کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5916320 1570720 2016 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
14-3-3-zeta participates in TLR3-mediated TICAM-1 signal-platform formation
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شناسی مولکولی
پیش نمایش صفحه اول مقاله
14-3-3-zeta participates in TLR3-mediated TICAM-1 signal-platform formation
چکیده انگلیسی


- 14-3-3-zeta is a component of TICAM-1 signalosome.
- TLR3-TICAM-1 pathway is reduced by 14-3-3-zeta knockdown.
- 14-3-3-zeta participates in TICAM-1 signalosome formation.

Recognition of pathogen-associated molecular patterns (PAMPs) by pattern-recognition receptors (PRRs) is important in innate immune signaling. Toll-like receptors (TLRs) are well-characterized PRRs and are pivotal in antiviral and antitumor host defense. TIR domain-containing adaptor molecule 1 (TICAM-1, also called TRIF) is an adapter molecule in TLR3- and TLR4-mediated IRF3 activation, late-phase NF-κB activation and MAPK-mediated AP-1 activation. When a TLR3 ligand is added to TLR3-positive cells, TICAM-1 transiently interacts with TLR3 and forms multimers in the cytosol. However, the precise mechanism of TICAM-1 multimer formation remains unknown. In this study, we identified 14-3-3-zeta as a molecule that functions in TLR3-mediated signaling. Knockdown of 14-3-3-zeta reduced production of type I interferon and inflammatory cytokines, nuclear translocation of IRF3 and phosphorylation of IκB via the TLR3-TICAM-1 pathway. Furthermore, TICAM-1 multimerization by ligand stimulation was prohibited by 14-3-3-zeta knockdown. These results suggest that 14-3-3-zeta is involved in the TLR3-TICAM-1 pathway in promoting multimerization of TICAM-1 for the formation of a TICAM-1 signalosome.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Immunology - Volume 73, May 2016, Pages 60-68
نویسندگان
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