ArticleJournal of virology2001
Activation of membrane fusion by murine leukemia viruses is controlled in cis or in trans by interactions between the receptor-binding domain and a conserved disulfide loop of the carboxy terminus of the surface glycoprotein.
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 43 papers.
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Who cites it
43 citing papers in PubMed, 76 citations in OpenAlex.
- Unique Structure and Distinctive Properties of the Ancient and Ubiquitous Gamma-Type Envelope Glycoprotein.Viruses · 2023Review
- Deep-Time Structural Evolution of Retroviral and Filoviral Surface Envelope Proteins.Journal of virology · 2022Article
- 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
- Sequential activation of the three protomers in the Moloney murine leukemia virus Env.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Permissive XPR1 gammaretrovirus receptors in four mammalian species are functionally distinct in interference tests.Virology · 2016Article
- Role of Cysteines in Stabilizing the Randomized Receptor Binding Domains within Feline Leukemia Virus Envelope Proteins.Journal of virology · 2015Article
- Furin cleavage of the Moloney murine leukemia virus Env precursor reorganizes the spike structure.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Maturation cleavage of the murine leukemia virus Env precursor separates the transmembrane subunits to prime it for receptor triggering.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Regulation of cell proliferation and cell density by the inorganic phosphate transporter PiT1.Cell division · 2012Article
- The receptors for gibbon ape leukemia virus and amphotropic murine leukemia virus are not downregulated in productively infected cells.Retrovirology · 2011Article
- Naturally Occurring Polymorphisms of the Mouse Gammaretrovirus Receptors CAT-1 and XPR1 Alter Virus Tropism and Pathogenicity.Advances in virology · 2011Article
- Infection of XC cells by MLVs and Ebola virus is endosome-dependent but acidification-independent.PloS one · 2011Article
- Misfolding of CasBrE SU is reversed by interactions with 4070A Env: implications for gammaretroviral neuropathogenesis.Retrovirology · 2010Article
- Mifepristone increases gamma-retroviral infection efficiency by enhancing the integration of virus into the genome of infected cells.Gene therapy · 2010Article
- Turning of the receptor-binding domains opens up the murine leukaemia virus Env for membrane fusion.The EMBO journal · 2008Article
- Identification of residues outside of the receptor binding domain that influence the infectivity and tropism of porcine endogenous retrovirus.Journal of virology · 2008Article
- Intersubunit disulfide isomerization controls membrane fusion of human T-cell leukemia virus Env.Journal of virology · 2008Article
- Characterization of fusion determinants points to the involvement of three discrete regions of both E1 and E2 glycoproteins in the membrane fusion process of hepatitis C virus.Journal of virology · 2007Article
- Molecular gymnastics at the herpesvirus surface.EMBO reports · 2006Review
- Linkage of reduced receptor affinity and superinfection to pathogenesis of TR1.3 murine leukemia virus.Journal of virology · 2006Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell entry of retroviruses is initiated by the recognition of cellular receptors and the subsequent membrane fusion between viral and cellular membranes. These two steps are mediated by the surface (SU) and transmembrane (TM) subunits of the retroviral envelope glycoprotein (Env), respectively. Determinants regulating membrane fusion have been described throughout SU and TM, but the processes coupling receptor recognition to fusion are still elusive. Here we establish that a critical interaction is formed between the receptor-binding domain (RBD) and the major disulfide loop of the carboxy-terminal domain (C domain) of the murine leukemia virus SU. Receptor binding causes an alteration of this interaction and, in turn, promotes further events of Env fusion activation. We characterize mutations which, by lowering this interaction and reducing the compatibility between the RBD and C domains of Env glycoprotein chimeras, affect both Env fusogenicity and sensitivity to receptor interference. Additionally, we demonstrate that suboptimal interactions in such mutant Env proteins can be compensated in trans by soluble RBDs in a manner that depends on their compatibility with the C domain. Our results therefore indicate that RBD/C domain interactions may occur in cis, via the proper RBD of the viral Env itself, or in trans, via a distinct RBD expressed by virion-free Env glycoproteins expressed endogenously by the infected cells or provided by neighboring Env trimers.
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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.