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Literature summary for 2.7.1.74 extracted from

  • Neschadim, A.; Wang, J.; Sato, T.; Fowler, D.; Lavie, A.; Medin, J.
    Cell fate control gene therapy based on engineered variants of human deoxycytidine kinase (2012), Mol. Ther., 20, 1002-1013.
    View publication on PubMedView publication on EuropePMC
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Cloned(Commentary)

Cloned (Comment) Organism
overexpression of wild-type and mutant enzymes in Jurkat, Molt-4, and U87-MG cells Homo sapiens

Protein Variants

Protein Variants Comment Organism
D133A site-directed mutagenesis, the mutant is active with thymidine derivatives, in contrast to the wild-type enzyme Homo sapiens
additional information mutants of dCK with rationally designed active sites, that make them thymidine-activating, are stably introduced into cells by recombinant lentiviral vectors. Transduced cells maintain growth kinetics and function. These dCK mutants efficiently activate bromovinyl-deoxyuridine, L-deoxythymidine, and L-deoxyuridine, which are otherwise not toxic to wild-type cells, overview. Mutant dCK-expressing Jurkat, Molt-4, and U87-MG cells could be efficiently eliminated in vitro and in xenogeneic leukemia and tumor models in vivo Homo sapiens
R104M site-directed mutagenesis, the mutant is active with thymidine derivatives, in contrast to the wild-type enzyme Homo sapiens
R104M/D133A/S74E site-directed mutagenesis, the mutant is active with thymidine derivatives, in contrast to the wild-type enzyme Homo sapiens
S74E site-directed mutagenesis, the mutant is active with thymidine derivatives, in contrast to the wild-type enzyme Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
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-
-

Synonyms

Synonyms Comment Organism
dCK
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 Homo sapiens
deoxycytidine kinase
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 Homo sapiens

General Information

General Information Comment Organism
malfunction mechanisms of cell killing by activated bromovinyl-deoxyuridine in Jurkat cells expressing thymidine-activating deoxycytidine kinase, cell fate control gene therapy strategy, overview. Tumor formation is repressed by dCK-based cell fate control gene therapy strategy in vivo in a xenogeneic murine model and thymidine-activating dCK mutant increased survival in a stringent model of T cell leukemia Homo sapiens