ArticleMedComm2021
SARS-CoV-2 spike protein harnesses SNX27-mediated endocytic recycling pathway.
Article in MedComm, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- A systematic review on impact of SARS-CoV-2 infection.Microbiological research · 2023Pooled it
- VPS26A retromer complex and SNX27 mediate stress-induced Golgi bypass of membrane proteins.Nature communications · 2026Article
- UNC0638 inhibits SARS-CoV-2 entry by blocking cathepsin L maturation.Journal of virology · 2025Article
- Sequences in the Cytoplasmic Tail Contribute to the Intracellular Trafficking and the Cell Surface Localization of SARS-CoV-2 Spike Protein.Biomolecules · 2025Review
- Antibiotics daptomycin interacts with S protein of SARS-CoV-2 to promote cell invasion of Omicron (B1.1.529) pseudovirus.Virulence · 2024Article
- FAM91A1-TBC1D23 complex structure reveals human genetic variations susceptible for PCH.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- TMED3 Complex Mediates ER Stress-Associated Secretion of CFTR, Pendrin, and SARS-CoV-2 Spike.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Inhibition of endocytic recycling of ACE2 by SARS-CoV-2 S protein partially explains multiple COVID-19 related diseases caused by ACE2 reduction.The Journal of infection · 2022Article
- ESCPE-1 mediates retrograde endosomal sorting of the SARS-CoV-2 host factor Neuropilin-1.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The emerging roles of retromer and sorting nexins in the life cycle of viruses.Virologica Sinica · 2022Review
- Endomembrane remodeling in SARS-CoV-2 infection.Cell insight · 2022Review
- Review
- The molecular mechanism of SARS-CoV-2 evading host antiviral innate immunity.Virology journal · 2022Review
- Cytoplasmic tail determines the membrane trafficking and localization of SARS-CoV-2 spike protein.Frontiers in molecular biosciences · 2022Review
- Article
- PDZ-Containing Proteins Targeted by the ACE2 Receptor.Viruses · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SARS-CoV-2 is an enveloped positive-sense RNA virus that depends on host factors for all stages of its life. Membrane receptor ACE2 is a well-established factor for SARS-CoV-2 docking. In addition to ACE2, whole-genome genetic screens have identified additional proteins, such as endosomal trafficking regulators SNX27 and retromer, as key host factors required for SARS-CoV-2 infection. However, it is poorly understood how SARS-CoV-2 utilize host endocytic transport pathways to produce productive infection. Here, we report that SNX27 interacts with the SARS-CoV-2 spike (S) protein to facilitate S protein surface expression. Interestingly, S protein binds to the PDZ domain of SNX27, although it does not contain a PDZ-binding motif (PDZbm). Either abrogation of the SNX27 PDZ domain or S protein "MTSC" motif, which is critical for SNX27 binding, decreases surface expression of S protein and viral production. Collectively, our study highlights a novel approach utilized by SARS-CoV-2 to facilitate virion trafficking to establish virus infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.