ArticleJournal of virology1992
Tunicamycin treatment of CHO cells abrogates multiple blocks to retrovirus infection, one of which is due to a secreted inhibitor.
Article in Journal of virology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
62 citing papers in PubMed, 101 citations in OpenAlex.
- Receptor usage of Syncytin-1: ASCT2, but not ASCT1, is a functional receptor and effector of cell fusion in the human placenta.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Identification of Copper Transporter 1 as a Receptor for Feline Endogenous Retrovirus ERV-DC14.Journal of virology · 2022Article
- Mutational analysis and glycosylation sensitivity of restrictive XPR1 gammaretrovirus receptors in six mammalian species.Virology · 2019Article
- Identification of the Receptor Used by the Ecotropic Mouse GLN Endogenous Retrovirus.Journal of virology · 2019Article
- Xenotropic Mouse Gammaretroviruses Isolated from Pre-Leukemic Tissues Include a Recombinant.Viruses · 2018Article
- Retroviral vectors: from cancer viruses to therapeutic tools.Human gene therapy · 2014Review
- The avian XPR1 gammaretrovirus receptor is under positive selection and is disabled in bird species in contact with virus-infected wild mice.Journal of virology · 2013Article
- Second site mutation in the virus envelope expands the host range of a cytopathic variant of Moloney murine leukemia virus.Virology · 2012Article
- Membrane fusion and cell entry of XMRV are pH-independent and modulated by the envelope glycoprotein's cytoplasmic tail.PloS one · 2012Article
- Feline leukemia virus infection requires a post-receptor binding envelope-dependent cellular component.Journal of virology · 2011Article
- Naturally Occurring Polymorphisms of the Mouse Gammaretrovirus Receptors CAT-1 and XPR1 Alter Virus Tropism and Pathogenicity.Advances in virology · 2011Article
- The mouse "xenotropic" gammaretroviruses and their XPR1 receptor.Retrovirology · 2010Review
- Evolution of functional and sequence variants of the mammalian XPR1 receptor for mouse xenotropic gammaretroviruses and the human-derived retrovirus XMRV.Journal of virology · 2010Article
- Six host range variants of the xenotropic/polytropic gammaretroviruses define determinants for entry in the XPR1 cell surface receptor.Retrovirology · 2009Article
- Article
- Identification of a feline leukemia virus variant that can use THTR1, FLVCR1, and FLVCR2 for infection.Journal of virology · 2009Article
- Role of receptor polymorphism and glycosylation in syncytium induction and host range variation of ecotropic mouse gammaretroviruses.Retrovirology · 2008Article
- Differential resistance to cell entry by porcine endogenous retrovirus subgroup A in rodent species.Retrovirology · 2007Article
- Isolation of genes controlling apoptosis through their effects on cell survival.Gene therapy & molecular biology · 2006Article
- Improved enzootic nasal tumor virus pseudotype packaging cell lines reveal virus entry requirements in addition to the primary receptor Hyal2.Journal of virology · 2005Article
2 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chinese hamster ovary (CHO) cells are resistant to infection by all of the major classes of murine retroviruses and are partially resistant to infection by gibbon ape leukemia virus. Treatment of CHO cells with the glycosylation inhibitor tunicamycin rendered these cells susceptible to infection by retroviral vectors with ecotropic, xenotropic, and amphotropic host ranges and increased the titer of gibbon ape leukemia virus pseudotyped vectors 10-fold. Vectors having a polytropic host range did not infect CHO cells in the presence or absence of tunicamycin, showing that the effect of tunicamycin was specific and related to the pseudotype of the vector. We present evidence for three mechanisms of resistance to infection: lack of viral receptors on CHO cells, the presence of nonfunctional receptors which can be made functional by treatment with tunicamycin, and the secretion of a protein factor that blocks retroviral infection of CHO cells. Several criteria indicate that the secreted inhibitor is not an interferon, and secretion of this factor was not detected in several other cell lines that were examined.
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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.