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Literature summary for 2.7.7.B22 extracted from

  • Abrusan, G.; Yant, S.R.; Szilagyi, A.; Marsh, J.A.; Mates, L.; Izsvak, Z.; Barabas, O.; Ivics, Z.
    Structural determinants of sleeping beauty transposase activity (2016), Mol. Ther., 24, 1369-1377.
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
molecular biology transposases are important tools in genome engineering. The first DNA transposon tool capable for gene transfer in vertebrates is Sleeping Beauty (SB), which is reconstructed from extinct Tc1/mariner transposons in fish. Sleeping Beauty, and especially its hyperactive variant is still one of the most widely used transposon tools, in human clinical trials Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
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Subunits

Subunits Comment Organism
dimer tertiary structure of SB transposase and protein core, overview Homo sapiens

Synonyms

Synonyms Comment Organism
SB transposase
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Homo sapiens
sleeping beauty transposase
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Homo sapiens

General Information

General Information Comment Organism
evolution protein coevolutionary information can be used to classify groups of physically connected, coevolving residues into elements called sectors, which are useful for understanding the folding, allosteric interactions, and enzymatic activity of proteins. 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. Sector residues are highly sensitive to mutations, and most mutations of these residues strongly reduce transposition rate. Mutations with a strong effect on free energy of folding in the DDE domain of the transposase significantly reduce transposition rate. 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. Hyperactivity results from the modification of protein interactions, rather than the stabilization of protein fold. Mutations in sector, conserved and core residues usually have a destabilizing effect on the structure, effects of mutations on folding energies, and effect of protein-protein and protein-DNA interactions on transposition rate, overview Homo sapiens