ArticleJournal of virology2001
CD150 (SLAM) is a receptor for measles virus but is not involved in viral contact-mediated proliferation inhibition.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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.
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Who cites it
88 citing papers in PubMed, 184 citations in OpenAlex.
- Protection against lethal canine distemper virus infection by a dual epitope-targeting synthetic antibody.Nature communications · 2026Article
- Measles virus reprograms CD4Frontiers in cell and developmental biology · 2026Article
- A splice donor variant inFrontiers in veterinary science · 2025Article
- CD150-dependent hematopoietic stem cell sensing of Brucella instructs myeloid commitment.The Journal of experimental medicine · 2023Article
- Structure and supramolecular organization of the canine distemper virus attachment glycoprotein.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- SLAM-family receptors come of age as a potential molecular target in cancer immunotherapy.Frontiers in immunology · 2023Review
- Overcoming the Barrier of the Respiratory Epithelium during Canine Distemper Virus Infection.mBio · 2022Article
- Review
- Measles immunity and immunosuppression.Current opinion in virology · 2021Review
- On invariant T cells and measles: A theory of "innate immune amnesia".PLoS pathogens · 2020Article
- Review
- Use of Acid Ceramidase and Sphingosine Kinase Inhibitors as Antiviral Compounds Against Measles Virus Infection of LymphocytesFrontiers in cell and developmental biology · 2019Article
- Contrasting Gene Expression Profiles of Monocytes and Lymphocytes From Peste-Des-Petits-Ruminants Virus Infected Goats.Frontiers in immunology · 2019Article
- Measles Virus Persistent Infection of Human Induced Pluripotent Stem Cells.Cellular reprogramming · 2018Article
- Measles vaccination: Threat from related veterinary viruses and need for continued vaccination post measles eradication.Human vaccines & immunotherapeutics · 2018Review
- Nonhuman Primate Models of Respiratory Disease: Past, Present, and Future.ILAR journal · 2017Review
- MiR-31 and miR-128 regulates poliovirus receptor-related 4 mediated measles virus infectivity in tumors.Molecular oncology · 2016Article
- Flexibility of the Head-Stalk Linker Domain of Paramyxovirus HN Glycoprotein Is Essential for Triggering Virus Fusion.Journal of virology · 2016Article
- Article
- Mapping the evolutionary trajectories of morbilliviruses: what, where and whither.Current opinion in virology · 2016Review
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Measles virus (MV) interacts with cellular receptors on the surface of peripheral blood lymphocytes (PBL) which mediate virus binding and uptake. Simultaneously, the direct contact of the viral glycoproteins with the cell surface induces a negative signal blocking progression to the S phase of the cell cycle, resulting in a pronounced proliferation inhibition. We selected a monoclonal antibody (MAb 5C6) directed to the surface of highly MV-susceptible B cells (B95a), which inhibits binding to and infection of cells with MV wild-type and vaccine strains. By screening a retroviral cDNA library from human splenocytes (ViraPort; Stratagene) with this antibody, we cloned and identified the recognized molecule as signaling lymphocytic activation molecule (SLAM; CD150), which is identical to the MV receptor recently found by H. Tatsuo et al. (Nature 406:893-897, 2000). After infection of cells, and after surface contact with MV envelope proteins, SLAM is downregulated from the cell surface of activated PBL and cell lines. Although anti-SLAM and/or anti-CD46 antibodies block virus binding, they do not interfere with the contact-mediated proliferation inhibition. In addition, the cell-type-specific expression of SLAM does not correlate with the sensitivity of cells for proliferation inhibition. The data indicate that proliferation inhibition induced by MV contact is independent of the presence or absence of the virus-binding receptors SLAM and CD46.
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What OpenQuestion holds
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.