Unit Gene Vector (AGV)
POF Topic(s) 30203 - Molecular Targets and Therapies
Forschungsfeld(er) Enabling and Novel Technologies
Immune Response and Infection
PSP-Element(e) G-509800-004
G-503000-001
G-501500-001
Förderungen Deutsches Zentrum für Infektionsforschung (German Center for Infection Research)
Deutsche Forschungsgemeinschaft (German Research Foundation)
DOI 10.1038/s41467-023-44455-w
WOS ID 001139519000001
Scopus ID 85181956718
PubMed ID 38195569
Erfassungsdatum 2024-01-16
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