PuSH - Publication Server of Helmholtz Zentrum München: Noncanonical NF-κB activation by the oncoprotein Tio occurs through a nonconserved TRAF3-binding motif.

Navigation

Home

Deutsch

Research

Advanced Search

Browse by ...

... Journal

... Publication Type

... Research Data

... Publication Year

Publication overview

Support & Contact

Contact persons

Help

Data protection

de Jong, S.J.* ; Albrecht, J.-C.* ; Giehler, F. ; Kieser, A. ; Sticht, H.* ; Biesinger, B.*

Noncanonical NF-κB activation by the oncoprotein Tio occurs through a nonconserved TRAF3-binding motif.

Sci. Signal. 6:ra27 (2013)

DOI

PMC

Open Access Green as soon as Postprint is submitted to ZB.

Abstract
Metrics
Extra information

Members of the nuclear factor B (NF-B) family of transcription factors regulate many cellular functions. Activation of NF-B signaling is commonly classified as occurring through canonical or noncanonical pathways. Most NF-B–inducing stimuli, including the viral oncoprotein Tio, lead to a concerted activation of both NF-B pathways; however, extensive crosstalk at multiple levels between these signaling cascades restricts the ability to discriminate between the canonical and the noncanonical effects. We showed that noncanonical NF-B activation by Tio depends on a distinct sequence motif that directly recruits tumor necrosis factor receptor–associated factor 3 (TRAF3). Through its TRAF3-binding motif, Tio triggered a ubiquitin-independent depletion of TRAF3 from the cytosol, which prevented TRAF3 from inhibiting signaling through the noncanonical NF-B cascade. Furthermore, the Tio-TRAF3 interaction did not affect components of the canonical NF-B signaling pathway or the expression of target genes; thus, Tio induced noncanonical NF-B independently of crosstalk with the canonical pathway. Together, these data identify a distinct molecular mechanism of noncanonical NF-B activation that should enable studies into the particular functions of this pathway.

Altmetric

Additional Metrics?

[➜Log in]

Edit extra informations Login

Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords Epstein-barr-virus ; Human T-cells ; Herpesvirus-saimiri ; Signaling Pathway ; Protein ; Receptor ; Traf3 ; Nik ; Tnf ; Transformation

ISSN (print) / ISBN 1945-0877

e-ISSN 1937-9145

Journal Science Signaling

Quellenangaben Volume: 6, Issue: 272, Article Number: ra27

Publisher American Association for the Advancement of Science (AAAS)

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) Research Unit Gene Vector (AGV)