ArticleRetrovirology2009
The formation of cysteine-linked dimers of BST-2/tetherin is important for inhibition of HIV-1 virus release but not for sensitivity to Vpu.
Article in Retrovirology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 1 of them a synthesis that pooled it.
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Who cites it
115 citing papers in PubMed, 1 synthesis or guideline pooled it, 159 citations in OpenAlex.
- Identifying potential survival strategies of HIV-1 through virus-host protein interaction networks.BMC systems biology · 2010Pooled it
- Label-free proteomics and single-cell mass cytometry analysis of 5 immune tissues from mice with artesunate administration reveal immunosuppression of artesunate via BST2 and MDSCs.Fundamental research · 2026Article
- Bone Marrow Stromal Cell Antigen 2 Promotes Esophageal Squamous Cell Carcinoma Progression by Mediating the Cell-Cell Interaction between Cancer Cells and Cancer-Associated Fibroblasts.The American journal of pathology · 2026Article
- cGAS-STING Pathway-Induced BST2 Enhances HPV-Infected Keratinocyte Proliferation in Condyloma Acuminata.Biomedicines · 2026Article
- Emerging Oncogenic and Immunoregulatory Roles of BST2 in Human Cancers.Biomedicines · 2026Review
- Article
- Bone marrow stromal cell antigen 2: Tumor biology, signaling pathway and therapeutic targeting (Review).Oncology reports · 2024Review
- Mutations accumulated in the Spike of SARS-CoV-2 Omicron allow for more efficient counteraction of the restriction factor BST2/Tetherin.PLoS pathogens · 2024Article
- BST2 negatively regulates porcine reproductive and respiratory syndrome virus replication by restricting the expression of viral proteins.Virus research · 2023Article
- ATG5 selectively engages virus-tethered BST2/tetherin in an LC3C-associated pathway.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Evaluation of SARS-CoV-2 ORF7a Deletions from COVID-19-Positive Individuals and Its Impact on Virus Spread in Cell Culture.Viruses · 2023Article
- Human BST2 inhibits rabies virus release independently of cysteine-linked dimerization and asparagine-linked glycosylation.PloS one · 2023Article
- Unique Evolution of Antiviral Tetherin in Bats.Journal of virology · 2022Article
- Distinct Molecular Mechanisms Characterizing Pathogenesis of SARS-CoV-2.Journal of microbiology and biotechnology · 2022Review
- BST2 Suppresses LINE-1 Retrotransposition by Reducing the Promoter Activity of LINE-1 5' UTR.Journal of virology · 2022Article
- Multi-functional BST2/tetherin against HIV-1, other viruses and LINE-1.Frontiers in cellular and infection microbiology · 2022Review
- Review
- Zn-Induced Interactions Between SARS-CoV-2 orf7a and BST2/Tetherin.ChemistryOpen · 2021Article
- Antiviral Activity and Adaptive Evolution of Avian Tetherins.Journal of virology · 2020Article
- The viral protein U (Vpu)-interacting host protein ATP6V0C down-regulates cell-surface expression of tetherin and thereby contributes to HIV-1 release.The Journal of biological chemistry · 2020Article
55 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe Human Immunodeficiency virus type 1 (HIV-1) Vpu protein enhances virus release from infected cells and induces proteasomal degradation of CD4. Recent work identified BST-2/CD317 as a host factor that inhibits HIV-1 virus release in a Vpu sensitive manner. A current working model proposes that BST-2 inhibits virus release by tethering viral particles to the cell surface thereby triggering their subsequent endocytosis.
resultsHere we defined structural properties of BST-2 required for inhibition of virus release and for sensitivity to Vpu. We found that BST-2 is modified by N-linked glycosylation at two sites in the extracellular domain. However, N-linked glycosylation was not important for inhibition of HIV-1 virus release nor did it affect surface expression or sensitivity to Vpu. Rodent BST-2 was previously found to form cysteine-linked dimers. Analysis of single, double, or triple cysteine mutants revealed that any one of three cysteine residues present in the BST-2 extracellular domain was sufficient for BST-2 dimerization, for inhibition of virus release, and sensitivity to Vpu. In contrast, BST-2 lacking all three cysteines in its ectodomain was unable to inhibit release of wild type or Vpu-deficient HIV-1 virions. This defect was not caused by a gross defect in BST-2 trafficking as the mutant protein was expressed at the cell surface of transfected 293T cells and was down-modulated by Vpu similar to wild type BST-2.
conclusionWhile BST-2 glycosylation was functionally irrelevant, formation of cysteine-linked dimers appeared to be important for inhibition of virus release. However lack of dimerization did not prevent surface expression or Vpu sensitivity of BST-2, suggesting Vpu sensitivity and inhibition of virus release are separable properties of BST-2.
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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.