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Details on Person Coimmunoprecipitation experiments revealed that apoptosis-as...
| Class:Id | Summation:9712387 |
|---|---|
| _displayName | Coimmunoprecipitation experiments revealed that apoptosis-as... |
| _timestamp | 2021-01-21 00:51:15 |
| created | [InstanceEdit:9712304] Shamovsky, Veronica, 2021-01-18 |
| literatureReference | [LiteratureReference:9685266] MAVS Promotes Inflammasome Activation by Targeting ASC for K63-Linked Ubiquitination via the E3 Ligase TRAF3 [LiteratureReference:9708085] The adaptor MAVS promotes NLRP3 mitochondrial localization and inflammasome activation [LiteratureReference:9708063] The mitochondrial antiviral protein MAVS associates with NLRP3 and regulates its inflammasome activity [LiteratureReference:9685267] Severe acute respiratory syndrome coronavirus ORF3a protein activates the NLRP3 inflammasome by promoting TRAF3-dependent ubiquitination of ASC [LiteratureReference:9708857] Negative regulation of MAVS-mediated innate immune response by ASC |
| modified | [InstanceEdit:9712441] Shamovsky, Veronica, 2021-01-21 |
| text | Coimmunoprecipitation experiments revealed that apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (CARD) (ASC, also known as PYCARD) interacted with the endogenous tumor necrosis factor receptor (TNFR)-associated factor 3 (TRAF3) in human monocytic THP-1 cells (Guan K et al. 2015). Upon NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome activation, both TRAF3 and PYCARD (ASC) are recruited to the mitochondrial antiviral-signaling protein (MAVS) in mammalian cells (Subramanian N et al. 2013; Park S et al. 2013; Guan K et al. 2015; Han Y et al. 2018). TRAF3 binding to PYCARD occured in the MAVS-dependent manner (Guan K et al. 2015). The E3 ubiquitin ligase activity of TRAF3 modified PYCARD with K63-linked polyubiquitin chains (Guan K et al. 2015). Deficiency in MAVS or TRAF3 impaired PYCARD ubiquitination and cytosolic speck formation, and the subsequent inflammasome activation in THP-1 and mouse embryonic fibroblasts (MEF) cells in response to vesicular stomatitis virus (VSV) infection (Guan K et al. 2015). Ubiquitination of PYCARD at Lys174 (K174) was indispensable for inflammasome activation in VSV-infected THP-1 and human embryonic kidney HEK293T cells transfected with wild type (WT) PYCARD or PYCARD K174R mutant (Guan K et al. 2015). Further, severe acute respiratory syndrome coronavirus type 1 (SARS-CoV-1) open reading frame 3a protein is thought to facilitate TRAF3-mediated K63-linked polyubiquitination of PYCARD via a direct interaction with both TRAF3 and PYCARD (Siu KL et al. 2019). The Reactome event shows TRAF3-mediated K63-linked polyubiquitination of PYCARD at K174 within the NLRP3 inflammasome complex on the outer mitochondrial membrane. |
| (summation) | [BlackBoxEvent:9685243] TRAF3 polyubiquitinates PYCARD [Homo sapiens] |
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