後複製修復(post-replication repair, PRR) 機制是以繞過DNA損傷，解決複製叉(replication fork)停滯。後複製修復有兩個子路徑，分別為跨損傷修復(translesion synthesis, TLS)及模板置換(template switching, TS)修復路徑。在TS修復路徑是藉由複製叉倒轉(fork reversal)及同源重組(homologous recombination, HR)的參與以解決複製叉停滯的現象，但TS修復路徑是如何利用HR重新啟動DNA複製，其中的詳細分子機制還尚未明瞭。HLTF (Helicase-like transcription factor)是E3泛素化連接酶，會對PCNA (Proliferating cell nuclear antigen)的K164位置進行多鏈泛素化修飾，在TS修復路徑中扮演著重要的角色。我們的研究結果發現，HLTF確實與PARP1具有交互作用，並且PARP1會對HLTF的DEXDc, RING and HELICc domains進行ADP-核醣基化(ADP-ribosylation)的修飾，而HLTF上的ADP-核醣基化修飾會去招集BARD1與其進行交互作用。若在具有順鉑(cisplatin)抗藥性的HONE6細胞株中，將模板置換途徑的HLTF、PARP1及同源重組的BARD1表現量降低後則會對順鉑藥物產生敏感性，抑制姊妹染色分體的交換率(sister chromatid exchange, SCE)，而將HLTF的表現量降低時，則會增加複製叉的停滯，減少新的複製起始點形成。結論，HLTF與PARP1的交互作用招集BARD1連結HR與TS修復途徑重新啟動複製叉停滯。

Post-replication repair (PRR) resolves stalled DNA replication forks through the lesion bypass mechanism. PRR is divided into two subpathways, translesion synthesis (TLS) and template switching (TS). Template-switching pathway, involves fork reversal and homologous recombination to resolve stalled forks. Although BRCA1 and RAD51 are required for restart stalled forks, it remains unclear how the TS pathway utilizes homologous recombination to resume DNA replication. Helicase-like transcription factor (HLTF), the E3 ubiquitin ligase, catalyzing the synthesis of polyubiquitination chain onto lysine 164 of PCNA, plays an important role in the TS pathway. In this study, we found that HLTF can interact with PARP1, BARD1, suggesting that the TS pathway is physically associated with HR components. In addition, the DEXDc, RING and HELICc domains of HLTF is modified with ADP-ribosylation by PARP1. Depletion of HLTF, PARP1, and BARD1 sensitized cisplatin-resistant HONE6 cells to cisplatin, decreases frequency of SCE. Depletion of HLTF increases the number of stalled replication forks and decreases the number of the new origin firing. Given that the BRCT domain of BARD1 can interact with ADP-ribosylation and HLTF is ADP-ribosylated, our results suggest that HLTF could recruit the BARD1 through the BRCT-ADP-ribosylation interaction. Therefore, the TS pathway incorporates HR to resume stalled forks.

Abraham, R.T. 2001. Cell cycle checkpoint signaling through the ATM and ATR kinases. Genes & Development. 15:2177-2196.
Ali, A.A., G. Timinszky, R. Arribas-Bosacoma, M. Kozlowski, P.O. Hassa, M. Hassler, A.G. Ladurner, L.H. Pearl, and A.W. Oliver. 2012. The zinc-finger domains of PARP1 cooperate to recognize DNA strand breaks. Nat Struct Mol Biol. 19:685-692.
Asimuddin, M., and K. Jamil. 2012. Insight into the DNA repair mechanism operating during cell cycle checkpoints in eukaryotic cells. Biology and Medicine. 4:147.
Bekker-Jensen, S., C. Lukas, R. Kitagawa, F. Melander, M.B. Kastan, J. Bartek, and J. Lukas. 2006. Spatial organization of the mammalian genome surveillance machinery in response to DNA strand breaks. The Journal of cell biology. 173:195-206.
Bienko, M., C.M. Green, N. Crosetto, F. Rudolf, G. Zapart, B. Coull, P. Kannouche, G. Wider, M. Peter, A.R. Lehmann, K. Hofmann, and I. Dikic. 2005. Ubiquitin-binding domains in Y-family polymerases regulate translesion synthesis. Science. 310:1821-1824.
Bray, C.M., and C.E. West. 2005. DNA repair mechanisms in plants: crucial sensors and effectors for the maintenance of genome integrity. The New phytologist. 168:511-528.
Bryant, H.E., N. Schultz, H.D. Thomas, K.M. Parker, D. Flower, E. Lopez, S. Kyle, M. Meuth, N.J. Curtin, and T. Helleday. 2005. Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase. Nature. 434:913-917.
Bunting, S.F., E. Callen, M.L. Kozak, J.M. Kim, N. Wong, A.J. Lopez-Contreras, T. Ludwig, R. Baer, R.B. Faryabi, A. Malhowski, H.T. Chen, O. Fernandez-Capetillo, A. D'Andrea, and A. Nussenzweig. 2012. BRCA1 functions independently of homologous recombination in DNA interstrand crosslink repair. Mol Cell. 46:125-135.
Burkovics, P., M. Sebesta, D. Balogh, L. Haracska, and L. Krejci. 2014. Strand invasion by HLTF as a mechanism for template switch in fork rescue. Nucleic Acids Research. 42:1711-1720.
Chang, D.J., and K.A. Cimprich. 2009. DNA damage tolerance: when it's OK to make mistakes. Nat Chem Biol. 5:82-90.
Chapman, J.R., M.R. Taylor, and S.J. Boulton. 2012. Playing the end game: DNA double-strand break repair pathway choice. Molecular cell. 47:497-510.
Chen, L., C.J. Nievera, A.Y. Lee, and X. Wu. 2008. Cell cycle-dependent complex formation of BRCA1.CtIP.MRN is important for DNA double-strand break repair. The Journal of biological chemistry. 283:7713-7720.
Chen, S., A.A. Davies, D. Sagan, and H.D. Ulrich. 2005. The RING finger ATPase Rad5p of Saccharomyces cerevisiae contributes to DNA double-strand break repair in a ubiquitin-independent manner. Nucleic Acids Res. 33:5878-5886.
Ciccia, A., and S.J. Elledge. 2010. The DNA damage response: making it safe to play with knives. Mol Cell. 40:179-204.
Cimprich, K.A., and D. Cortez. 2008. ATR: an essential regulator of genome integrity. Nature reviews. Molecular cell biology. 9:616-627.
Cortez, D., Y. Wang, J. Qin, and S.J. Elledge. 1999. Requirement of ATM-dependent phosphorylation of brca1 in the DNA damage response to double-strand breaks. Science. 286:1162-1166.
de Murcia, J.M., M. Ricoul, L. Tartier, C. Niedergang, A. Huber, F. Dantzer, V. Schreiber, J.C. Amé, A. Dierich, and M. LeMeur. 2003. Functional interaction between PARP‐1 and PARP‐2 in chromosome stability and embryonic development in mouse. The EMBO journal. 22:2255-2263.
Debauve, G., A. Capouillez, A. Belayew, and S. Saussez. 2008. The helicase-like transcription factor and its implication in cancer progression. Cellular and molecular life sciences : CMLS. 65:591-604.
Debauve, G., D. Nonclercq, F. Ribaucour, M. Wiedig, C. Gerbaux, O. Leo, G. Laurent, F. Journe, A. Belayew, and G. Toubeau. 2006. Early expression of the Helicase-Like Transcription Factor (HLTF/SMARCA3) in an experimental model of estrogen-induced renal carcinogenesis. Mol Cancer. 5:23.
Ding, H., K. Descheemaeker, P. Marynen, L. Nelles, T. Carvalho, M. Carmo-Fonseca, D. Collen, and A. Belayew. 1996. Characterization of a helicase-like transcription factor involved in the expression of the human plasminogen activator inhibitor-1 gene. DNA Cell Biol. 15:429-442.
Esteller, M., J.M. Silva, G. Dominguez, F. Bonilla, X. Matias-Guiu, E. Lerma, E. Bussaglia, J. Prat, I.C. Harkes, E.A. Repasky, E. Gabrielson, M. Schutte, S.B. Baylin, and J.G. Herman. 2000. Promoter hypermethylation and BRCA1 inactivation in sporadic breast and ovarian tumors. Journal of the National Cancer Institute. 92:564-569.
Farmer, H., N. McCabe, C.J. Lord, A.N.J. Tutt, D.A. Johnson, T.B. Richardson, M. Santarosa, K.J. Dillon, I. Hickson, C. Knights, N.M.B. Martin, S.P. Jackson, G.C.M. Smith, and A. Ashworth. 2005. Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy. Nature. 434:917-921.
Fisher, A.E., H. Hochegger, S. Takeda, and K.W. Caldecott. 2007. Poly(ADP-ribose) polymerase 1 accelerates single-strand break repair in concert with poly(ADP-ribose) glycohydrolase. Mol Cell Biol. 27:5597-5605.
Fukuoka, T., K. Hibi, and A. Nakao. 2006. Aberrant methylation is frequently observed in advanced esophageal squamous cell carcinoma. Anticancer Research. 26:3333-3335.
Gao, C., K. Furge, J. Koeman, K. Dykema, Y. Su, M.L. Cutler, A. Werts, P. Haak, and G.F. Vande Woude. 2007. Chromosome instability, chromosome transcriptome, and clonal evolution of tumor cell populations. Proceedings of the National Academy of Sciences of the United States of America. 104:8995-9000.
Ghosal, G., and J. Chen. 2013. DNA damage tolerance: a double-edged sword guarding the genome. Translational cancer research. 2:107-129.
Gudmundsdottir, K., and A. Ashworth. 2006. The roles of BRCA1 and BRCA2 and associated proteins in the maintenance of genomic stability. Oncogene. 25:5864-5874.
Haince, J.F., S. Kozlov, V.L. Dawson, T.M. Dawson, M.J. Hendzel, M.F. Lavin, and G.G. Poirier. 2007. Ataxia telangiectasia mutated (ATM) signaling network is modulated by a novel poly(ADP-ribose)-dependent pathway in the early response to DNA-damaging agents. Journal of Biological Chemistry. 282:16441-16453.
Hamai, Y., N. Oue, Y. Mitani, H. Nakayama, R. Ito, K. Matsusaki, K. Yoshida, T. Toge, and W. Yasui. 2003. DNA hypermethylation and histone hypoacetylation of the HLTF gene are associated with reduced expression in gastric carcinoma. Cancer Sci. 94:692-698.
Hassa, P.O., S.S. Haenni, M. Elser, and M.O. Hottiger. 2006. Nuclear ADP-ribosylation reactions in mammalian cells: where are we today and where are we going? Microbiology and Molecular Biology Reviews. 70:789-829.
Hassa, P.O., and M.O. Hottiger. 2008. The diverse biological roles of mammalian PARPS, a small but powerful family of poly-ADP-ribose polymerases. Frontiers in bioscience : a journal and virtual library. 13:3046-3082.
Houtgraaf, J.H., J. Versmissen, and W.J. van der Giessen. 2006. A concise review of DNA damage checkpoints and repair in mammalian cells. Cardiovascular revascularization medicine : including molecular interventions. 7:165-172.
Hu, Y., S.A. Petit, S.B. Ficarro, K.J. Toomire, A. Xie, E. Lim, S.A. Cao, E. Park, M.J. Eck, and R. Scully. 2014. PARP1-Driven Poly-ADP-Ribosylation Regulates BRCA1 Function in Homologous Recombination–Mediated DNA Repair. Cancer discovery. 4:1430-1447.
Huertas, P., and S.P. Jackson. 2009. Human CtIP mediates cell cycle control of DNA end resection and double strand break repair. The Journal of biological chemistry. 284:9558-9565.
Jackson, A.L., and L.A. Loeb. 1998. On the origin of multiple mutations in human cancers. In Seminars in cancer biology. Vol. 8. Elsevier. 421-429.
Johnson, R.E., S. Prakash, and L. Prakash. 1999. Efficient bypass of a thymine-thymine dimer by yeast DNA polymerase, Poleta. Science. 283:1001-1004.
Johnson, R.E., M.T. Washington, L. Haracska, S. Prakash, and L. Prakash. 2000. Eukaryotic polymerases iota and zeta act sequentially to bypass DNA lesions. Nature. 406:1015-1019.
Jungmichel, S., F. Rosenthal, M. Altmeyer, J. Lukas, M.O. Hottiger, and M.L. Nielsen. 2013. Proteome-wide identification of poly(ADP-Ribosyl)ation targets in different genotoxic stress responses. Mol Cell. 52:272-285.
Kang, S., J.W. Kim, G.H. Kang, S. Lee, N.H. Park, Y.S. Song, S.Y. Park, S.B. Kang, and H.P. Lee. 2006. Comparison of DNA hypermethylation patterns in different types of uterine cancer: cervical squamous cell carcinoma, cervical adenocarcinoma and endometrial adenocarcinoma. International journal of cancer. Journal international du cancer. 118:2168-2171.
Kannouche, P.L., J. Wing, and A.R. Lehmann. 2004. Interaction of human DNA polymerase η with monoubiquitinated PCNA: a possible mechanism for the polymerase switch in response to DNA damage. Molecular cell. 14:491-500.
Kolodner, R.D., C.D. Putnam, and K. Myung. 2002. Maintenance of genome stability in Saccharomyces cerevisiae. Science. 297:552-557.
Kraus, W.L. 2008. Transcriptional control by PARP-1: chromatin modulation, enhancer-binding, coregulation, and insulation. Curr Opin Cell Biol. 20:294-302.
Krishnakumar, R., and W.L. Kraus. 2010. The PARP side of the nucleus: molecular actions, physiological outcomes, and clinical targets. Mol Cell. 39:8-24.
Lavin, M.F., G. Birrell, P. Chen, S. Kozlov, S. Scott, and N. Gueven. 2005. ATM signaling and genomic stability in response to DNA damage. Mutation research. 569:123-132.
Li, B., S. Navarro, N. Kasahara, and L. Comai. 2004. Identification and biochemical characterization of a Werner's syndrome protein complex with Ku70/80 and poly(ADP-ribose) polymerase-1. The Journal of biological chemistry. 279:13659-13667.
Li, M., and X.C. Yu. 2013. Function of BRCA1 in the DNA Damage Response Is Mediated by ADP-Ribosylation. Cancer Cell. 23:693-704.
Li, N., and J. Chen. 2014. ADP-ribosylation: activation, recognition, and removal. Mol Cells. 37:9-16.
Liu, Y., and S.C. West. 2004. Happy Hollidays: 40th anniversary of the Holliday junction. Nature reviews. Molecular cell biology. 5:937-944.
Loeb, L.A. 2001. A mutator phenotype in cancer. Cancer Res. 61:3230-3239.
Loeb, L.A. 2011. Human cancers express mutator phenotypes: origin, consequences and targeting. Nature reviews. Cancer. 11:450-457.
Loeb, L.A., J.H. Bielas, and R.A. Beckman. 2008. Cancers exhibit a mutator phenotype: clinical implications. Cancer Res. 68:3551-3557; discussion 3557.
Loeb, L.A., K.R. Loeb, and J.P. Anderson. 2003. Multiple mutations and cancer. Proceedings of the National Academy of Sciences of the United States of America. 100:776-781.
Loeb, L.A., Springga.Cf, and N. Battula. 1974. Errors in DNA-Replication as a Basis of Malignant Changes. Cancer Research. 34:2311-2321.
Lukas, J., C. Lukas, and J. Bartek. 2011. More than just a focus: The chromatin response to DNA damage and its role in genome integrity maintenance. Nature Cell Biology. 13:1161-1169.
Luo, X., and W.L. Kraus. 2012. On PAR with PARP: cellular stress signaling through poly(ADP-ribose) and PARP-1. Genes & Development. 26:417-432.
Minca, E.C., and D. Kowalski. 2010. Multiple Rad5 activities mediate sister chromatid recombination to bypass DNA damage at stalled replication forks. Molecular cell. 38:649-661.
Mohrmann, L., and C.P. Verrijzer. 2005. Composition and functional specificity of SWI2/SNF2 class chromatin remodeling complexes. Biochimica et biophysica acta. 1681:59-73.
Moinova, H.R., W.D. Chen, L. Shen, D. Smiraglia, J. Olechnowicz, L. Ravi, L. Kasturi, L. Myeroff, C. Plass, R. Parsons, J. Minna, J.K. Willson, S.B. Green, J.P. Issa, and S.D. Markowitz. 2002. HLTF gene silencing in human colon cancer. Proceedings of the National Academy of Sciences of the United States of America. 99:4562-4567.
Motegi, A., H.J. Liaw, K.Y. Lee, H.P. Roest, A. Maas, X. Wu, H. Moinova, S.D. Markowitz, H. Ding, J.H. Hoeijmakers, and K. Myung. 2008. Polyubiquitination of proliferating cell nuclear antigen by HLTF and SHPRH prevents genomic instability from stalled replication forks. Proceedings of the National Academy of Sciences of the United States of America. 105:12411-12416.
Motegi, A., R. Sood, H. Moinova, S.D. Markowitz, P.P. Liu, and K. Myung. 2006. Human SHPRH suppresses genomic instability through proliferating cell nuclear antigen polyubiquitination. J Cell Biol. 175:703-708.
Moynahan, M.E., and M. Jasin. 2010. Mitotic homologous recombination maintains genomic stability and suppresses tumorigenesis. Nature reviews. Molecular cell biology. 11:196-207.
Niimi, A., S. Brown, S. Sabbioneda, P.L. Kannouche, A. Scott, A. Yasui, C.M. Green, and A.R. Lehmann. 2008. Regulation of proliferating cell nuclear antigen ubiquitination in mammalian cells. Proceedings of the National Academy of Sciences of the United States of America. 105:16125-16130.
Nyberg, K.A., R.J. Michelson, C.W. Putnam, and T.A. Weinert. 2002. Toward maintaining the genome: DNA damage and replication checkpoints. Annu Rev Genet. 36:617-656.
O'Donovan, P.J., and D.M. Livingston. 2010. BRCA1 and BRCA2: breast/ovarian cancer susceptibility gene products and participants in DNA double-strand break repair. Carcinogenesis. 31:961-967.
O'Driscoll, M., and P.A. Jeggo. 2006. The role of double-strand break repair—insights from human genetics. Nature Reviews Genetics. 7:45-54.
Ogi, T., Y. Shinkai, K. Tanaka, and H. Ohmori. 2002. Polkappa protects mammalian cells against the lethal and mutagenic effects of benzo[a]pyrene. Proceedings of the National Academy of Sciences of the United States of America. 99:15548-15553.
Parsons, J.L., Dianova, II, S.L. Allinson, and G.L. Dianov. 2005. Poly(ADP-ribose) polymerase-1 protects excessive DNA strand breaks from deterioration during repair in human cell extracts. The FEBS journal. 272:2012-2021.
Patel, A.G., J.N. Sarkaria, and S.H. Kaufmann. 2011. Nonhomologous end joining drives poly(ADP-ribose) polymerase (PARP) inhibitor lethality in homologous recombination-deficient cells. Proceedings of the National Academy of Sciences of the United States of America. 108:3406-3411.
Petermann, E., and T. Helleday. 2010. Pathways of mammalian replication fork restart. Nature reviews. Molecular cell biology. 11:683-687.
Petrini, J.H., and T.H. Stracker. 2003. The cellular response to DNA double-strand breaks: defining the sensors and mediators. Trends Cell Biol. 13:458-462.
Pfeiffer, P., W. Goedecke, and G. Obe. 2000. Mechanisms of DNA double-strand break repair and their potential to induce chromosomal aberrations. Mutagenesis. 15:289-302.
Prakash, S., R.E. Johnson, and L. Prakash. 2005. Eukaryotic translesion synthesis DNA polymerases: specificity of structure and function. Annual review of biochemistry. 74:317-353.
Rogakou, E.P., D.R. Pilch, A.H. Orr, V.S. Ivanova, and W.M. Bonner. 1998. DNA double-stranded breaks induce histone H2AX phosphorylation on serine 139. The Journal of biological chemistry. 273:5858-5868.
Rouleau, M., A. Patel, M.J. Hendzel, S.H. Kaufmann, and G.G. Poirier. 2010. PARP inhibition: PARP1 and beyond. Nature reviews. Cancer. 10:293-301.
Russell, P.A., P.D. Pharoah, K. De Foy, S.J. Ramus, I. Symmonds, A. Wilson, I. Scott, B.A. Ponder, and S.A. Gayther. 2000. Frequent loss of BRCA1 mRNA and protein expression in sporadic ovarian cancers. International journal of cancer. Journal international du cancer. 87:317-321.
Sale, J.E. 2013. Translesion DNA synthesis and mutagenesis in eukaryotes. Cold Spring Harbor perspectives in biology. 5:a012708.
San Filippo, J., P. Sung, and H. Klein. 2008. Mechanism of eukaryotic homologous recombination. Annual review of biochemistry. 77:229-257.
Sancar, A., L.A. Lindsey-Boltz, K. Unsal-Kacmaz, and S. Linn. 2004. Molecular mechanisms of mammalian DNA repair and the DNA damage checkpoints. Annu Rev Biochem. 73:39-85.
Schmitt, M., N. Harbeck, C. Thomssen, O. Wilhelm, V. Magdolen, U. Reuning, K. Ulm, H. Hofler, F. Janicke, and H. Graeff. 1997. Clinical impact of the plasminogen activation system in tumor invasion and metastasis: prognostic relevance and target for therapy. Thromb Haemost. 78:285-296.
Schreiber, V., J.C. Ame, P. Dolle, I. Schultz, B. Rinaldi, V. Fraulob, J. Menissier-de Murcia, and G. de Murcia. 2002. Poly(ADP-ribose) polymerase-2 (PARP-2) is required for efficient base excision DNA repair in association with PARP-1 and XRCC1. Journal of Biological Chemistry. 277:23028-23036.
Schreiber, V., F. Dantzer, J.C. Ame, and G. de Murcia. 2006. Poly(ADP-ribose): novel functions for an old molecule. Nature reviews. Molecular cell biology. 7:517-528.
Scully, R., and D.M. Livingston. 2000. In search of the tumour-suppressor functions of BRCA1 and BRCA2. Nature. 408:429-432.
Sheridan, P.L., M. Schorpp, M.L. Voz, and K.A. Jones. 1995. Cloning of an Snf2/Swi2-Related Protein That Binds Specifically to the Sph Motifs of the Sv40 Enhancer and to the Hiv-1 Promoter. Journal of Biological Chemistry. 270:4575-4587.
Storchova, Z., and D. Pellman. 2004. From polyploidy to aneuploidy, genome instability and cancer. Nature reviews. Molecular cell biology. 5:45-54.
Su, W.P., S.H. Hsu, C.K. Wu, S.B. Chang, Y.J. Lin, W.B. Yang, J.J. Hung, W.T. Chiu, S.F. Tzeng, Y.L. Tseng, J.Y. Chang, W.C. Su, and H. Liaw. 2014. Chronic treatment with cisplatin induces replication-dependent sister chromatid recombination to confer cisplatin-resistant phenotype in nasopharyngeal carcinoma. Oncotarget. 5:6323-6337.
Sung, P., L. Krejci, S. Van Komen, and M.G. Sehorn. 2003. Rad51 recombinase and recombination mediators. The Journal of biological chemistry. 278:42729-42732.
Tang, L., E. Nogales, and C. Ciferri. 2010. Structure and function of SWI/SNF chromatin remodeling complexes and mechanistic implications for transcription. Prog Biophys Mol Biol. 102:122-128.
Thompson, M.E., R.A. Jensen, P.S. Obermiller, D.L. Page, and J.T. Holt. 1995. Decreased expression of BRCA1 accelerates growth and is often present during sporadic breast cancer progression. Nature genetics. 9:444-450.
Tian, F., S. Sharma, J. Zou, S.Y. Lin, B. Wang, K. Rezvani, H. Wang, J.D. Parvin, T. Ludwig, C.E. Canman, and D. Zhang. 2013. BRCA1 promotes the ubiquitination of PCNA and recruitment of translesion polymerases in response to replication blockade. Proceedings of the National Academy of Sciences of the United States of America. 110:13558-13563.
Unk, I., I. Hajdu, K. Fátyol, B. Szakál, A. Blastyák, V. Bermudez, J. Hurwitz, L. Prakash, S. Prakash, and L. Haracska. 2006. Human SHPRH is a ubiquitin ligase for Mms2–Ubc13-dependent polyubiquitylation of proliferating cell nuclear antigen. Proceedings of the National Academy of Sciences. 103:18107-18112.
Wang, W. 2007. Emergence of a DNA-damage response network consisting of Fanconi anaemia and BRCA proteins. Nature reviews. Genetics. 8:735-748.
Waters, L.S., B.K. Minesinger, M.E. Wiltrout, S. D'Souza, R.V. Woodruff, and G.C. Walker. 2009. Eukaryotic translesion polymerases and their roles and regulation in DNA damage tolerance. Microbiology and molecular biology reviews : MMBR. 73:134-154.
Wilson, C.A., L. Ramos, M.R. Villasenor, K.H. Anders, M.F. Press, K. Clarke, B. Karlan, J.J. Chen, R. Scully, D. Livingston, R.H. Zuch, M.H. Kanter, S. Cohen, F.J. Calzone, and D.J. Slamon. 1999. Localization of human BRCA1 and its loss in high-grade, non-inherited breast carcinomas. Nature genetics. 21:236-240.
Winge, Ö. 1927. Zytologische Untersuchungen über die Natur maligner Tumoren. Zeitschrift für Zellforschung und Mikroskopische Anatomie. 6:397-423.
Wray, J., J. Liu, J.A. Nickoloff, and Z. Shen. 2008. Distinct RAD51 associations with RAD52 and BCCIP in response to DNA damage and replication stress. Cancer research. 68:2699-2707.
Yu, X., and J. Chen. 2004. DNA damage-induced cell cycle checkpoint control requires CtIP, a phosphorylation-dependent binding partner of BRCA1 C-terminal domains. Molecular and cellular biology. 24:9478-9486.
Zhou, B.B., and S.J. Elledge. 2000. The DNA damage response: putting checkpoints in perspective. Nature. 408:433-439.