Corrigendum to “The Ku-dependent non-homologous end-joining but not other repair pathway is inhibited by high linear energy transfer ionizing radiation” [DNA Repair 27 (2008) 725–733] (DNA Repair (2008) 7(5) (725–733), (S1568786408000153), (10.1016/j.dnarep.2008.01.010));The Ku-dependent non-homologous end-joining but not other repair pathway is inhibited by high linear energy transfer ionizing radiation

DNA Repair

Volumn 7, Issue 5, 2008, Pages 725-733

  Wang, Hongyan ^a   Wang, Xiang ^a   Zhang, Piyan ^a   Wang, Ya ^a  

^a THOMAS JEFFERSON UNIVERSITY   (United States)

Author keywords

DNA repair; Homologous recombination repair (HRR); Ionizing radiation (IR); Linear energy transfer (LET); Non homologous end joining (NHEJ)

Indexed keywords

KU ANTIGEN; NICOTINAMIDE ADENINE DINUCLEOTIDE ADENOSINE DIPHOSPHATE RIBOSYLTRANSFERASE 1;

ANIMAL CELL; ARTICLE; CELL CYCLE ARREST; CELL CYCLE G2 PHASE; CELL DEATH; CELL KILLING; COMPARATIVE STUDY; CONTROLLED STUDY; DNA REPAIR; DOUBLE STRANDED DNA BREAK; EMBRYO; GAMMA RADIATION; HOMOLOGOUS RECOMBINATION; INFRARED RADIATION; IONIZING RADIATION; LINEAR ENERGY TRANSFER; MAMMAL CELL; MOUSE; NONHUMAN; PHENOTYPE; PRIORITY JOURNAL; PROTEIN DNA BINDING; SIGNAL TRANSDUCTION; WILD TYPE; X RAY;

MAMMALIA;

EID: 42249098075     PISSN: 15687864     EISSN: 15687856     Source Type: Journal    
DOI: 10.1016/j.dnarep.2020.102857     Document Type: Erratum

References (34)

1. Audebert M., Salles B., and Calsou P. Involvement of poly(ADP-ribose) polymerase-1 and XRCC1/DNA Ligase III in an alternative route for DNA double-strand breaks rejoining. J. Biol. Chem. 279 (2004) 55117-55126
2. Wang H., Rosidi B., Perrault R., Wang M., Zhang L., Windhofer F., and Iliakis G. DNA ligase III as a candidate component of backup pathways of nonhomologous end joining. Cancer Res. 65 (2005) 4020-4030
3. Wang M., Wu W., Rosidi B., Zhang L., Wang H., and Iliakis G. PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways. Nucleic Acids Res. 34 (2006) 6170-6182
4. Goodhead D.T., Thacker J., and Cox R. Effects of radiations of different qualities on cells: molecular mechanisms of damage and repair. Int. J. Radiat. Biol. 63 (1993) 543-556
5. Rydberg B., Loebrich M., and Cooper P.K. DNA double-strand breaks induced by high-energy neon and iron ions in human fibroblasts. I. Pulsed-field gel electrophoresis method. Radiat. Res. 139 (1994) 133-141
6. Stenerlow B., and Hoglund E. Rejoining of double-stranded DNA-fragments studied in different size-intervals. Int. J. Radiat. Biol. 78 (2002) 1-7
7. Hill M.A., Herdman M.T., Stevens D.L., Jones N.J., Thacker J., and Goodhead D.T. Relative sensitivities of repair-deficient mammalian cells for clonogenic survival after alpha-particle irradiation. Radiat. Res. 162 (2004) 667-676
8. Okayasu R., Okada M., Okabe A., Noguchi M., Takakura K., and Takahashi S. Repair of DNA damage induced by accelerated heavy ions in mammalian cells proficient and deficient in the non-homologous end-joining pathway. Radiat. Res. 165 (2006) 59-67
9. Rydberg B., Holley W.R., Mian I.S., and Chatterjee A. Chromatin conformation in living cells: support for a zig-zag model of the 30 nm chromatin fiber. J. Mol. Biol. 284 (1998) 71-84
10. Wachsberger P.R., Li W.-H., Guo M., Chen D., Cheong N., Ling C.C., and Iliakis G. Rejoining of DNA double strand breaks in Ku80-deficient mouse fibroblasts. Radiat. Res. 151 (1999) 398-407
11. Wang Z.-Q., Auer B., Stingl L., Berghammer H., Haidacher D., Schweiger M., and Wagner E.F. Mice lacking ADPRT and poly(ADP-ribosyl)ation develop normally but are susceptible to skin disease. Genes Dev. 9 (1995) 509-520
12. Liu N., Lamerdin J.E., Tebbs R.S., Schild D., Tucker J.D., Shen M.R., Brookman K.W., Siciliano M.J., Walter C.A., Fan W., Narayana L.S., Zhou Z.-Q., Adamson A.W., Sorensen K.J., Chen D.J., Jones N.J., and Thompson L.H. XRCC2 and XRCC3, new human Rad51-family members, promote chromosome stability and protect against DNA cross-links and other damages. Mol. Cell 1 (1998) 783-793
13. Nussenzweig A., Chen C., da Costa Soares V., Sanchez M., Kokol K., Nussenzweig M.C., and Li G.C. Requirement for Ku80 in growth and immunoglobulin V(D)J recombination. Nature 382 (1996) 551-555
14. Xu B., Kim S.-T., Lim D.-S., and Kastan M.B. Two molecularly distinct G2/M checkpoints are induced by ionizing radiation. Mol. Cell Biol. 22 (2002) 1049-1059
15. Brown E.J., and Baltimore D. Essential and dispensable roles of ATR in cell cycle arrest and genome maintenance. Genes Dev. 17 (2003) 615-628
16. Wang X., Khadpe J., Hu B., Iliakis G., and Wang Y. An over-activated ATR/CHK1 pathway is responsible for the prolonged G2 accumulation in irradiated AT cells. J. Biol. Chem. 278 (2003) 30869-30874
17. Karlsson K.H., and Stenerlöw B. Focus formation of DNA repair proteins in normal and repair-deficient cells irradiated with high-LET ions. Radiat. Res. 161 (2004) 517-527
18. Arosio D., Costantini S., Kong Y., and Vindigni A. Fluorescence anisotropy studies on the Ku-DNA interaction: ANION AND CATION EFFECTS. J. Biol. Chem. 279 (2004) 42826-42835
19. Hammarsten O., and Chu G. DNA-dependent protein kinase: DNA binding and activation in the absence of Ku. Proc. Natl. Acad. Sci. U.S.A. 95 (1998) 525-530
20. Fukushima T., Takata M., Morrison C., Araki R., Fujimori A., Abe M., Tatsumi K., Jasin M., Dhar P.K., Sonoda E., Chiba T., and Takeda S. Genetic analysis of the DNA-dependent protein kinase reveals an inhibitory role of Ku in Late S-G2 phase DNA double-strand break repair. J. Biol. Chem. 276 (2001) 44413-44418
21. Pierce A.J., Hu P., Han M., Ellis N., and Jasin M. Ku DNA end-binding protein modulates homologous repair of double-strand breaks in mammalian cells. Genes Dev. 15 (2001) 3237-3242
22. Wang X., Li G.C., Iliakis G., and Wang Y. Ku affects G2 checkpoint response following ionizing radiation. Cancer Res. 62 (2002) 6031-6034
23. Lu H.-R., Wang X., and Wang Y. A stronger DNA damage-induced G2 checkpoint due to over-activated CHK1 in the absence of PARP-1. Cell Cycle 5 (2006) 2364-2370
24. Zhu C., Bogue M.A., Lim D.-S., Hasty P., and Roth D.B. Ku86-deficient mice exhibit severe combined immunodeficiency and defective processing of V(D)J recombination intermediates. Cell 86 (1996) 379-389
25. Tong W.-M., Cortes U., Hande M.P., Ohgaki H., Cavalli L.R., Lansdorp P.M., Haddad B.R., and Wang Z.-Q. Synergistic role of Ku80 and poly(ADP-ribose) polymerase in suppressing chromosomal aberrations and liver cancer formation. Cancer Res. 62 (2002) 6990-6996
26. Henrie M.S., Kurimasa A., Burma S., Menissier-de Murcia J., de Murcia G., Li G.C., and Chen D.J. Lethality in PARP-1/Ku80 double mutant mice reveals physiological synergy during early embryogenesis. DNA Repair 2 (2003) 151-158
27. Bryant H.E., Schultz N., Thomas H.D., Parker K.M., Flower D., Lopez E., Kyle S., Meuth M., Curtin N.J., and Helleday T. Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase. Nature 434 (2005) 913-917
28. Walker J.R., Corpina R.A., and Goldberg J. Structure of the Ku heterodimer bound to DNA and its implications for double-strand break repair. Nature 412 (2001) 607-614
29. Rivera-Calzada A., Spagnolo L., Pearl L.H., and Llorca O. Structural model of full-length human Ku70-Ku80 heterodimer and its recognition of DNA and DNA-PKcs. EMBO Rep. 8 (2007) 56-62
30. Rydberg B. Radiation-induced heat-labile sites that convert into DNA double-strand breaks. Radiat. Res. 153 (2000) 805-812
31. Stenerlöw B., Karlsson K.H., Cooper B., and Rydberg B. Measurement of prompt DNA double-strand breaks in mammalian cells without including heat-labile sites: results for cells deficient in nonhomologous end joining. Radiat. Res. 159 (2003) 502-510
32. Fry R.J., Powers-Risius P., Alpen E.L., Ainsworth E.J., and Ullrich R.L. High-LET radiation carcinogenesis. Adv. Space Res. 3 (1983) 241-248
33. Sutherland B.M., Bennett P.V., Sidorkina O., and Laval J. Clustered DNA damages induced in isolated DNA and in human cells by low doses of ionizing radiation. Proc. Natl. Acad. Sci. U.S.A. 97 (2000) 103-108
34. Asaad N.A., Zeng Z.-C., Guan J., Thacker J., and Iliakis G. Homologous recombination as a potential target for caffeine radiosensitization in mammalian cells: reduced caffeine radiosensitization in XRCC2 and XRCC3 mutants. Oncogene 19 (2000) 5788-5800