ArticleJournal of virology2003
Variable sensitivity to substitutions in the N-terminal heptad repeat of Mason-Pfizer monkey virus transmembrane protein.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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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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
17 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- Nucleic Acid Binding by Mason-Pfizer Monkey Virus CA Promotes Virus Assembly and Genome Packaging.Journal of virology · 2016Article
- Host and viral determinants of Mx2 antiretroviral activity.Journal of virology · 2014Article
- The G-patch domain of Mason-Pfizer monkey virus is a part of reverse transcriptase.Journal of virology · 2012Article
- The impact of altered polyprotein ratios on the assembly and infectivity of Mason-Pfizer monkey virus.Virology · 2009Article
- D-retrovirus morphogenetic switch driven by the targeting signal accessibility to Tctex-1 of dynein.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Analysis of human cell heterokaryons demonstrates that target cell restriction of cyclosporine-resistant human immunodeficiency virus type 1 mutants is genetically dominant.Journal of virology · 2007Article
- Basic residues in the Mason-Pfizer monkey virus gag matrix domain regulate intracellular trafficking and capsid-membrane interactions.Journal of virology · 2007Article
- Balancing selection and the evolution of functional polymorphism in Old World monkey TRIM5alpha.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- The betaretrovirus Mason-Pfizer monkey virus selectively excludes simian APOBEC3G from virion particles.Journal of virology · 2006Article
- Genetic variability of the envelope gene of Type D simian retrovirus-2 (SRV-2) subtypes associated with SAIDS-related retroperitoneal fibromatosis in different macaque species.Virology journal · 2006Article
- A primate virus generates transformed human cells by fusion.The Journal of cell biology · 2005Article
- The pp24 phosphoprotein of Mason-Pfizer monkey virus contributes to viral genome packaging.Retrovirology · 2005Article
- Amino acid residues in the cytoplasmic domain of the Mason-Pfizer monkey virus glycoprotein critical for its incorporation into virions.Journal of virology · 2005Article
- Activity of the Mason-Pfizer monkey virus fusion protein is modulated by single amino acids in the cytoplasmic tail.Journal of virology · 2005Article
- Role of the simian virus 5 fusion protein N-terminal coiled-coil domain in folding and promotion of membrane fusion.Journal of virology · 2005Article
- An early stage of Mason-Pfizer monkey virus budding is regulated by the hydrophobicity of the Gag matrix domain core.Journal of virology · 2004Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The transmembrane protein of Mason-Pfizer monkey virus contains two heptad repeats that are predicted to form amphipathic alpha-helices that mediate the conformational change necessary for membrane fusion. To analyze the relative sensitivity of the predicted hydrophobic face of the N-terminal heptad repeat to the insertion of uncharged, polar, and charged substitutions, mutations that introduced alanine, serine, or glutamic acid into positions 436, 443, 450, and 457 of the envelope protein were examined. Novel systems using Tat protein and the GHOST cell line were developed to test and quantitate the effects of the mutations on Env-mediated fusion and infectivity of the virus. While no single amino acid change at any of the positions interfered significantly with the synthesis, processing, or transport to the plasma membrane of glycoprotein complexes, 9 of the 12 nonconservative mutations in these residues completely abolished fusion activity and virus infectivity. Mutations in the central positions (443 and 450) of the heptad repeat region were the most detrimental to Env function, and even single alanine substitutions in these positions dramatically altered the fusogenicity of the protein. These results demonstrate that this N-terminal heptad repeat plays a critical role in Env-mediated membrane fusion and highlight the key function of central hydrophobic residues in this process and the sensitivity of all positions to charge substitutions.
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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.