DNA nucleotide excision repair-dependent signaling to checkpoint activation
Open accessAbstract
Eukaryotic cells respond to a variety of DNA insults by triggering a common signal transduction cascade, known as checkpoint response, which temporarily halts cell-cycle progression. Although the main players involved in the cascade have been identified, there is still uncertainty about the nature of the structures that activate these surveillance mechanisms. To understand the role of nucleotide excision repair (NER) in checkpoint activation, we analyzed the UV-induced phosphorylation of the key checkpoint proteins Chk1 and p53, in primary fibroblasts from patients with xeroderma pigmentosum (XP), Cockayne syndrome (CS), trichothiodystrophy (TTD), or UV light-sensitive syndrome. These disorders are due to defects in transcription-coupled NER (TC-NER) and/or global genome NER (GG-NER), the NER subpathways repairing the transcribed strand of active genes or the rest of the genome, respectively. We show here that in G 0 /G 1 and G 2 /M phases of the cell cycle, triggering of the DNA damage cascade requires recognition and processing of the lesions by the GG-NER. Loss of TC-NER does not affect checkpoint activation. Mutations in XPD , XPB , and in TTDA , encoding subunits of the TFIIH complex, involved in both transcription and NER, impair checkpoint triggering. The only exception is represented by mutations in XPD , resulting in combined features of XP and CS (XP/CS) that lead to activation of the checkpoint cascade after UV radiation. Inhibition of RNA polymerase II transcription significantly reduces the phosphorylation of key checkpoint factors in XP/CS fibroblasts on exposure to UV damage.
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XPA interacts with EXO1 to generate ssDNA lesions at UV damage sites in G1.
“interacts with EXO1 to generate the ssDNA lesions at UV damage sites in G1 [49;50].”
From ATR- and ATM-Mediated DNA Damage Response Is Dependent on Excision Repair Assembly during G1 but Not in S Phase of Cell Cycle (2016) · cites this paper as [50]
H2AX phosphorylation upon UV radiation is triggered by both NER-dependent and independent pathways.
“Previous studies in this area showed that H2AX phosphorylation upon UV radiation is triggered by both NER-dependent and independent pathways [50;61–63].”
From ATR- and ATM-Mediated DNA Damage Response Is Dependent on Excision Repair Assembly during G1 but Not in S Phase of Cell Cycle (2016) · cites this paper as [50]
Chk1 and p53 phosphorylation are not dependent on DDB2, XPC, and XPA in S phase cells.
“This is supported by Marini et. al., who showed that Chk1 and p53 phosphorylation are not dependent on DDB2, XPC, and XPA in S phase cells [50].”
From ATR- and ATM-Mediated DNA Damage Response Is Dependent on Excision Repair Assembly during G1 but Not in S Phase of Cell Cycle (2016) · cites this paper as [50]
UV-induced Chk1 phosphorylation is restricted in G1 and G2/M phases in XP-A mutated cells, but not in S phase cells.
“This data is supported by Marini et. al. showing that UV-induced Chk1 phosphorylation is restricted in G1 and G2/M phases in XP-A mutated cells, but not in S phase cells [50].”
From ATR- and ATM-Mediated DNA Damage Response Is Dependent on Excision Repair Assembly during G1 but Not in S Phase of Cell Cycle (2016) · cites this paper as [50]
Several studies have reported that NER factor-mediated lesion processing might be required for γH2AX foci formation.
“However, several studies reported that lesion processing by NER factors might be an essential step in γH2AX foci formation [35-39].”
From NER initiation factors, DDB2 and XPC, regulate UV radiation response by recruiting ATR and ATM kinases to DNA damage sites (2013) · cites this paper as [38]
There is a correlation between the ability of XP and CS cells to control G1 and G2/M transitions after UV, their genomic instability, and the tumor proneness of XP and CS patients.
“Intriguingly, there seems to be a correlation between the capacity of these cells to properly control G1 and G2/M transitions after UV, their genomic instability and the proneness of XP and CS patients to develop tumors [56].”
From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [56]
In human XP cells, lack of NER-dependent processing prevents UV-induced checkpoint activity in non-cycling fibroblasts, and XP cells are deficient in both repair and G1/G2/M UV-induced checkpoint.
“Extension of this kind of analysis to human cells derived from XP patients confirmed that lack of NER-dependent processing prevented UV-induced checkpoint activity in non cycling fibroblasts, revealing that XP cells are not only deficient in repairing UV lesions, but they are also deficient in the G1 and G2/M UV-induced checkpoint [56,57].”
From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [56]
XPC cells defective in GG-NER show checkpoint failure, while Cockayne syndrome cells defective in TC-NER can activate the checkpoint, possibly via GG-NER.
“Interestingly, while XPC cells, defective in GG-NER, exhibit a checkpoint failure, cells obtained from Cockayne syndrome patients, which are defective in TC-NER, are instead able to activate the checkpoint, possibly thanks to the activity of GG-NER.”
From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [56]
Outside S phase and in non-cycling cells, UV lesions alone cannot activate the checkpoint; NER plays a major role in triggering the checkpoint response, though contrasting results exist.
“Outside of S phase and in non cycling cells the situation is quite different. Recent analysis showed that UV lesions themselves cannot activate the checkpoint and NER plays a major role in triggering the checkpoint response, although contrasting results have also been reported [52–57].”
From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [56]
XPA, but not CSB, is necessary for UV-induced phosphorylation of Chk1 at serine 317 and p53 at serine 15.
“XPA, but not CSB, is required for UV-induced Chk1 phosphorylation at Serine 317 and p53 phosphorylation at Serine 15”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [200]
Global genome NER, but not transcription-coupled NER, is necessary for ATR-Chk1 checkpoint signaling.
“suggesting that GG-NER but not TC-NER (transcription-coupled NER) is required for ATR-Chk1 checkpoint signaling [200]”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [200]
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Cites
Friedberg, E. C., Walker, G. C., Siede, W., Wood, R. D., Schultz, R. A., & Ellenberger, T. (2005) · doi:10.1128/9781555816704 · Cited by 5,683 · see citing works
The DNA damage response: putting checkpoints in perspective
Zhou, B.-B. S., & Elledge, S. J. (2000) · Nature · doi:10.1038/35044005 · Cited by 3,213 · see citing works
Sensing DNA Damage Through ATRIP Recognition of RPA-ssDNA Complexes
Zou, L., & Elledge, S. J. (2003) · Science · doi:10.1126/science.1083430 · Cited by 2,693 · see citing works
Sugasawa, K., Ng, J. M. Y., Masutani, C., Iwai, S., van der Spek, P. J., Eker, A. P. M., Hanaoka, F., Bootsma, D., & Hoeijmakers, J. H. J. (1998) · Molecular Cell · doi:10.1016/s1097-2765(00)80132-x · Cited by 899 · see citing works
O'Driscoll, M., Ruiz-Perez, V. L., Woods, C. G., Jeggo, P. A., & Goodship, J. A. (2003) · Nature Genetics · doi:10.1038/ng1129 · Cited by 794 · see citing works
Hwang, B. J., Ford, J. M., Hanawalt, P. C., & Chu, G. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.2.424 · Cited by 581 · see citing works
The xeroderma pigmentosum group D (XPD) gene: one gene, two functions, three diseasesPreprint
Lehmann, A. R. (2001) · Genes & Development · doi:10.1101/gad.859501 · Cited by 370 · see citing works
Marti, T. M., Hefner, E., Feeney, L., Natale, V., & Cleaver, J. E. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0603779103 · Cited by 359 · see citing works
A new, tenth subunit of TFIIH is responsible for the DNA repair syndrome trichothiodystrophy group A
Giglia‐Mari, G., Coin, F., Ranish, J. A., Hoogstraten, D., Theil, A. F., Wijgers, N., Jaspers, N. G. J., Raams, A., Argentini, M., van der Spek, P. J., et al. (2004) · Nature Genetics · doi:10.1038/ng1387 · Cited by 334 · see citing works
Self-citationTaylor, E. M., Broughton, B. C., Botta, E., Stefanini, M., Sarasin, A. R., Jaspers, N. G. J., Fawcett, H., Harcourt, S. A., Arlett, C. F., & Lehmann, A. R. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.16.8658 · Cited by 262 · see citing works
Self-citationWard, I. M., Minn, K. T., & Chen, J. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.c300554200 · Cited by 205 · see citing works
Garinis, G. A., Mitchell, J. R., Moorhouse, M. J., Hanada, K., de Waard, H., Vandeputte, D., Jans, J. J. M., Brand, K., Smid, M., van der Spek, P. J., et al. (2005) · The EMBO Journal · doi:10.1038/sj.emboj.7600849 · Cited by 163 · see citing works
Chavanne, F., Broughton, B. C., Pietra, D., Nardò, T., Browitt, A., Lehmann, A. R., & Stefanini, M. (2000) · PubMed · Cited by 133 · see citing works
Self-citationVermeulen, W., Scott, R. J., Rodgers, S., Müller, H., Cole, J., Arlett, C. F., Kleijer, W. J., Bootsma, D., Hoeijmakers, J. H. J., & Weeda, G. (1994) · PubMed Central · Cited by 129 · see citing works
Genetic heterogeneity of the excision repair defect associated with trichothiodystrophy
Stefanini, M., Lagomarsini, P., Giliani, S. C., Nardò, T., Botta, E., Peserico, A., Kleijer, W. J., Lehmann, A. R., & Sarasin, A. R. (1993) · Carcinogenesis · doi:10.1093/carcin/14.6.1101 · Cited by 117 · see citing works
Self-citationPhysical and functional interactions between nucleotide excision repair and DNA damage checkpoint
Giannattasio, M., Lazzaro, F., Longhese, M. P., Plevani, P., & Muzi‐Falconi, M. (2004) · The EMBO Journal · doi:10.1038/sj.emboj.7600051 · Cited by 113 · see citing works
Self-citationRapic-Otrin, V. (2003) · Human Molecular Genetics · doi:10.1093/hmg/ddg174 · Cited by 113 · see citing works
p8/TTD-A as a Repair-Specific TFIIH Subunit
Coin, F., Proietti‐De‐Santis, L., Nardò, T., Zlobinskaya, O., Stefanini, M., & Egly, J. (2006) · Molecular Cell · doi:10.1016/j.molcel.2005.10.024 · Cited by 109 · see citing works
Self-citationBotta, E., Nardò, T., Broughton, B. C., Marinoni, S., Lehmann, A. R., & Stefanini, M. (1998) · The American Journal of Human Genetics · doi:10.1086/302063 · Cited by 107 · see citing works
Self-citationItoh, T., Ono, T., & Yamaizumi, M. (1994) · Mutation Research/DNA Repair · doi:10.1016/0921-8777(94)90068-x · Cited by 97 · see citing works
XPA protein as a limiting factor for nucleotide excision repair and UV sensitivity in human cells
Köberle, B., Roginskaya, V. Y., & Wood, R. D. (2006) · DNA repair · doi:10.1016/j.dnarep.2005.12.001 · Cited by 91 · see citing works
Bomgarden, R. D., Lupardus, P. J., Soni, D. V., Yee, M., Ford, J. M., & Cimprich, K. A. (2006) · The EMBO Journal · doi:10.1038/sj.emboj.7601123 · Cited by 87 · see citing works
Spivak, G. (2005) · Mutation research. Fundamental and molecular mechanisms of mutagenesis · doi:10.1016/j.mrfmmm.2005.03.017 · Cited by 86 · see citing works
Unwind and slow down: checkpoint activation by helicase and polymerase uncoupling: Figure 1.
Cortez, D. (2005) · Genes & Development · doi:10.1101/gad.1316905 · Cited by 84 · see citing works
Recruitment of DNA damage checkpoint proteins to damage in transcribed and nontranscribed sequences
Jiang, G., & Sancar, A. (2006) · Molecular and Cellular Biology · doi:10.1128/mcb.26.1.39-49.2006 · Cited by 70 · see citing works
Lalle, P., Nouspikel, T. P., Constantinou, A., Thorel, F., & Clarkson, S. G. (2002) · Journal of Investigative Dermatology · doi:10.1046/j.0022-202x.2001.01673.x · Cited by 55 · see citing works
Bowman, K. K., Sicard, D. M., Ford, J. M., & Hanawalt, P. C. (2000) · Molecular Carcinogenesis · doi:10.1002/1098-2744(200009)29:1 · Cited by 54 · see citing works
Conforti, G., Nardò, T., D’Incalci, M., & Stefanini, M. (2000) · Oncogene · doi:10.1038/sj.onc.1203583 · Cited by 54 · see citing works
Self-citationColella, S., Nardò, T., Mallery, D. L., Borrone, C., Ricci, R., Ruffa, G., Lehmann, A. R., & Stefanini, M. (1999) · Human Molecular Genetics · doi:10.1093/hmg/8.5.935 · Cited by 52 · see citing works
Self-citationHuman cell mutagenicity of mono- and dinitropyrenes in metabolically competent MCL-5 cells
Busby, W. F., Penman, B. W., & Crespi, C. L. (1994) · Mutation Research/Genetic Toxicology · doi:10.1016/0165-1218(94)90099-x · Cited by 47 · see citing works
Theron, T., Fousteri, M. I., Volker, M., Harries, L. W., Botta, E., Stefanini, M., Fujimoto, M., Andressoo, J., Mitchell, J., Jaspers, N. G. J., et al. (2005) · Molecular and Cellular Biology · doi:10.1128/mcb.25.18.8368-8378.2005 · Cited by 44 · see citing works
Self-citationThe cancer-free phenotype in trichothiodystrophy is unrelated to its repair defect.
Berneburg, M., Clingen, P. H., Harcourt, S. A., Lowe, J. E., Taylor, E. M., Green, M. H. L., Krutmann, J., Arlett, C. F., & Lehmann, A. R. (2000) · PubMed · Cited by 41 · see citing works
Heritable genetic alterations in a xeroderma pigmentosum group G/Cockayne syndrome pedigree
Okinaka, R. T., Perez-Castro, A. V., Sena, A., Laubscher, K. H., Strniste, G. F., Park, M. S., Hernandez, R. R., MacInnes, M. A., & Kraemer, K. H. (1997) · Mutation Research/DNA Repair · doi:10.1016/s0921-8777(97)00031-1 · Cited by 35 · see citing works
Lambert, B., & Ringborg, U. K. (1976) · Acta Medica Scandinavica · doi:10.1111/j.0954-6820.1976.tb08259.x · Cited by 9 · see citing works
Stefanini, M. (2006) · Springer eBooks · doi:10.1007/0-387-36802-7_3 · Cited by 6 · see citing works
Self-citation
Flagged first, then by citations
Research works printed but not linked: 4
- [12]Bowman KK, Sicard DM, Ford JM, Hanawalt PC. Mol Carcinog. 2000;29:17–24. [PubMed] [Google Scholar]
- [18]Chavanne F, Broughton BC, Pietra D, Nardo T, Browitt A, Lehmann AR, Stefanini M. Cancer Res. 2000;60:1974–1982. [PubMed] [Google Scholar]
- [30]Vermeulen W, Scott RJ, Rodgers S, Muller HJ, Cole J, Arlett CF, Kleijer WJ, Bootsma D, Hoeijmakers JHJ, Weeda G. Am J Hum Genet. 1994;54:191–200. [PMC free article] [PubMed] [Google Scholar]
- [32]Berneburg M, Clingen PH, Harcourt SA, Lowe JE, Taylor EM, Green MH, Krutmann J, Arlett CF, Lehmann AR. Cancer Res. 2000;60:431–438. [PubMed] [Google Scholar]
Cited by
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The DNA Damage Response: Making It Safe to Play with Knives
Ciccia, A., & Elledge, S. J. (2010) · Molecular Cell · doi:10.1016/j.molcel.2010.09.019 · Cited by 4,368 · see citing works
Mechanisms of DNA damage, repair, and mutagenesis
Chatterjee, N., & Walker, G. C. (2017) · Environmental and Molecular Mutagenesis · doi:10.1002/em.22087 · Cited by 2,039 · see citing works
Understanding nucleotide excision repair and its roles in cancer and ageing
Marteijn, J. A., Lans, H., Vermeulen, W., & Hoeijmakers, J. H. J. (2014) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3822 · Cited by 1,192 · see citing works
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MacDougall, C. A., Byun, T. S., Van, C., Yee, M.-C., & Cimprich, K. A. (2007) · Genes & Development · doi:10.1101/gad.1522607 · Cited by 240 · see citing works
Yan, S., Sorrell, M., & Berman, Z. (2014) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-014-1666-4 · Cited by 247 · see citing works
Roles of UVA radiation and DNA damage responses in melanoma pathogenesis
Khan, A. Q., Travers, J. B., & Kemp, M. G. (2018) · Environmental and Molecular Mutagenesis · doi:10.1002/em.22176 · Cited by 152 · see citing works
Yajima, H., Lee, K.-J., Zhang, S., Kobayashi, J., & Chen, B. P. C. (2009) · Journal of Molecular Biology · doi:10.1016/j.jmb.2008.11.036 · Cited by 124 · see citing works
Giannattasio, M., Follonier, C., Tourrière, H., Puddu, F., Lazzaro, F., Pasero, P., Lopes, M., Plevani, P., & Muzi-Falconi, M. (2010) · Molecular Cell · doi:10.1016/j.molcel.2010.09.004 · Cited by 121 · see citing works
Self-citationChk2-dependent phosphorylation of XRCC1 in the DNA damage response promotes base excision repair
Chou, W., Wang, H., Wong, F., Ding, S., Wu, P., Shieh, S., & Shen, C. (2008) · The EMBO Journal · doi:10.1038/emboj.2008.229 · Cited by 104 · see citing works
Vrouwe, M. G., Pines, A., Overmeer, R. M., Hanada, K., & Mullenders, L. H. F. (2011) · Journal of Cell Science · doi:10.1242/jcs.075325 · Cited by 100 · see citing works
Kerzendorfer, C., & O’Driscoll, M. (2009) · DNA Repair · doi:10.1016/j.dnarep.2009.04.018 · Cited by 97 · see citing works
Checkpoint mechanisms at the intersection between DNA damage and repair
Lazzaro, F., Giannattasio, M., Puddu, F., Granata, M., Pellicioli, A., Plevani, P., & Muzi-Falconi, M. (2009) · DNA Repair · doi:10.1016/j.dnarep.2009.04.022 · Cited by 94 · see citing works
Self-citationNavadgi-Patil, V. M., & Burgers, P. M. (2009) · DNA Repair · doi:10.1016/j.dnarep.2009.03.011 · Cited by 93 · see citing works
Ray, A., Milum, K., Battu, A., Wani, G., & Wani, A. A. (2013) · DNA Repair · doi:10.1016/j.dnarep.2013.01.003 · Cited by 85 · see citing works
“However, several studies reported that lesion processing by NER factors might be an essential step in γH2AX foci formation [35-39].”
BackgroundXeroderma pigmentosum genes: Functions inside and outside DNA repair
Sugasawa, K. (2007) · Carcinogenesis · doi:10.1093/carcin/bgm282 · Cited by 83 · see citing works
Sertic, S., Pizzi, S., Cloney, R., Lehmann, A. R., Marini, F., Plevani, P., & Muzi-Falconi, M. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1108547108 · Cited by 80 · see citing works
Self-citationRay, A., Mir, S. N., Wani, G., Zhao, Q., Battu, A., Zhu, Q., Wang, Q.-E., & Wani, A. A. (2009) · Molecular and Cellular Biology · doi:10.1128/mcb.00503-09 · Cited by 71 · see citing works
E2F1 Localizes to Sites of UV-induced DNA Damage to Enhance Nucleotide Excision Repair
Guo, R., Chen, J., Zhu, F., Biswas, A. K., Berton, T. R., Mitchell, D. L., & Johnson, D. G. (2010) · Journal of Biological Chemistry · doi:10.1074/jbc.m110.121939 · Cited by 69 · see citing works
Reconstitution of a human ATR-mediated checkpoint response to damaged DNA.
Choi, J.-H., Lindsey-Boltz, L. A., & Sancar, A. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0706013104 · Cited by 64 · see citing works
Coupling of Human DNA Excision Repair and the DNA Damage Checkpoint in a Defined in Vitro System
Lindsey-Boltz, L. A., Kemp, M. G., Reardon, J. T., DeRocco, V., Iyer, R. R., Modrich, P., & Sancar, A. (2014) · Journal of Biological Chemistry · doi:10.1074/jbc.m113.542787 · Cited by 59 · see citing works
Stergiou, L., Eberhard, R., Doukoumetzidis, K., & Hengartner, M. O. (2011) · Cell Death & Differentiation · doi:10.1038/cdd.2010.158 · Cited by 48 · see citing works
Sertic, S., Mollica, A., Campus, I., Roma, S., Tumini, E., Aguilera, A., & Muzi-Falconi, M. (2018) · Molecular Cell · doi:10.1016/j.molcel.2018.02.017 · Cited by 45 · see citing works
Self-citationRay, A., Blevins, C., Wani, G., & Wani, A. A. (2016) · PLOS ONE · doi:10.1371/journal.pone.0159344 · Cited by 44 · see citing works
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Novarina, D., Amara, F., Lazzaro, F., Plevani, P., & Muzi-Falconi, M. (2011) · DNA Repair · doi:10.1016/j.dnarep.2011.04.030 · Cited by 43 · see citing works
Self-citationLow, G. K. M., Fok, E. D. Z., Ting, A. P. L., & Hande, M. P. (2008) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2008.05.009 · Cited by 27 · see citing works
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Prætorius-Ibba, M., Wang, Q.-E., Wani, G., El-Mahdy, M. A., Zhu, Q., Qin, S., & Wani, A. A. (2007) · DNA Repair · doi:10.1016/j.dnarep.2006.11.009 · Cited by 24 · see citing works
Morino, M., Nukina, K., Sakaguchi, H., Maeda, T., Takahara, M., Shiomi, Y., & Nishitani, H. (2015) · PLOS ONE · doi:10.1371/journal.pone.0120553 · Cited by 7 · see citing works
- Authors
- Marini, F., Nardo, T., Giannattasio, M., Minuzzo, M., Stefanini, M., Plevani, P., & Falconi, M. M.
- Affiliations
- University of Milan (IT)
- Istituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche, Via Abbiategrasso 207, 27100 Pavia, Italy
- Istituto di Genetica Molecolare (IT)
- *Dipartimento di Scienze Biomolecolari e Biotecnologie, Universitá degli Studi di Milano, Via Celoria 26, 20133 Milano, Italy; and
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2006-11-14
- Volume
- 103
- Issue
- 46
- Pages
- 17325-17330
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC1859929
- OpenAlex
- W2130027970
- Cited by
- 114
- References
- 35
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2023: 1 · 2022: 10 · 2021: 4 · 2020: 2 · 2019: 3 · 2018: 4 · 2017: 5 · 2016: 8 · 2015: 5 · 2014: 9 · 2013: 8 · 2012: 5
- FWCI
- 3.67
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Consorzio Interuniversitario Biotecnologie
- European Commission
- International Centre for Genetic Engineering and Biotechnology
- Fondazione Cariplo
- Fondazione Italiana per la Ricerca sul Cancro
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- nucleotide excision repair, DNA damage checkpoint, checkpoint signaling, Chk1, p53, xeroderma pigmentosum, Cockayne syndrome, trichothiodystrophy, TFIIH, XPD, XPB, RNA polymerase II transcription, cell cycle arrest
- MeSH terms
- Cells, Cultured, DNA, DNA Repair, Fibroblasts, Humans, Transcription, Genetic, Xeroderma Pigmentosum, Signal Transduction, Genome, Human
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