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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).
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Genome Integrity

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