Evidence map›Paper›PMID 27401040›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2016

Structural Determinants of Sleeping Beauty Transposase Activity.

György Abrusán, Stephen R Yant, András Szilágyi, Joseph A Marsh, Lajos Mátés, Zsuzsanna Izsvák, Orsolya Barabás, Zoltán Ivics

Abstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. A novel hyperactive variant of theMolecular therapy. Nucleic acids · 2024
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  3. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

György AbrusánMRC Human Genetics Unit, Institute of Genetics & Molecular Medicine, University of Edinburgh, Western General Hospital, Edinburgh, UK.
Stephen R YantDepartment of Pediatrics and Genetics, Stanford University School of Medicine, Stanford, California, USA.
András SzilágyiInstitute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, Hungary.
Joseph A MarshMRC Human Genetics Unit, Institute of Genetics & Molecular Medicine, University of Edinburgh, Western General Hospital, Edinburgh, UK.
Lajos MátésInstistute of Genetics, Biological Research Center of the Hungarian Academy of Sciences, Szeged, Hungary.
Zsuzsanna IzsvákMax Delbrück Center for Molecular Medicine, Berlin, Germany.
Orsolya BarabásEuropean Molecular Biology Laboratory, Structural and Computational Biology Unit, Heidelberg, Germany.
Zoltán IvicsDivision of Medical Biotechnology, Paul Ehrlich Institute, Langen, Germany.

Funding

Medical Research Council MR/M02122X/1
6 · The paper itself

Abstract

Transposases are important tools in genome engineering, and there is considerable interest in engineering more efficient ones. Here, we seek to understand the factors determining their activity using the Sleeping Beauty transposase. Recent work suggests that protein coevolutionary information can be used to classify groups of physically connected, coevolving residues into elements called "sectors", which have proven useful for understanding the folding, allosteric interactions, and enzymatic activity of proteins. Using extensive mutagenesis data, protein modeling and analysis of folding energies, we show that (i) The Sleeping Beauty transposase contains two sectors, which span across conserved domains, and are enriched in DNA-binding residues, indicating that the DNA binding and endonuclease functions of the transposase coevolve; (ii) Sector residues are highly sensitive to mutations, and most mutations of these residues strongly reduce transposition rate; (iii) Mutations with a strong effect on free energy of folding in the DDE domain of the transposase significantly reduce transposition rate. (iv) Mutations that influence DNA and protein-protein interactions generally reduce transposition rate, although most hyperactive mutants are also located on the protein surface, including residues with protein-protein interactions. This suggests that hyperactivity results from the modification of protein interactions, rather than the stabilization of protein fold.

Indexed as

DNA Transposable ElementsCarrier ProteinsConserved SequenceGenetic VectorsHomologous RecombinationModels, MolecularMutagenesisMutationProtein BindingProtein ConformationProtein Interaction Domains and MotifsProtein MultimerizationProtein StabilityStructure-Activity RelationshipTransposasesCarrier ProteinsDNA Transposable ElementsTransposases

Identifiers

PMID27401040
PMCPMC5010145

What OpenQuestion holds

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Registered trials

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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.