Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 2.7.7.31 extracted from

  • Maezawa, S.; Nakano, S.; Kuniya, T.; Koiwai, O.; Koiwai, K.
    Double-strand break repair based on short-homology regions is suppressed under terminal deoxynucleotidyltransferase expression, as revealed by a novel vector system for analysing DNA repair by nonhomologous end joining (2016), FEBS open bio, 6, 16-23.
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
analysis construction of a nonhomologous end-joining assay vector NAV, containing mKate2, Venus and ccdB genes. Cotransfection of NAV with a construct expressing the restriction enzyme I-SceI generates a double-strand break in NAV that excises mKate2 and ccdB. Repair of this double-strand break produces an intact vector that expresses Venus, a green fluorescent protein. Cells bearing the repaired NAV lack the ccdB gene which slows cell proliferation, the cultures are enriched in cells containing repaired double-strand breaks Homo sapiens

Cloned(Commentary)

Cloned (Comment) Organism
transfection of U2OS cell Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

General Information

General Information Comment Organism
physiological function in cells overexpressing terminal deoxynucleotidyltransferase, the enzyme suppresses DNA repair that is based on short (one- or two-base) homology regions, to efficiently add deoxynucleotides during VDJ recombination in lymphoid cells Homo sapiens