ArticleJournal of virology1998
Role of variable regions A and B in receptor binding domain of amphotropic murine leukemia virus envelope protein.
Article in Journal of virology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
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- The Bipartite Sequence Motif in the N and C Termini of gp85 of Subgroup J Avian Leukosis Virus Plays a Crucial Role in Receptor Binding and Viral Entry.Journal of virology · 2020Article
- Infectious KoRV-related retroviruses circulating in Australian bats.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Hybridization capture reveals evolution and conservation across the entire Koala retrovirus genome.PloS one · 2014Article
- Article
- Cell type-specific induction and inhibition of apoptosis by Herpes Simplex virus type 2 ICP10.Journal of virology · 2009Article
- Characterizing the anti-HIV activity of papuamide A.Marine drugs · 2008Article
- Molecular and phylogenetic analyses of a new amphotropic murine leukemia virus (MuLV-1313).Virology journal · 2006Article
- Functional domains within the human immunodeficiency virus type 2 envelope protein required to enhance virus production.Journal of virology · 2005Article
- Probing sequence variation in the receptor-targeting domain of feline leukemia virus envelope proteins with peptide display libraries.Journal of virology · 2005Article
- G100R mutation within 4070A murine leukemia virus Env increases virus receptor binding, kinetics of entry, and viral transduction efficiency.Journal of virology · 2003Article
- Cytoplasmic tail of Moloney murine leukemia virus envelope protein influences the conformation of the extracellular domain: implications for mechanism of action of the R Peptide.Journal of virology · 2003Article
- Similar regulation of cell surface human T-cell leukemia virus type 1 (HTLV-1) surface binding proteins in cells highly and poorly transduced by HTLV-1-pseudotyped virions.Journal of virology · 2002Article
- Functional murine leukemia virus vectors pseudotyped with the visna virus envelope show expanded visna virus cell tropism.Journal of virology · 2001Article
- Functional characterization of the N termini of murine leukemia virus envelope proteins.Journal of virology · 2001Article
- Sequences in the cytoplasmic tail of the gibbon ape leukemia virus envelope protein that prevent its incorporation into lentivirus vectors.Journal of virology · 2001Article
- Efficient cell infection by Moloney murine leukemia virus-derived particles requires minimal amounts of envelope glycoprotein.Journal of virology · 2000Article
- Second-site changes affect viability of amphotropic/ecotropic chimeric enveloped murine leukemia viruses.Journal of virology · 2000Article
- A comprehensive approach to mapping the interacting surfaces of murine amphotropic and feline subgroup B leukemia viruses with their cell surface receptors.Journal of virology · 2000Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
For the amphotropic murine leukemia virus (MuLV), a 208-amino-acid amino-terminal fragment of the surface unit (SU) of the envelope glycoprotein is sufficient to bind to its receptor, Pit2. Within this binding domain, two hypervariable regions, VRA and VRB, have been proposed to be important for receptor recognition. In order to specifically locate residues that are important for the interaction with Pit2, we generated a number of site-specific mutations in both VRA and VRB and analyzed the resulting envelope proteins when expressed on retroviral vectors. Concurrently, we substituted portions of the amphotropic SU with homologous regions from the polytropic MuLV envelope protein. The amphotropic SU was unaffected by most of the point mutations we introduced. In addition, the deletion of eight residues in a region of VRA that was previously suggested to be essential for Pit2 utilization only decreased titer on NIH 3T3 cells by 1 order of magnitude. Although the replacement of the amino-terminal two-thirds of VRA with the polytropic sequence abolished receptor binding, smaller nonoverlapping substitutions did not affect the function of the protein. We were not able to identify a single critical receptor contact point within VRA, and we suggest that the amphotropic receptor binding domain probably makes multiple contacts with the receptor and that the loss of some of these contacts can be tolerated.
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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.