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Literature summary for 3.2.2.23 extracted from

  • Ropolo, M.; Degan, P.; Foresta, M.; DErrico, M.; Lasiglie, D.; Dogliotti, E.; Casartelli, G.; Zupo, S.; Poggi, A.; Frosina, G.
    Complementation of the oxidatively damaged DNA repair defect in Cockayne syndrome A and B cells by Escherichia coli formamidopyrimidine DNA glycosylase (2007), Free Radic. Biol. Med., 42, 1807-1817.
    View publication on PubMed

Application

Application Comment Organism
medicine expression of enzyme in human cells from patients belonging to Cockayne syndrome complementation groups A and B completely corrects the repair deficiency in both CS-A and CS-B cells. The sensitivity of CS-B cells to elevated concentrations of potassium bromate is not compensated by expression of enzyme Escherichia coli

Protein Variants

Protein Variants Comment Organism
additional information expression of enzyme in human cells from patients belonging to Cockayne syndrome complementation groups A and B completely corrects the repair deficiency in both CS-A and CS-B cells. The sensitivity of CS-B cells to elevated concentrations of potassium bromate is not compensated by expression of enzyme Escherichia coli

Organism

Organism UniProt Comment Textmining
Escherichia coli
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