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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
cytosol
,
lysosomal membrane
ReviewStatus
5/5
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Disease (Homo sapiens)
Diseases of programmed cell death (Homo sapiens)
Defective RIPK1-mediated regulated necrosis (Homo sapiens)
Microbial modulation of RIPK1-mediated regulated necrosis (Homo sapiens)
SARS-CoV-1 3a binds the lysosomal membrane (Homo sapiens)
Infectious disease (Homo sapiens)
Viral Infection Pathways (Homo sapiens)
SARS-CoV Infections (Homo sapiens)
SARS-CoV-1 Infection (Homo sapiens)
SARS-CoV-1-host interactions (Homo sapiens)
SARS-CoV-1-mediated effects on programmed cell death (Homo sapiens)
SARS-CoV-1 3a binds the lysosomal membrane (Homo sapiens)
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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
Input
3a tetramer:(RIPK1:RIPK3) oligomer [cytosol]
(Homo sapiens)
Output
3a tetramer:(RIPK1:RIPK3) oligomer [lysosomal membrane]
(Homo sapiens)
Participates
as an event of
Microbial modulation of RIPK1-mediated regulated necrosis (Homo sapiens)
SARS-CoV-1-mediated effects on programmed cell death (Homo sapiens)
Disease
Name
Identifier
Synonyms
severe acute respiratory syndrome
DOID:2945
SARS-CoV infection, SARS
Authored
Shamovsky, V (2020-05-21)
Reviewed
Murphy, JM (2020-08-28)
D'Eustachio, P (2020-06-26)
Created
Shamovsky, V (2020-04-30)
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