ArticleJournal of virology2006
Revealing domain structure through linker-scanning analysis of the murine leukemia virus (MuLV) RNase H and MuLV and human immunodeficiency virus type 1 integrase proteins.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 24 citations in OpenAlex.
- M-MuLV reverse transcriptase: Selected properties and improved mutants.Computational and structural biotechnology journal · 2021Review
- Disrupting MLV integrase:BET protein interaction biases integration into quiescent chromatin and delays but does not eliminate tumor activation in a MYC/Runx2 mouse model.PLoS pathogens · 2019Article
- Structural basis of suppression of host translation termination by Moloney Murine Leukemia Virus.Nature communications · 2016Article
- Structural and sequencing analysis of local target DNA recognition by MLV integrase.Nucleic acids research · 2015Article
- Altering murine leukemia virus integration through disruption of the integrase and BET protein family interaction.Nucleic acids research · 2014Article
- Molecular mechanisms of retroviral integration site selection.Nucleic acids research · 2014Article
- Structural analysis of monomeric retroviral reverse transcriptase in complex with an RNA/DNA hybrid.Nucleic acids research · 2013Article
- Crystal structure of xenotropic murine leukaemia virus-related virus (XMRV) ribonuclease H.Bioscience reports · 2012Article
- Transcription factor YY1 interacts with retroviral integrases and facilitates integration of moloney murine leukemia virus cDNA into the host chromosomes.Journal of virology · 2010Article
- Protein transduction from retroviral Gag precursors.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- HIV-1 Integrase-DNA Recognition Mechanisms.Viruses · 2009Article
- Expression artifact with retroviral vectors based on pBMN.Analytical biochemistry · 2009Article
- In vivo biotinylation and capture of HIV-1 matrix and integrase proteins.Journal of virological methods · 2009Article
- Ribonuclease H: properties, substrate specificity and roles in retroviral reverse transcription.The FEBS journal · 2009Review
- Defining the DNA substrate binding sites on HIV-1 integrase.Journal of molecular biology · 2009Article
- Murine leukemia virus reverse transcriptase: structural comparison with HIV-1 reverse transcriptase.Virus research · 2008Review
- RNase H activity: structure, specificity, and function in reverse transcription.Virus research · 2008Review
- Subunit-specific protein footprinting reveals significant structural rearrangements and a role for N-terminal Lys-14 of HIV-1 Integrase during viral DNA binding.The Journal of biological chemistry · 2008Article
- Human T-cell leukemia virus type 1 integration target sites in the human genome: comparison with those of other retroviruses.Journal of virology · 2007Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Linker-scanning libraries were generated within the 3' terminus of the Moloney murine leukemia virus (M-MuLV) pol gene encoding the connection-RNase H domains of reverse transcriptase (RT) as well as the structurally related M-MuLV and human immunodeficiency virus type 1 (HIV-1) integrase (IN) proteins. Mutations within the M-MuLV proviral vectors were Tn7 based and resulted in 15-bp insertions. Mutations within an HIV-1 IN bacterial expression vector were based on Tn5 and resulted in 57-bp insertions. The effects of the insertions were examined in vivo (M-MuLV) and in vitro (HIV-1). A total of 178 individual M-MuLV constructs were analyzed; 40 in-frame insertions within RT connection-RNase H, 108 in-frame insertions within IN, 13 insertions encoding stop codons within RNase H, and 17 insertions encoding stop codons within IN. For HIV-1 IN, 56 mutants were analyzed. In both M-MuLV and HIV-1 IN, regions are identified which functionally tolerate multiple-linker insertions. For MuLV, these correspond to the RT-IN proteolytic junction, the junction between the IN core and C terminus, and the C terminus of IN. For HIV-1 IN, in addition to the junction between the IN core and C terminus and the C terminus of IN, insertions between the N terminus and core domains maintained integration and disintegration activity. Of the 40 in-frame insertions within the M-MuLV RT connection-RNase H domains, only the three C-terminal insertions mapping to the RT-IN proteolytic junction were viable. These results correlate with deletion studies mapping the domain and subdomain boundaries of RT and IN. Importantly, these genetic footprints provide a means to identify nonessential regions within RT and IN for targeted gene therapy applications.
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