Lựa chọn con đường sửa chữa gãy đôi chuỗi DNA: ngã ba đường

Ahnesorg, P., Smith, P., & Jackson, S. P. (2006). XLF interacts with the XRCC4-DNA ligase IV complex to promote DNA nonhomologous end-joining. Cell,124(2), 301–313. https://doi.org/10.1016/j.cell.2005.12.031. Anand, R., Ranjha, L., Cannavo, E., & Cejka, P. (2016). Phosphorylated CtIP functions as a co-factor of the MRE11-RAD50-NBS1 endonuclease in DNA end resection. Molecular Cell,64(5), 940–950. https://doi.org/10.1016/j.molcel.2016.10.017. Andres, S. N., Modesti, M., Tsai, C. J., Chu, G., & Junop, M. S. (2007). Crystal structure of human XLF: A twist in nonhomologous DNA end-joining. Molecular Cell,28(6), 1093–1101. https://doi.org/10.1016/j.molcel.2007.10.024. Arnoult, N., et al. (2017). Regulation of DNA repair pathway choice in S and G2 phases by the NHEJ inhibitor CYREN. Nature,549(7673), 548–552. https://doi.org/10.1038/nature24023. Audebert, M., Salles, B., & Calsou, P. (2004). Involvement of poly(ADP-ribose) polymerase-1 and XRCC1/DNA ligase III in an alternative route for DNA double-strand breaks rejoining. The Journal of Biological Chemistry,279(53), 55117–55126. https://doi.org/10.1074/jbc.M404524200. Aylon, Y., Liefshitz, B., & Kupiec, M. (2004). The CDK regulates repair of double-strand breaks by homologous recombination during the cell cycle. The EMBO Journal,23(24), 4868–4875. https://doi.org/10.1038/sj.emboj.7600469. Aymard, F., et al. (2014). Transcriptionally active chromatin recruits homologous recombination at DNA double-strand breaks. Nature Structural & Molecular Biology,21(4), 366–374. https://doi.org/10.1038/nsmb.2796. Badie, S., et al. (2010). BRCA2 acts as a RAD51 loader to facilitate telomere replication and capping. Nature Structural & Molecular Biology,17(12), 1461–1469. https://doi.org/10.1038/nsmb.1943. Bennardo, N., Cheng, A., Huang, N., & Stark, J. M. (2008). Alternative-NHEJ is a mechanistically distinct pathway of mammalian chromosome break repair. PLoS Genetics,4(6), e1000110. https://doi.org/10.1371/journal.pgen.1000110. Bhargava, R., Onyango, D. O., & Stark, J. M. (2016). Regulation of single-strand annealing and its role in genome maintenance. Trends in Genetics: TIG,32(9), 566–575. https://doi.org/10.1016/j.tig.2016.06.007. Biehs, R., et al. (2017). DNA double-strand break resection occurs during non-homologous end joining in G1 but is distinct from resection during homologous recombination. Molecular Cell,65(4), 671–684. https://doi.org/10.1016/j.molcel.2016.12.016 Boboila, C., et al. (2010). Alternative end-joining catalyzes class switch recombination in the absence of both Ku70 and DNA ligase 4. The Journal of Experimental Medicine,207(2), 417–427. https://doi.org/10.1084/jem.20092449. Botuyan, M. V., et al. (2006). Structural basis for the methylation state-specific recognition of histone H4-K20 by 53BP1 and Crb2 in DNA repair. Cell,127(7), 1361–1373. https://doi.org/10.1016/j.cell.2006.10.043. Brown, J. S., et al. (2015). Neddylation promotes ubiquitylation and release of Ku from DNA-damage sites. Cell Reports,11(5), 704–714. https://doi.org/10.1016/j.celrep.2015.03.058. Bunting, S. F., et al. (2010). 53BP1 inhibits homologous recombination in Brca1-deficient cells by blocking resection of DNA breaks. Cell,141(2), 243–254. https://doi.org/10.1016/j.cell.2010.03.012. Cabello-Lobato, M. J., Wang, S., & Schmidt, C. K. (2017). SAMHD1 sheds moonlight on DNA double-strand break repair. Trends in Genetics: TIG,33(12), 895–897. https://doi.org/10.1016/j.tig.2017.09.007. Callen, E., et al. (2013). 53BP1 mediates productive and mutagenic DNA repair through distinct phosphoprotein interactions. Cell,153(6), 1266–1280. https://doi.org/10.1016/j.cell.2013.05.023. Ceccaldi, R., Rondinelli, B., & D'Andrea, A. D. (2016). Repair pathway choices and consequences at the double-strand break. Trends in Cell Biology,26(1), 52–64. https://doi.org/10.1016/j.tcb.2015.07.009. Chambers, A. L., & Downs, J. A. (2012). The RSC and INO80 chromatin-remodeling complexes in DNA double-strand break repair. Progress in Molecular Biology and Translational Science,110, 229–261. https://doi.org/10.1016/B978-0-12-387665-2.00009-2. Chan, S. H., Yu, A. M., & McVey, M. (2010). Dual roles for DNA polymerase theta in alternative end-joining repair of double-strand breaks in Drosophila. PLoS Genetics,6(7), e1001005. https://doi.org/10.1371/journal.pgen.1001005. Chanut, P., Britton, S., Coates, J., Jackson, S. P., & Calsou, P. (2016). Coordinated nuclease activities counteract Ku at single-ended DNA double-strand breaks. Nature Communications,7, 12889. https://doi.org/10.1038/ncomms12889. Chapman, J. R., Taylor, M. R., & Boulton, S. J. (2012). Playing the end game: DNA double-strand break repair pathway choice. Molecular Cell,47(4), 497–510. https://doi.org/10.1016/j.molcel.2012.07.029. Chapman, J. R., et al. (2013). RIF1 is essential for 53BP1-dependent nonhomologous end joining and suppression of DNA double-strand break resection. Molecular Cell,49(5), 858–871. https://doi.org/10.1016/j.molcel.2013.01.002. Chen, X., et al. (2012). The Fun30 nucleosome remodeller promotes resection of DNA double-strand break ends. Nature,489(7417), 576–580. https://doi.org/10.1038/nature11355. Ciccia, A., & Elledge, S. J. (2010). The DNA damage response: Making it safe to play with knives. Molecular Cell,40(2), 179–204. https://doi.org/10.1016/j.molcel.2010.09.019. Clapier, C. R., & Cairns, B. R. (2009). The biology of chromatin remodeling complexes. Annual Review of Biochemistry,78, 273–304. https://doi.org/10.1146/annurev.biochem.77.062706.153223. Costelloe, T., et al. (2012). The yeast Fun30 and human SMARCAD1 chromatin remodellers promote DNA end resection. Nature,489(7417), 581–584. https://doi.org/10.1038/nature11353. Daddacha, W., et al. (2017). SAMHD1 promotes DNA end resection to facilitate DNA repair by homologous recombination. Cell Reports,20(8), 1921–1935. https://doi.org/10.1016/j.celrep.2017.08.008. Daley, J. M., & Sung, P. (2014). 53BP1, BRCA1, and the choice between recombination and end joining at DNA double-strand breaks. Molecular and Cellular Biology,34(8), 1380–1388. https://doi.org/10.1128/MCB.01639-13. Davies, A. A., et al. (2001). Role of BRCA2 in control of the RAD51 recombination and DNA repair protein. Molecular Cell,7(2), 273–282. Davis, A. J., & Chen, D. J. (2013). DNA double strand break repair via non-homologous end-joining. Translational Cancer Research,2(3), 130–143. https://doi.org/10.3978/j.issn.2218-676X.2013.04.02. Deng, S. K., Gibb, B., de Almeida, M. J., Greene, E. C., & Symington, L. S. (2014). RPA antagonizes microhomology-mediated repair of DNA double-strand breaks. Nature Structural & Molecular Biology,21(4), 405–412. https://doi.org/10.1038/nsmb.2786. Deriano, L., & Roth, D. B. (2013). Modernizing the nonhomologous end-joining repertoire: Alternative and classical NHEJ share the stage. Annual Review of Genetics,47, 433–455. https://doi.org/10.1146/annurev-genet-110711-155540. Dev, H., et al. (2018). Shieldin complex promotes DNA end-joining and counters homologous recombination in BRCA1-null cells. Nature Cell Biology,20(8), 954–965. https://doi.org/10.1038/s41556-018-0140-1. Difilippantonio, M. J., et al. (2000). DNA repair protein Ku80 suppresses chromosomal aberrations and malignant transformation. Nature,404(6777), 510–514. https://doi.org/10.1038/35006670. Dong, S., et al. (2014). The human SRCAP chromatin remodeling complex promotes DNA-end resection. Current Biology: CB,24(18), 2097–2110. https://doi.org/10.1016/j.cub.2014.07.081. Escribano-Diaz, C., et al. (2013). A cell cycle-dependent regulatory circuit composed of 53BP1-RIF1 and BRCA1-CtIP controls DNA repair pathway choice. Molecular Cell,49(5), 872–883. https://doi.org/10.1016/j.molcel.2013.01.001. Escribano-Diaz, C., & Durocher, D. (2013). DNA repair pathway choice—a PTIP of the hat to 53BP1. EMBO Reports,14(8), 665–666. https://doi.org/10.1038/embor.2013.99. Falck, J., et al. (2012). CDK targeting of NBS1 promotes DNA-end resection, replication restart and homologous recombination. EMBO Reports,13(6), 561–568. https://doi.org/10.1038/embor.2012.58. Feng, L., Fong, K. W., Wang, J., Wang, W., & Chen, J. (2013). RIF1 counteracts BRCA1-mediated end resection during DNA repair. The Journal of Biological Chemistry,288(16), 11135–11143. https://doi.org/10.1074/jbc.M113.457440. Feng, L., & Chen, J. (2012). The E3 ligase RNF8 regulates KU80 removal and NHEJ repair. Nature Structural & Molecular Biology,19(2), 201–206. https://doi.org/10.1038/nsmb.2211. Ferretti, L. P., Lafranchi, L., & Sartori, A. A. (2013). Controlling DNA-end resection: A new task for CDKs. Frontiers in Genetics,4, 99. https://doi.org/10.3389/fgene.2013.00099. Fradet-Turcotte, A., et al. (2013). 53BP1 is a reader of the DNA-damage-induced H2A Lys 15 ubiquitin mark. Nature,499(7456), 50–54. https://doi.org/10.1038/nature12318. Gao, S., et al. (2018). An OB-fold complex controls the repair pathways for DNA double-strand breaks. Nature Communications,9(1), 3925. https://doi.org/10.1038/s41467-018-06407-7. Ghezraoui, H., et al. (2018). 53BP1 cooperation with the REV7-shieldin complex underpins DNA structure-specific NHEJ. Nature,560(7716), 122–127. https://doi.org/10.1038/s41586-018-0362-1. Goodarzi, A. A., et al. (2006). DNA-PK autophosphorylation facilitates Artemis endonuclease activity. The EMBO Journal,25(16), 3880–3889. https://doi.org/10.1038/sj.emboj.7601255. Grawunder, U., Zimmer, D., Fugmann, S., Schwarz, K., & Lieber, M. R. (1998a). DNA ligase IV is essential for V (D) J recombination and DNA double-strand break repair in human precursor lymphocytes. Molecular Cell,2(4), 477–484. Grawunder, U., Zimmer, D., & Lieber, M. R. (1998b). DNA ligase IV binds to XRCC4 via a motif located between rather than within its BRCT domains. Current Biology: CB,8(15), 873–876. Gu, J., et al. (2004). Cell cycle-dependent regulation of a human DNA helicase that localizes in DNA damage foci. Molecular Biology of the Cell,15(7), 3320–3332. https://doi.org/10.1091/mbc.e04-03-0227. Guler, G. D., et al. (2012). Human DNA helicase B (HDHB) binds to replication protein A and facilitates cellular recovery from replication stress. The Journal of Biological Chemistry,287(9), 6469–6481. https://doi.org/10.1074/jbc.M111.324582. Gupta, R., et al. (2018). DNA repair network analysis reveals shieldin as a key regulator of NHEJ and PARP inhibitor sensitivity. Cell,173(4), 972–988. https://doi.org/10.1016/j.cell.2018.03.050 Hakem, R. (2008). DNA-damage repair; the good, the bad, and the ugly. The EMBO Journal,27(4), 589–605. https://doi.org/10.1038/emboj.2008.15. Han, J., et al. (2017). BRCA2 antagonizes classical and alternative nonhomologous end-joining to prevent gross genomic instability. Nature Communications,8(1), 1470. https://doi.org/10.1038/s41467-017-01759-y. Hauer, M. H., et al. (2017). Histone degradation in response to DNA damage enhances chromatin dynamics and recombination rates. Nature Structural & Molecular Biology,24(2), 99–107. https://doi.org/10.1038/nsmb.3347. Heyer, W. D., Ehmsen, K. T., & Liu, J. (2010). Regulation of homologous recombination in eukaryotes. Annual Review of Genetics,44, 113–139. https://doi.org/10.1146/annurev-genet-051710-150955. Hoeijmakers, J. H. (2009). DNA damage, aging, and cancer. The New England Journal of Medicine,361(15), 1475–1485. https://doi.org/10.1056/NEJMra0804615. Huertas, P. (2010). DNA resection in eukaryotes: Deciding how to fix the break. Nature Structural & Molecular Biology,17(1), 11–16. https://doi.org/10.1038/nsmb.1710. Huertas, P., & Jackson, S. P. (2009). Human CtIP mediates cell cycle control of DNA end resection and double strand break repair. The Journal of Biological Chemistry,284(14), 9558–9565. https://doi.org/10.1074/jbc.M808906200. Hustedt, N., & Durocher, D. (2016). The control of DNA repair by the cell cycle. Nature Cell Biology,19(1), 1–9. https://doi.org/10.1038/ncb3452. Ira, G., et al. (2004). DNA end resection, homologous recombination and DNA damage checkpoint activation require CDK1. Nature,431(7011), 1011–1017. https://doi.org/10.1038/nature02964. Ismail, I. H., et al. (2015). The RNF138 E3 ligase displaces Ku to promote DNA end resection and regulate DNA repair pathway choice. Nature Cell Biology,17(11), 1446–1457. https://doi.org/10.1038/ncb3259. Jackson, S. P., & Bartek, J. (2009). The DNA-damage response in human biology and disease. Nature,461(7267), 1071–1078. https://doi.org/10.1038/nature08467. Jensen, R. B., Carreira, A., & Kowalczykowski, S. C. (2010). Purified human BRCA2 stimulates RAD51-mediated recombination. Nature,467(7316), 678–683. https://doi.org/10.1038/nature09399. Jin, S., & Weaver, D. T. (1997). Double-strand break repair by Ku70 requires heterodimerization with Ku80 and DNA binding functions. The EMBO Journal,16(22), 6874–6885. https://doi.org/10.1093/emboj/16.22.6874. Kanakkanthara, A., et al. (2016). Cyclin A2 is an RNA binding protein that controls Mre11 mRNA translation. Science,353(6307), 1549–1552. https://doi.org/10.1126/science.aaf7463. Kent, T., Chandramouly, G., McDevitt, S. M., Ozdemir, A. Y., & Pomerantz, R. T. (2015). Mechanism of microhomology-mediated end-joining promoted by human DNA polymerase theta. Nature Structural & Molecular Biology,22(3), 230–237. https://doi.org/10.1038/nsmb.2961. Kumar, V., Alt, F. W., & Frock, R. L. (2016). PAXX and XLF DNA repair factors are functionally redundant in joining DNA breaks in a G1-arrested progenitor B-cell line. Proceedings of the National Academy of Sciences of the United States of America,113(38), 10619–10624. https://doi.org/10.1073/pnas.1611882113. Langerak, P., Mejia-Ramirez, E., Limbo, O., & Russell, P. (2011). Release of Ku and MRN from DNA ends by Mre11 nuclease activity and Ctp1 is required for homologous recombination repair of double-strand breaks. PLoS Genetics,7(9), e1002271. https://doi.org/10.1371/journal.pgen.1002271. Li, Y., et al. (2008). Crystal structure of human XLF/Cernunnos reveals unexpected differences from XRCC4 with implications for NHEJ. The EMBO Journal,27(1), 290–300. https://doi.org/10.1038/sj.emboj.7601942. Lieber, M. R. (2010). The mechanism of double-strand DNA break repair by the nonhomologous DNA end-joining pathway. Annual Review of Biochemistry,79, 181–211. https://doi.org/10.1146/annurev.biochem.052308.093131. Liu, T., & Huang, J. (2014). Quality control of homologous recombination. Cellular and Molecular Life Sciences: CMLS,71(19), 3779–3797. https://doi.org/10.1007/s00018-014-1649-5. Liu, T., & Huang, J. (2016). DNA end resection: Facts and mechanisms. Genomics, Proteomics & Bioinformatics,14(3), 126–130. https://doi.org/10.1016/j.gpb.2016.05.002. Longhese, M. P., Bonetti, D., Manfrini, N., & Clerici, M. (2010). Mechanisms and regulation of DNA end resection. The EMBO Journal,29(17), 2864–2874. https://doi.org/10.1038/emboj.2010.165. Lord, C. J., & Ashworth, A. (2013). Mechanisms of resistance to therapies targeting BRCA-mutant cancers. Nature Medicine,19(11), 1381–1388. https://doi.org/10.1038/nm.3369. Lou, J., et al. (2017). AUNIP/C1orf135 directs DNA double-strand breaks towards the homologous recombination repair pathway. Nature Communications,8(1), 985. https://doi.org/10.1038/s41467-017-01151-w. Lu, G., et al. (2016). Ligase I and ligase III mediate the DNA double-strand break ligation in alternative end-joining. Proceedings of the National Academy of Sciences of the United States of America,113(5), 1256–1260. https://doi.org/10.1073/pnas.1521597113. Ma, Y., Pannicke, U., Schwarz, K., & Lieber, M. R. (2002). Hairpin opening and overhang processing by an Artemis/DNA-dependent protein kinase complex in nonhomologous end joining and V (D) J recombination. Cell,108(6), 781–794. Ma, Y., Schwarz, K., & Lieber, M. R. (2005). The Artemis: DNA-PKcs endonuclease cleaves DNA loops, flaps, and gaps. DNA Repair,4(7), 845–851. https://doi.org/10.1016/j.dnarep.2005.04.013. McVey, M., & Lee, S. E. (2008). MMEJ repair of double-strand breaks (director's cut): Deleted sequences and alternative endings. Trends in Genetics: TIG,24(11), 529–538. https://doi.org/10.1016/j.tig.2008.08.007. Mimitou, E. P., & Symington, L. S. (2009). DNA end resection: Many nucleases make light work. DNA Repair,8(9), 983–995. https://doi.org/10.1016/j.dnarep.2009.04.017. Mimitou, E. P., & Symington, L. S. (2010). Ku prevents Exo1 and Sgs1-dependent resection of DNA ends in the absence of a functional MRX complex or Sae2. The EMBO Journal,29(19), 3358–3369. https://doi.org/10.1038/emboj.2010.193. Mimitou, E. P., & Symington, L. S. (2011). DNA end resection—unraveling the tail. DNA Repair,10(3), 344–348. https://doi.org/10.1016/j.dnarep.2010.12.004. Mirman, Z., et al. (2018). 53BP1-RIF1-shieldin counteracts DSB resection through CST- and Polalpha-dependent fill-in. Nature,560(7716), 112–116. https://doi.org/10.1038/s41586-018-0324-7. Morrison, A. J., et al. (2004). INO80 and gamma-H2AX interaction links ATP-dependent chromatin remodeling to DNA damage repair. Cell,119(6), 767–775. https://doi.org/10.1016/j.cell.2004.11.037. Noordermeer, S. M., et al. (2018). The shieldin complex mediates 53BP1-dependent DNA repair. Nature,560(7716), 117–121. https://doi.org/10.1038/s41586-018-0340-7. Ochi, T., et al. (2015). DNA repair. PAXX, a paralog of XRCC4 and XLF, interacts with Ku to promote DNA double-strand break repair. Science,347(6218), 185–188. https://doi.org/10.1126/science.1261971 O'Driscoll, M. (2012). Diseases associated with defective responses to DNA damage. Cold Spring Harbor Perspectives in Biology,. https://doi.org/10.1101/cshperspect.a012773 Panier, S., & Durocher, D. (2013). Push back to respond better: Regulatory inhibition of the DNA double-strand break response. Nature Reviews Molecular Cell Biology,14(10), 661–672. https://doi.org/10.1038/nrm3659. Paull, T. T. (2018). 20 years of Mre11 biology: No end in sight. Molecular Cell,71(3), 419–427. https://doi.org/10.1016/j.molcel.2018.06.033. Ramakrishnan, S., Kockler, Z., Evans, R., Downing, B. D., & Malkova, A. (2018). Single-strand annealing between inverted DNA repeats: Pathway choice, participating proteins, and genome destabilizing consequences. PLoS Genetics,14(8), e1007543. https://doi.org/10.1371/journal.pgen.1007543. Rass, E., Grabarz, A., Plo, I., Gautier, J., Bertrand, P., & Lopez, B. S. (2009). Role of Mre11 in chromosomal nonhomologous end joining in mammalian cells. Nature Structural & Molecular Biology,16(8), 819–824. https://doi.org/10.1038/nsmb.1641. Reczek, C. R., Szabolcs, M., Stark, J. M., Ludwig, T., & Baer, R. (2013). The interaction between CtIP and BRCA1 is not essential for resection-mediated DNA repair or tumor suppression. The Journal of Cell Biology,201(5), 693–707. https://doi.org/10.1083/jcb.201302145. Renkawitz, J., Lademann, C. A., & Jentsch, S. (2014). Mechanisms and principles of homology search during recombination. Nature Reviews Molecular Cell Biology,15(6), 369–383. https://doi.org/10.1038/nrm3805. San Filippo, J., Sung, P., & Klein, H. (2008). Mechanism of eukaryotic homologous recombination. Annual Review of Biochemistry,77, 229–257. https://doi.org/10.1146/annurev.biochem.77.061306.125255. Sartori, A. A., et al. (2007). Human CtIP promotes DNA end resection. Nature,450(7169), 509–514. https://doi.org/10.1038/nature06337. Schar, P., Herrmann, G., Daly, G., & Lindahl, T. (1997). A newly identified DNA ligase of Saccharomyces cerevisiae involved in RAD52-independent repair of DNA double-strand breaks. Genes & Development,11(15), 1912–1924. Sfeir, A., & Symington, L. S. (2015). Microhomology-mediated end joining: A back-up survival mechanism or dedicated pathway? Trends in Biochemical Sciences,40(11), 701–714. https://doi.org/10.1016/j.tibs.2015.08.006. Shibata, A., et al. (2011). Factors determining DNA double-strand break repair pathway choice in G2 phase. The EMBO Journal,30(6), 1079–1092. https://doi.org/10.1038/emboj.2011.27. Shibata, A. (2017). Regulation of repair pathway choice at two-ended DNA double-strand breaks. Mutation Research,803–805, 51–55. https://doi.org/10.1016/j.mrfmmm.2017.07.011. Shiloh, Y., & Lehmann, A. R. (2004). Maintaining integrity. Nature Cell Biology,6(10), 923–928. https://doi.org/10.1038/ncb1004-923. Shim, E. Y., Ma, J. L., Oum, J. H., Yanez, Y., & Lee, S. E. (2005). The yeast chromatin remodeler RSC complex facilitates end joining repair of DNA double-strand breaks. Molecular and Cellular Biology,25(10), 3934–3944. https://doi.org/10.1128/MCB.25.10.3934-3944.2005. Shim, E. Y., Hong, S. J., Oum, J. H., Yanez, Y., Zhang, Y., & Lee, S. E. (2007). RSC mobilizes nucleosomes to improve accessibility of repair machinery to the damaged chromatin. Molecular and Cellular Biology,27(5), 1602–1613. https://doi.org/10.1128/MCB.01956-06. Silverman, J., Takai, H., Buonomo, S. B., Eisenhaber, F., & de Lange, T. (2004). Human Rif1, ortholog of a yeast telomeric protein, is regulated by ATM and 53BP1 and functions in the S-phase checkpoint. Genes & Development,18(17), 2108–2119. https://doi.org/10.1101/gad.1216004. Simpson, R. T., Whitlock, J. P., Jr., Bina-Stein, M., & Stein, A. (1978). Histone-DNA interactions in chromatin core particles. Cold Spring Harbor Symposia on Quantitative Biology,42(Pt 1), 127–136. Simsek, D., & Jasin, M. (2010). Alternative end-joining is suppressed by the canonical NHEJ component Xrcc4-ligase IV during chromosomal translocation formation. Nature Structural & Molecular Biology,17(4), 410–416. https://doi.org/10.1038/nsmb.1773. Spagnolo, L., Rivera-Calzada, A., Pearl, L. H., & Llorca, O. (2006). Three-dimensional structure of the human DNA-PKcs/Ku70/Ku80 complex assembled on DNA and its implications for DNA DSB repair. Molecular Cell,22(4), 511–519. https://doi.org/10.1016/j.molcel.2006.04.013. Steger, M., et al. (2013). Prolyl isomerase PIN1 regulates DNA double-strand break repair by counteracting DNA end resection. Molecular Cell,50(3), 333–343. https://doi.org/10.1016/j.molcel.2013.03.023. Sugiyama, T., New, J. H., & Kowalczykowski, S. C. (1998). DNA annealing by RAD52 protein is stimulated by specific interaction with the complex of replication protein A and single-stranded DNA. Proceedings of the National Academy of Sciences of the United States of America,95(11), 6049–6054. Sun, J., Lee, K. J., Davis, A. J., & Chen, D. J. (2012). Human Ku70/80 protein blocks exonuclease 1-mediated DNA resection in the presence of human Mre11 or Mre11/Rad50 protein complex. The Journal of Biological Chemistry,287(7), 4936–4945. https://doi.org/10.1074/jbc.M111.306167. Sunada, S., et al. (2016). Nontoxic concentration of DNA-PK inhibitor NU7441 radio-sensitizes lung tumor cells with little effect on double strand break repair. Cancer Science,107(9), 1250–1255. https://doi.org/10.1111/cas.12998. Sung, P., & Klein, H. (2006). Mechanism of homologous recombination: Mediators and helicases take on regulatory functions. Nature Reviews Molecular Cell Biology,7(10), 739–750. https://doi.org/10.1038/nrm2008. Sy, S. M., Huen, M. S., & Chen, J. (2009). PALB2 is an integral component of the BRCA complex required for homologous recombination repair. Proceedings of the National Academy of Sciences of the United States of America,106(17), 7155–7160. https://doi.org/10.1073/pnas.0811159106. Symington, L. S., & Gautier, J. (2011). Double-strand break end resection and repair pathway choice. Annual Review of Genetics,45, 247–271. https://doi.org/10.1146/annurev-genet-110410-132435. Symington, L. S. (2002). Role of RAD52 epistasis group genes in homologous recombination and double-strand break repair. Microbiology and Molecular Biology Reviews: MMBR,66(4), 630–670. Taylor, M. R. G., et al. (2015). Rad51 paralogs remodel pre-synaptic Rad51 filaments to stimulate homologous recombination. Cell,162(2), 271–286. https://doi.org/10.1016/j.cell.2015.06.015. Teo, S. H., & Jackson, S. P. (1997). Identification of Saccharomyces cerevisiae DNA ligase IV: Involvement in DNA double-strand break repair. The EMBO Journal,16(15), 4788–4795. https://doi.org/10.1093/emboj/16.15.4788. Thorslund, T., et al. (2010). The breast cancer tumor suppressor BRCA2 promotes the specific targeting of RAD51 to single-stranded DNA. Nature Structural & Molecular Biology,17(10), 1263–1265. https://doi.org/10.1038/nsmb.1905. Tkac, J., et al. (2016). HELB is a feedback inhibitor of DNA end resection. Molecular Cell,61(3), 405–418. https://doi.org/10.1016/j.molcel.2015.12.013. Tomimatsu, N., et al. (2014). Phosphorylation of EXO1 by CDKs 1 and 2 regulates DNA end resection and repair pathway choice. Nature Communications,5, 3561. https://doi.org/10.1038/ncomms4561. Truong, L. N., et al. (2013). Microhomology-mediated end joining and homologous recombination share the initial end resection step to repair DNA double-strand breaks in mammalian cells. Proceedings of the National Academy of Sciences of the United States of America,110(19), 7720–7725. https://doi.org/10.1073/pnas.1213431110. van Attikum, H., Fritsch, O., Hohn, B., & Gasser, S. M. (2004). Recruitment of the INO80 complex by H2A phosphorylation links ATP-dependent chromatin remodeling with DNA double-strand break repair. Cell,119(6), 777–788. https://doi.org/10.1016/j.cell.2004.11.033. van Attikum, H., & Gasser, S. M. (2005). The histone code at DNA breaks: A guide to repair? Nature Reviews Molecular Cell Biology,6(10), 757–765. https://doi.org/10.1038/nrm1737. van der Burg, M., van Dongen, J. J., & van Gent, D. C. (2009). DNA-PKcs deficiency in human: Long predicted, finally found. Current Opinion in Allergy and Clinical Immunology,9(6), 503–509. https://doi.org/10.1097/ACI.0b013e3283327e41. van Gent, D. C., Hoeijmakers, J. H., & Kanaar, R. (2001). Chromosomal stability and the DNA double-stranded break connection. Nature Reviews Genetics,2(3), 196–206. https://doi.org/10.1038/35056049. Wang, H., et al. (2001a). Nonhomologous end-joining of ionizing radiation-induced DNA double-stranded breaks in human tumor cells deficient in BRCA1 or BRCA2. Cancer Research,61(1), 270–277. Wang, H., et al. (2001b). Efficient rejoining of radiation-induced DNA double-strand breaks in vertebrate cells deficient in genes of the RAD52 epistasis group. Oncogene,20(18), 2212–2224. https://doi.org/10.1038/sj.onc.1204350. Wang, H., Perrault, A. R., Takeda, Y., Qin, W., Wang, H., & Iliakis, G. (2003). Biochemical evidence for Ku-independent backup pathways of NHEJ. Nucleic Acids Research,31(18), 5377–5388. Wang, H., et al. (2005). DNA ligase III as a candidate component of backup pathways of nonhomologous end joining. Cancer Research,65(10), 4020–4030. https://doi.org/10.1158/0008-5472.CAN-04-3055. Wang, H., et al. (2013). The interaction of CtIP and Nbs1 connects CDK and ATM to regulate HR-mediated double-strand break repair. PLoS Genetics,9(2), e1003277. https://doi.org/10.1371/journal.pgen.1003277. Wang, J., et al. (2014). PTIP associates with Artemis to dictate DNA repair pathway choice. Genes & Development,28(24), 2693–2698. https://doi.org/10.1101/gad.252478.114. West, S. C. (2003). Molecular views of recombination proteins and their control. Nature Reviews Molecular Cell Biology,4(6), 435–445. https://doi.org/10.1038/nrm1127. Wilson, T. E., Grawunder, U., & Lieber, M. R. (1997). Yeast DNA ligase IV mediates non-homologous DNA end joining. Nature,388(6641), 495–498. https://doi.org/10.1038/41365. Wilson, M. D., et al. (2016). The structural basis of modified nucleosome recognition by 53BP1. Nature,536(7614), 100–103. https://doi.org/10.1038/nature18951. Wohlbold, L., et al. (2012). Chemical genetics reveals a specific requirement for Cdk2 activity in the DNA damage response and identifies Nbs1 as a Cdk2 substrate in human cells. PLoS Genetics,8(8), e1002935. https://doi.org/10.1371/journal.pgen.1002935. Wyman, C., & Kanaar, R. (2006). DNA double-strand break repair: All's well that ends well. Annual Review of Genetics,40, 363–383. https://doi.org/10.1146/annurev.genet.40.110405.090451. Xia, B., et al. (2006). Control of BRCA2 cellular and clinical functions by a nuclear partner, PALB2. Molecular Cell,22(6), 719–729. https://doi.org/10.1016/j.molcel.2006.05.022. Xie, A., Kwok, A., & Scully, R. (2009). Role of mammalian Mre11 in classical and alternative nonhomologous end joining. Nature Structural & Molecular Biology,16(8), 814–818. https://doi.org/10.1038/nsmb.1640. Yu, X., Wu, L. C., Bowcock, A. M., Aronheim, A., & Baer, R. (1998). The C-terminal (BRCT) domains of BRCA1 interact in vivo with CtIP, a protein implicated in the CtBP pathway of transcriptional repression. The Journal of Biological Chemistry,273(39), 25388–25392. Yu, X., & Chen, J. (2004). DNA damage-induced cell cycle checkpoint control requires CtIP, a phosphorylation-dependent binding partner of BRCA1 C-terminal domains. Molecular and Cellular Biology,24(21), 9478–9486. https://doi.org/10.1128/MCB.24.21.9478-9486.2004. Yu, A. M., & McVey, M. (2010). Synthesis-dependent microhomology-mediated end joining accounts for multiple types of repair junctions. Nucleic Acids Research,38(17), 5706–5717. https://doi.org/10.1093/nar/gkq379. Yun, M. H., & Hiom, K. (2009). CtIP-BRCA1 modulates the choice of DNA double-strand-break repair pathway throughout the cell cycle. Nature,459(7245), 460–463. https://doi.org/10.1038/nature07955. Zha, S., Alt, F. W., Cheng, H. L., Brush, J. W., & Li, G. (2007). Defective DNA repair and increased genomic instability in Cernunnos-XLF-deficient murine ES cells. Proceedings of the National Academy of Sciences of the United States of America,104(11), 4518–4523. https://doi.org/10.1073/pnas.0611734104. Zhang, Y., & Jasin, M. (2011). An essential role for CtIP in chromosomal translocation formation through an alternative end-joining pathway. Nature Structural & Molecular Biology,18(1), 80–84. https://doi.org/10.1038/nsmb.1940. Zhao, W., et al. (2015). Promotion of BRCA2-dependent homologous recombination by DSS1 via RPA targeting and DNA mimicry. Molecular Cell,59(2), 176–187. https://doi.org/10.1016/j.molcel.2015.05.032. Zimmermann, M., Lottersberger, F., Buonomo, S. B., Sfeir, A., & de Lange, T. (2013). 53BP1 regulates DSB repair using Rif1 to control 5ʹ end resection. Science,339(6120), 700–704. https://doi.org/10.1126/science.1231573. Zimmermann, M., & de Lange, T. (2014). 53BP1: pro choice in DNA repair. Trends in Cell Biology,24(2), 108–117. https://doi.org/10.1016/j.tcb.2013.09.003. Zlotorynski, E. (2018). Shieldin the ends for 53BP1. Nature Reviews Molecular Cell Biology,19(6), 346–347. https://doi.org/10.1038/s41580-018-0019-9.