SARS-CoV-1 3a binds the lysosomal membrane

Stable Identifier
R-HSA-9686338
Type
Reaction [omitted]
Species
Homo sapiens
Related Species
Human SARS coronavirus
Compartment
ReviewStatus
5/5
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Severe acute respiratory syndrome-associated coronavirus type 1 (SARS-CoV-1) open reading frame-3a has been implicated in host cell death pathways. Receptor interacting serine/threonine protein kinase 3 (RIPK3) was found to induce oligomerization of SARS-CoV-1 3a after co-transfection of viral 3a and RIPK3 in human embryonic kidney 293 (HEK293) that do not express endogenous RIPK3 or MLKL (Yue Y et al. 2018). Confocal imaging showed that co-expressed SARS-CoV-1 3a and RIPK3 co-localized with lysosomal-associated membrane protein 1 (LAMP1) in HeLa cells (Yue Y et al. 2018). Quantification of colocalization revealed that 3a likely targets RIPK3 to lysosomes. Further, a lysosomal galectin puncta assay showed that SARS-CoV-1 3a caused lysosomal membrane permeabilization. In addition, the SARS-CoV-1 3a-mediated release of cathepsins from lysosomes in HEK293 cells (Yue Y et al. 2018). Thus, RIPK3 is thought to induce oligomerization of SARS-CoV-1 3a, which facilitates membrane insertion and ion channel functionality of SARS-CoV-1 3a (Yue Y et al. 2018).
Literature References
PubMed ID Title Journal Year
30185776 SARS-Coronavirus Open Reading Frame-3a drives multimodal necrotic cell death

Shi, CS, Hwang, IY, Kehrl, JH, Xiao, X, Kamenyeva, O, Nabar, NR, Yue, Y, Wang, M

Cell Death Dis 2018
Participants
Participates
Disease
Name Identifier Synonyms
severe acute respiratory syndrome DOID:2945 SARS-CoV infection, SARS
Authored
Reviewed
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