Query author contributions in Reactome
Reactome depends on collaboration between our curation team and outside experts to assemble and peer-review its pathway modules. The integration of ORCID within Reactome enables us to meet a key challenge with authoring, curating and reviewing biological information by incentivizing and crediting the external experts that contribute their expertise and time to the Reactome curation process. More information is available at ORCID and Reactome.
If you have an ORCID ID that is not listed on this page, please forward this information to us and we will update your Reactome pathway records.
Details on Person The NLRP3 inflammasome is activated in response to SARS-CoV-...
| Class:Id | Summation:9757098 |
|---|---|
| _displayName | The NLRP3 inflammasome is activated in response to SARS-CoV-... |
| _timestamp | 2021-12-24 20:55:01 |
| created | [InstanceEdit:9757087] Shamovsky, Veronica, 2021-10-27 |
| literatureReference | [LiteratureReference:9757092] SARS-CoV-2 N protein promotes NLRP3 inflammasome activation to induce hyperinflammation [LiteratureReference:9712367] Inflammasomes are activated in response to SARS-CoV-2 infection and are associated with COVID-19 severity in patients [LiteratureReference:9757096] Inflammasome formation in the lungs of patients with fatal COVID-19 |
| modified | [InstanceEdit:9758527] Shamovsky, Veronica, 2021-11-18 [InstanceEdit:9760735] Shamovsky, Veronica, 2021-12-24 |
| text | The NLRP3 inflammasome is activated in response to SARS-CoV-2 infection and is associated with severity and outcomes in COVID-19 patients (Rodrigues TS et al. 2021; Stefano Toldo S et al. 2021; Pan P et al. 2021). The nucleocapsid protein (N) of SARS-CoV-2 was found to induce activation of the NLRP3 inflammasome (Pan P et al. 2021). Co-immunoprecipitation (Co-IP) assays showed that N interacted with the NLRP3 protein upon co-expression in human embryonic kidney 293T (HEK293T) cells and in human lung carcinoma A549 cells (Pan P et al. 2021). The binding of N to NLRP3 enhanced the interaction between NLRP3 and PYCARD (ASC) in a dose-dependent manner. Co-IP also revealed that viral N interacted with endogenous PYCARD (ASC) in the presence of NLRP3 in phorbol 12-myristate 13-acetate (PMA)-differentiated human monocytic (THP-1) cells. Moreover, confocal microscope analyses showed that N co-localized with NLRP3 and induced PYCARD speck formation in the cytoplasm of HEK293T, A549 cells. Similarly, N promoted oligomerization of PYCARD in THP-1 cells (Pan P et al. 2021). Expression of SARS-CoV-2 N induced cleavage and secretion of interleukin (IL)-1β as well as activation of caspase-1 in THP-1cells and HEK293T cells (Pan P et al. 2021). Further, viral N induced production of proinflammatory cytokines such as IL-1β, IL-6, TNF and CCL2, in human THP-1 cells and in the lung of mice injected with adenovirus-associated virus (AAV)-based vectors expressing SARS-CoV-2 N ((Pan P et al. 2021). Overall, these data suggest that SARS-CoV-2 N binds NLRP3 to promote the assembly and activation of the NLRP3 inflammasome. |
| (summation) | [Reaction:9757097] SARS-CoV-2 N binds NLRP3 [Homo sapiens] |
| [Change default viewing format] | |
No pathways have been reviewed or authored by The NLRP3 inflammasome is activated in response to SARS-CoV-... (9757098)
