SARS-CoV-1 7a binds BCL2L1

Stable Identifier
R-HSA-9704692
Type
Reaction [binding]
Species
Homo sapiens
Related Species
Human SARS coronavirus
Compartment
ReviewStatus
5/5
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Severe acute respiratory syndrome coronavirus type 1 (SARS-CoV-1) 7a protein can induce caspase-dependent apoptosis in cell lines derived from different organs, including lung, kidney and liver (Tan YJ et al. 2004; Schaecher SR et al. 2007; Tan YX et al. 2007). The induction of apoptosis by 7a was blocked by the overexpression of the Bcl-2-like protein 1 (BCL2L1, also known as BCLX, Bcl-xL), which is a prosurvival member of the Bcl-2 family (Tan YX et al. 2007). Coimmunoprecipitation experiments showed that viral 7a interacted with BCL2L1 upon co-expression in human embryonic kidney 293 (HEK293) cells and also in SARS-CoV-1-infected African green monkey kidney (Vero E6) cells. Subcellular fractionation and localization studies revealed that 7a colocalized with BCL2L1 at the endoplasmic reticulum (ER) as well as the mitochondria (Tan YX et al. 2007). The data suggest that SARS-CoV-1 7a induces pro-apoptotic signaling through interaction with anti-apoptotic BCL2L1.
Literature References
PubMed ID Title Journal Year
17428862 Induction of apoptosis by the severe acute respiratory syndrome coronavirus 7a protein is dependent on its interaction with the Bcl-XL protein

Birch, C, Lee, MJ, Catton, M, Tan, TH, Yu, VC, Tham, PY, Fu, NY, Tan, YJ, Gunalan, V, Druce, J, Tan, YX

2007
Participants
Participates
Disease
Name Identifier Synonyms
severe acute respiratory syndrome DOID:2945 SARS-CoV infection, SARS
Authored
Reviewed
Created
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