SARS-CoV-1 E binds BCL2L1

Stable Identifier
R-HSA-9704655
Type
Reaction [binding]
Species
Homo sapiens
Related Species
Human SARS coronavirus
Compartment
cytosol, endoplasmic reticulum-Golgi intermediate compartment membrane
ReviewStatus
5/5
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SARS-CoV-1 E binds BCL2L1
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Severe acute respiratory syndrome coronavirus type 1 (SARS-CoV-1) E protein induced apoptosis upon expression in the human Jurkat T-cells in the absence of growth factors (Yang Y et al. 2005). Overexpressed anti-apoptotic Bcl-2-like protein 1 (BCL2L1, also known as BCLX, Bcl-xL) inhibited T-cell apoptosis induced by SARS-CoV-1. BCL2L1 was found to interact with the viral E protein via the BH3 domain of BCL2L1 and a BH3-like domain of E protein. SARS-CoV-1 E protein is thought to induce apoptosis by sequestering anti-apoptotic BCL2L1 to membranes of the endoplasmic reticulum (ER) and Golgi, where the viral E protein is located (Yang Y et al. 2005). High levels of expression of pro‑apoptotic molecules may contribute to the depletion of T lymphocytes by apoptosis, leading to the lymphopenia observed in severely affected SARS patients (Diao B et al. 2020; Chen Z & Wherry EJ 2020).
Literature References
PubMed ID Title Journal Year
16048439 Bcl-xL inhibits T-cell apoptosis induced by expression of SARS coronavirus E protein in the absence of growth factors

Yang, F, Lu, H, Wang, H, Zhang, S, Brendese, J, Yan, Y, Ng, B, Nguyen, J, Yang, XF, Yang, Y, Xiong, Z

2005
Participants
Input
Output
Participates
as an event of
Disease
Name Identifier Synonyms
severe acute respiratory syndrome DOID:2945 SARS-CoV infection, SARS
Authored
Shamovsky, V  (2020-06-25)
Reviewed
D'Eustachio, P  (2021-01-26)
Created
Shamovsky, V  (2020-10-10)
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