ArticleCellular signalling2021
TRIM28 regulates SARS-CoV-2 cell entry by targeting ACE2.
Article in Cellular signalling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- TRIM28 and TRIM32: multifaceted regulators of innate immunity and antiviral defence.Immunologic research · 2026Review
- Immune transcriptomic differences in paediatric patients with SARS-CoV-2 compared to other lower respiratory tract infections.bioRxiv : the preprint server for biology · 2025Article
- KAP1 in antiviral immunity: dual roles in viral silencing and immune regulation.Frontiers in cellular and infection microbiology · 2025Review
- Multifaceted role ofMedComm · 2024Review
- Human E3 ubiquitin ligases: accelerators and brakes for SARS-CoV-2 infection.Biochemical Society transactions · 2024Review
- Genome-scale CRISPR-Cas9 screen identifies host factors as potential therapeutic targets for SARS-CoV-2 infection.iScience · 2024Article
- Exploring TRIM proteins' role in antiviral defense against influenza A virus and respiratory coronaviruses.Frontiers in cellular and infection microbiology · 2024Review
- Article
- Spontaneous cancer remission after COVID-19: insights from the pandemic and their relevance for cancer treatment.Journal of translational medicine · 2023Review
- Identification of Human Host Substrates of the SARS-CoV-2 MACS infectious diseases · 2023Article
- Comparing the expression levels of tripartite motif containing 28 in mild and severe COVID-19 infection.Virology journal · 2022Article
- Lysozyme Protects Against Severe Acute Respiratory Syndrome Coronavirus 2 Infection and Inflammation in Human Corneal Epithelial Cells.Investigative ophthalmology & visual science · 2022Article
- Human phospho-signaling networks of SARS-CoV-2 infection are rewired by population genetic variants.Molecular systems biology · 2022Article
- Post-treatment with propofol inhibits inflammatory response in LPS-induced alveolar type II epithelial cells.Experimental and therapeutic medicine · 2022Article
- Article
- KAP1/TRIM28: Transcriptional Activator and/or Repressor of Viral and Cellular Programs?Frontiers in cellular and infection microbiology · 2022Review
- SUMO: a novel target for anti-coronavirus therapy.Pathogens and global health · 2021Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of coronavirus disease 2019, it binds to angiotensin-converting enzyme 2 (ACE2) to enter into human cells. The expression level of ACE2 potentially determine the susceptibility and severity of COVID-19, it is thus of importance to understand the regulatory mechanism of ACE2 expression. Tripartite motif containing 28 (TRIM28) is known to be involved in multiple processes including antiviral restriction, endogenous retrovirus latency and immune response, it is recently reported to be co-expressed with SARS-CoV-2 receptor in type II pneumocytes; however, the roles of TRIM28 in ACE2 expression and SARS-CoV-2 cell entry remain unclear. This study showed that knockdown of TRIM28 induces ACE2 expression and increases pseudotyped SARS-CoV-2 cell entry of A549 cells and primary pulmonary alveolar epithelial cells (PAEpiCs). In a co-culture model of NK cells and lung epithelial cells, our results demonstrated that NK cells inhibit TRIM28 and promote ACE2 expression in lung epithelial cells, which was partially reversed by depletion of interleukin-2 and blocking of granzyme B in the co-culture medium. Furthermore, TRIM28 knockdown enhanced interferon-γ (IFN-γ)- induced ACE2 expression through a mechanism involving upregulating IFN-γ receptor 2 (IFNGR2) in both A549 and PAEpiCs. The upregulated ACE2 induced by TRIM28 knockdown and co-culture of NK cells was partially reversed by dexamethasone in A549 cells. Our study identified TRIM28 as a novel regulator of ACE2 expression and SARS-CoV-2 cell entry.
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