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

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