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Details on Person Coimmunoprecipitation experiments showed that TNF receptor-a...
| Class:Id | Summation:9729610 |
|---|---|
| _displayName | Coimmunoprecipitation experiments showed that TNF receptor-a... |
| _timestamp | 2021-05-07 14:02:50 |
| created | [InstanceEdit:9729613] Shamovsky, Veronica, 2021-05-03 |
| literatureReference | [LiteratureReference:9729608] TRAF3IP3, a novel autophagy up-regulated gene, is involved in marginal zone B lymphocyte development and survival [LiteratureReference:9729634] T cell development involves TRAF3IP3-mediated ERK signaling in the Golgi [LiteratureReference:9729630] TRAF3IP3 mediates the recruitment of TRAF3 to MAVS for antiviral innate immunity [LiteratureReference:9729625] T3JAM, a novel protein that specifically interacts with TRAF3 and promotes the activation of JNK(1) [LiteratureReference:9729618] TRAF3-interacting JNK-activating modulator promotes inflammation by stimulating translocation of Toll-like receptor 4 to lipid rafts [LiteratureReference:9729647] TRAF3IP3 negatively regulates cytosolic RNA induced anti-viral signaling by promoting TBK1 K48 ubiquitination |
| modified | [InstanceEdit:9730422] Shamovsky, Veronica, 2021-05-07 |
| text | Coimmunoprecipitation experiments showed that TNF receptor-associated factor 3 (TRAF3) associates with TRAF3-interacting JNK-activating modulator (TRAF3IP3, T3JAM) upon coexpression in human embryonic kidney 293T (HEK293T) cells (Dadgostar H et al. 2003; Zhu W et al. 2019; Deng M et al. 2020). Mutagenesis analysis revealed that the isoleucine zipper domain of TRAF3 mediates interaction with the coiled‐coil domain of TRAF3IP3 (Dadgostar H et al. 2003). TRAF3IP3 is required for T and B cell development (Zou Q et al. 2015; Peng S et al. 2015) and also modulates the pathogen sensing pathways in innate immunity (Li Y et al. 2019; Deng M et al. 2020). TRAF3IP3 localizes predominantly to the membranous fraction of cells (Dadgostar H et al. 2003; Zhu W et al. 2019). Upon coexpression in HEK293T cells, TRAF3IP3 altered the localization of TRAF3 to the insoluble fraction of cell lysates and promoted the activation of Jun N‐terminal kinase (JNK) (Dadgostar H et al. 2003). Further, TRAF3IP3 was found to mediate TRAF3 recruitment to mitochondrial antiviral-signaling protein (MAVS) upon virus infection (Zhu W et al. 2019). TRAF3 binding to MAVS is an essential step in DDX58 (RIG-1):MAVS dependent type I interferon (IFN) production. Traf3ip3‐deficient mice demonstrated attenuated IFN production and were vulnerable to RNA virus infection suggesting that TRAF3IP3 contributes to antiviral innate immune signaling (Zhu W et al. 2019). Similarly, TRAF3IP3 associated with Toll-like receptor 4 (TLR4) and promoted TLR4 translocation to lipid rafts in LPS-stimulated human (THP-1) and mouse macrophage thus enhancing the TLR4 signaling pathway (Li Y et al. 2019). However, TRAF3IP3 was also found to suppress type I IFN production upon overexpression in HEK293T cells in response to cytosolic poly(I:C), 5’ppp-dsRNA, and vesicular stomatitis virus (VSV) which are sensed by DDX58 and IFIH1 to induce MAVS-dependent signaling (Deng M et al. 2020). This Reactome event shows the interaction between TRAF3 and TRAF3IP3. Function of TRAF3IP3 f in innate immunity remains unclear. |
| (summation) | [Reaction:9729654] TRAF3IP3 binds TRAF3 [Homo sapiens] |
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