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Table 1 End processing factors

From: Resolution of complex ends by non-homologous end joining - better to be lucky than good?

Factor* Activity
APTX Removes 5-adenylate adducts [40]
PNKP Removes 3 phosphates and phosphorylates 5 hydroxyls [45]
APLF Histone chaperone [59] 3-5 exonuclease, endonuclease [56, 61]
TDP1 Removes Top I adducts [63], 3 deoxyribose fragments [47, 67, 68]
TDP2 Removes Top II adducts [64]
XRCC5,XRCC6 (Ku) Removes 5-dRP residues and abasic sites [27]
POLM (Pol λ) Fills in gaps when ends align with no complementarity [90]
POLL (Pol μ) Fills in gaps when ends are partly complementary [86, 90]
DCLRE1C (Artemis) Endonuclease, 5-3 exonuclease [100]
WRN 3-5 exonuclease [121, 122] and 3-5 helicase [120]
MRE11/RAD50/NBN (MRN) 3-5 exonuclease, endonuclease [101, 129]
SETMAR (Metnase) Endonuclease/exonuclease [103]
  1. *HUGO gene nomenclature: APTX, aprataxin; PNKP, polynucleotide kinase 3-phosphatase; APLF, aprataxin and PNKP like factor; TDP1, tyrosyl-DNA phosphodiesterase 1; TDP2, tyrosyl-DNA phosphodiesterase 2; XRCC5,XRCC6 (Ku80, Ku70), X-ray repair complementing defective repair in Chinese hamster cells 5/6; POLM, polymerase mu; POLL, polymerase lambda; DCLRE1C (Artemis), DNA cross-link repair 1C; WRN, Werner syndrome; MRE11/RAD50/NBN, meiotic recombination 11 homolog/RAD50 homolog/nibrin (Nbs1), SETMAR, SET domain and mariner transposase fusion gene (Metnase).