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Details on Person Severe acute respiratory syndrome coronavirus type 1 (SARS-C...
| Class:Id | Summation:9704656 |
|---|---|
| _displayName | Severe acute respiratory syndrome coronavirus type 1 (SARS-C... |
| _timestamp | 2021-01-27 01:40:26 |
| created | [InstanceEdit:9704665] Shamovsky, Veronica, 2020-10-10 |
| literatureReference | [LiteratureReference:9704670] Bcl-xL inhibits T-cell apoptosis induced by expression of SARS coronavirus E protein in the absence of growth factors [LiteratureReference:9704674] Reduction and Functional Exhaustion of T Cells in Patients With Coronavirus Disease 2019 (COVID-19) [LiteratureReference:9704654] T cell responses in patients with COVID-19 |
| modified | [InstanceEdit:9704696] Shamovsky, Veronica, 2020-10-10 [InstanceEdit:9710680] Shamovsky, Veronica, 2021-01-05 [InstanceEdit:9713615] Shamovsky, Veronica, 2021-01-27 |
| text | 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). |
| (summation) | [Reaction:9704655] SARS-CoV-1 E binds BCL2L1 [Homo sapiens] |
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No pathways have been reviewed or authored by Severe acute respiratory syndrome coronavirus type 1 (SARS-C... (9704656)
