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Cited by 377

The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

Apoptosis Induced by the Toll-Like Receptor Adaptor TRIF Is Dependent on Its Receptor Interacting Protein Homotypic Interaction Motif

Open access
Kaiser, William J, Offermann, Margaret K·2005·The Journal of Immunology
DOI 10.4049/jimmunol.174.8.4942
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Abstract

TLRs detect specific molecular features of microorganisms and subsequently engage distinct signaling networks through the differential use of Toll/IL-1R (TIR)-domain-containing adapter proteins. In this study, we investigated the control of apoptosis by the TIR domain-containing adapter proteins MyD88, TIR-domain containing adapter protein (TIRAP), TIR-domain-containing adapter-inducing IFN-β (TRIF), TRIF-related adapter molecule (TRAM), and sterile α motifs and β-catenin/armadillo repeats (SARM). Upon overexpression, TRIF was the sole TIR-adapter to potently engage mammalian cell death signaling pathways. TRIF-induced cell death required caspase activity initiated by the Fas/Apo-1-associated DD protein-caspase-8 axis and was unaffected by inhibitors of the intrinsic apoptotic machinery. The proapoptotic potential of TRIF mapped to the C-terminal region that was found to harbor a receptor interacting protein (RIP) homotypic interaction motif (RHIM). TRIF physically interacted with the RHIM-containing proteins RIP1 and RIP3, and deletion and mutational analyses revealed that the RHIM in TRIF was essential for TRIF-induced apoptosis and contributed to TRIF-induced NF-κB activation. The domain that was required for induction of apoptosis could activate NF-κB but not IFN regulatory factor-3, yet the activation of NF-κB could be blocked by superrepressor IκBα without blocking apoptosis. Thus, the ability of TRIF to induce apoptosis was not dependent on its ability to activate either IFN regulatory factor-3 or NF-κB but was dependent on the presence of an intact RHIM. TRIF serves as an adaptor for both TLR3 and TLR4, receptors that are activated by dsRNA and LPS, respectively. These molecular motifs are encountered during viral and bacterial infection, and the apoptosis that occurs when TRIF is engaged represents an important host defense to limit the spread of infection.

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Cited by

Metadata

Authors
Kaiser, W. J., & Offermann, M. K.
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
2005-04
Volume
174
Issue
8
Pages
4942-4952
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
DOI
10.4049/jimmunol.174.8.4942
OpenAlex
W1588312796
Cited by
377
References
11
FWCI
6.55
Type
journal article
Language
en
Open access
bronze
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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