Experts and Doctors on dna repair in Germany


Locale: Germany
Topic: dna repair

Top Publications

  1. Maacke H, Jost K, Opitz S, Miska S, Yuan Y, Hasselbach L, et al. DNA repair and recombination factor Rad51 is over-expressed in human pancreatic adenocarcinoma. Oncogene. 2000;19:2791-5 pubmed
    ..These data suggest that perturbations of Rad51 expression contribute to the malignant phenotype of pancreatic cancer. Oncogene (2000). ..
  2. Briegert M, Kaina B. Human monocytes, but not dendritic cells derived from them, are defective in base excision repair and hypersensitive to methylating agents. Cancer Res. 2007;67:26-31 pubmed
    ..The BER defect in monocytes may cause them to be selectively killed during tumor therapy with alkylating agents, provoking hematotoxicity and sustained immunosuppression. ..
  3. Nikolova T, Ensminger M, Lobrich M, Kaina B. Homologous recombination protects mammalian cells from replication-associated DNA double-strand breaks arising in response to methyl methanesulfonate. DNA Repair (Amst). 2010;9:1050-63 pubmed publisher
    ..Further, they show that HR is the major pathway of protection of cells against DSB formation, killing and genotoxicity following S(N)2-alkylating agents. ..
  4. Hocke S, Guo Y, Job A, Orth M, Ziesch A, Lauber K, et al. A synthetic lethal screen identifies ATR-inhibition as a novel therapeutic approach for POLD1-deficient cancers. Oncotarget. 2016;7:7080-95 pubmed publisher
    ..POLD1 deficiency might thus represent a predictive marker for treatment response towards ATR- or CHK1-inhibitors that are currently tested in clinical trials. ..
  5. Christmann M, Tomicic M, Aasland D, Kaina B. A role for UV-light-induced c-Fos: Stimulation of nucleotide excision repair and protection against sustained JNK activation and apoptosis. Carcinogenesis. 2007;28:183-90 pubmed
    ..The data support the hypothesis that non-repaired DNA damage is the cause for the late and sustained activation of the MAP kinase pathway in response to genotoxins. ..
  6. Beneke R, Geisen C, Zevnik B, Bauch T, Muller W, Kupper J, et al. DNA excision repair and DNA damage-induced apoptosis are linked to Poly(ADP-ribosyl)ation but have different requirements for p53. Mol Cell Biol. 2000;20:6695-703 pubmed
    ..Furthermore, we propose a p53-dependent link between PARP activity and DNA damage-induced cell death. ..
  7. Butkiewicz D, Popanda O, Risch A, Edler L, Dienemann H, Schulz V, et al. Association between the risk for lung adenocarcinoma and a (-4) G-to-A polymorphism in the XPA gene. Cancer Epidemiol Biomarkers Prev. 2004;13:2242-6 pubmed
    ..The underlying mechanisms as to why AA homozygotes are predisposed to lung adenocarcinoma and which specific carcinogens are involved remains to be determined. ..
  8. Kidane D, Graumann P. Dynamic formation of RecA filaments at DNA double strand break repair centers in live cells. J Cell Biol. 2005;170:357-66 pubmed
    ..Contrary to proteins forming RCs, DNA polymerase I did not form foci but was present throughout the nucleoids (even after induction of DSBs or after UV irradiation), suggesting that it continuously scans the chromosome for DNA lesions. ..
  9. Keimling M, Kaur J, Bagadi S, Kreienberg R, Wiesmuller L, Ralhan R. A sensitive test for the detection of specific DSB repair defects in primary cells from breast cancer specimens. Int J Cancer. 2008;123:730-6 pubmed publisher
    ..This method may, therefore, serve as a marker for breast cancer risk assessment and, even more importantly, for the prediction of responsiveness to targeted therapies such as to inhibitors of poly(ADP-ribose)polymerase (PARP1). ..

More Information

Publications233 found, 100 shown here

  1. Capalbo G, Dittmann K, Weiss C, Reichert S, Hausmann E, Rodel C, et al. Radiation-induced survivin nuclear accumulation is linked to DNA damage repair. Int J Radiat Oncol Biol Phys. 2010;77:226-34 pubmed publisher
    ..These data indicate that nuclear survivin is linked to DNA double-strand break repair by interaction with members of the DNA double-strand breaks repair machinery, thus regulating DNA-PKcs activity. ..
  2. Roth N, Klimesch J, Dukowic Schulze S, Pacher M, Mannuss A, Puchta H. The requirement for recombination factors differs considerably between different pathways of homologous double-strand break repair in somatic plant cells. Plant J. 2012;72:781-90 pubmed publisher
    ..Both SSA and SDSA were affected only weakly when the SMC6B protein, implicated in sister chromatid recombination, was absent, indicating that SSA and SDSA are in most cases intrachromatid recombination reactions. ..
  3. Day F, Ruth K, Thompson D, Lunetta K, Pervjakova N, Chasman D, et al. Large-scale genomic analyses link reproductive aging to hypothalamic signaling, breast cancer susceptibility and BRCA1-mediated DNA repair. Nat Genet. 2015;47:1294-1303 pubmed publisher
    ..Mendelian randomization analyses supported a causal effect of later ANM on breast cancer risk (∼6% increase in risk per year; P = 3 × 10(-14)), likely mediated by prolonged sex hormone exposure rather than DDR mechanisms. ..
  4. Fritz G, Grosch S, Tomicic M, Kaina B. APE/Ref-1 and the mammalian response to genotoxic stress. Toxicology. 2003;193:67-78 pubmed
    ..Because of its involvement in DNA repair and apoptosis-related signaling mechanisms, APE/Ref-1 is also being discussed as a novel target for tumor-therapeutic approaches. ..
  5. Bienko M, Green C, Crosetto N, Rudolf F, Zapart G, Coull B, et al. Ubiquitin-binding domains in Y-family polymerases regulate translesion synthesis. Science. 2005;310:1821-4 pubmed
    ..Our results indicate that Ub-binding domains of Y-family polymerases play crucial regulatory roles in TLS...
  6. Shannan B, Seifert M, Boothman D, Tilgen W, Reichrath J. Clusterin and DNA repair: a new function in cancer for a key player in apoptosis and cell cycle control. J Mol Histol. 2006;37:183-8 pubmed
    ..This review summarizes our current understanding of the role of clusterin in DNA repair, apoptosis, and cell cycle control and the relevance. ..
  7. Toulany M, Kehlbach R, Florczak U, Sak A, Wang S, Chen J, et al. Targeting of AKT1 enhances radiation toxicity of human tumor cells by inhibiting DNA-PKcs-dependent DNA double-strand break repair. Mol Cancer Ther. 2008;7:1772-81 pubmed publisher
    ..Thus, targeting of AKT enhances radiation sensitivity of lung cancer cell lines A549 and H460 most likely through specific inhibition of DNA-PKcs-dependent DNA-dsb repair but not through enhancement of radiation-induced apoptosis. ..
  8. Fleck O, Michael H, Heim L. The swi4+ gene of Schizosaccharomyces pombe encodes a homologue of mismatch repair enzymes. Nucleic Acids Res. 1992;20:2271-8 pubmed
    ..A strain with a disrupted swi4+ gene was constructed and analysed with respect to the switching process. As in swi4 mutants duplications occur in the mating-type region of the swi4 (null) strain, reducing the efficiency of switching. ..
  9. Hartwig A. Zinc finger proteins as potential targets for toxic metal ions: differential effects on structure and function. Antioxid Redox Signal. 2001;3:625-34 pubmed
  10. Fondufe Mittendorf Y, Härer C, Kramer W, Fritz H. Two amino acid replacements change the substrate preference of DNA mismatch glycosylase Mig.MthI from T/G to A/G. Nucleic Acids Res. 2002;30:614-21 pubmed
    ..The results also offer an explanation for why so many different substrate specificities are realized within the HhH superfamily of DNA repair glycosylases, and they widen the scope of these enzymes as practical tools. ..
  11. Hoege C, Pfander B, Moldovan G, Pyrowolakis G, Jentsch S. RAD6-dependent DNA repair is linked to modification of PCNA by ubiquitin and SUMO. Nature. 2002;419:135-41 pubmed
    ..We demonstrate that these modifications differentially affect resistance to DNA damage, and that damage-induced PCNA ubiquitination is elementary for DNA repair and occurs at the same conserved residue in yeast and humans. ..
  12. Assenmacher N, Wenig K, Lammens A, Hopfner K. Structural basis for transcription-coupled repair: the N terminus of Mfd resembles UvrB with degenerate ATPase motifs. J Mol Biol. 2006;355:675-83 pubmed
    ..Thus, our results suggest that Mfd might form a UvrA recruitment factor at stalled transcription complexes that architecturally but not catalytically resembles UvrB. ..
  13. Neveling K, Endt D, Hoehn H, Schindler D. Genotype-phenotype correlations in Fanconi anemia. Mutat Res. 2009;668:73-91 pubmed publisher
  14. Behrens A, van Deursen J, Rudolph K, Schumacher B. Impact of genomic damage and ageing on stem cell function. Nat Cell Biol. 2014;16:201-7 pubmed publisher
    ..We discuss DNA-damage-induced cell intrinsic and extrinsic alterations that influence these processes, and review recent advances in understanding systemic adjustments to DNA damage and how they affect stem cells. ..
  15. Meier P, Wackernagel W. Impact of mutS inactivation on foreign DNA acquisition by natural transformation in Pseudomonas stutzeri. J Bacteriol. 2005;187:143-54 pubmed
    ..We concluded that in P. stutzeri upregulation of MutS could enforce sexual isolation and downregulation could increase foreign DNA acquisition and that MutS affects mechanisms of HFIR...
  16. Frankenberger S, Davari K, Fischer Burkart S, Böttcher K, Tomi N, Zimber Strobl U, et al. Checkpoint kinase 1 negatively regulates somatic hypermutation. Nucleic Acids Res. 2014;42:3666-74 pubmed publisher
    ..Our data show that Chk1 signaling plays a crucial role in regulation of Ig diversification and sheds unexpected light on potential origins of aberrant somatic hypermutation in B cell lymphomagenesis. ..
  17. Ruf A, Mennissier de Murcia J, de Murcia G, Schulz G. Structure of the catalytic fragment of poly(AD-ribose) polymerase from chicken. Proc Natl Acad Sci U S A. 1996;93:7481-5 pubmed
    ..The enzyme is structurally related to bacterial ADP-ribosylating toxins but contains an additional alpha-helical domain that is suggested to relay the activation signal issued on binding to damaged DNA. ..
  18. Carell T, Burgdorf L, Kundu L, Cichon M. The mechanism of action of DNA photolyases. Curr Opin Chem Biol. 2001;5:491-8 pubmed
    ..The light-driven electron and energy transfer events that lead to the photolyase-catalyzed repair of lethal, mutagenic and carcinogenic UV-light-induced DNA lesions have all been examined in the past few years. ..
  19. Kruse R, Rutten A, Schweiger N, Jakob E, Mathiak M, Propping P, et al. Frequency of microsatellite instability in unselected sebaceous gland neoplasias and hyperplasias. J Invest Dermatol. 2003;120:858-64 pubmed
    ..Therefore, screening for microsatellite instability in sebaceous gland neoplasias will be of great value in the detection of an inherited DNA mismatch repair defect, which predisposes to various types of internal cancers...
  20. Liebe B, Petukhova G, Barchi M, Bellani M, Braselmann H, Nakano T, et al. Mutations that affect meiosis in male mice influence the dynamics of the mid-preleptotene and bouquet stages. Exp Cell Res. 2006;312:3768-81 pubmed
    ..Altogether, it appears that several pathways influence telomere dynamics in mammalian meiosis. ..
  21. Klassen R, Paluszynski J, Wemhoff S, Pfeiffer A, Fricke J, Meinhardt F. The primary target of the killer toxin from Pichia acaciae is tRNA(Gln). Mol Microbiol. 2008;69:681-97 pubmed publisher
    ..Most interestingly, a functional DSB repair pathway confers PaT but also zymocin resistance, suggesting DNA damage to occur generally concomitant with specific tRNA offence. ..
  22. Reiss C, Haneke T, Völker H, Spahn M, Rosenwald A, Edelmann W, et al. Conditional inactivation of MLH1 in thymic and naive T-cells in mice leads to a limited incidence of lymphoblastic T-cell lymphomas. Leuk Lymphoma. 2010;51:1875-86 pubmed publisher
  23. Weiler M, Blaes J, Pusch S, Sahm F, Czabanka M, Luger S, et al. mTOR target NDRG1 confers MGMT-dependent resistance to alkylating chemotherapy. Proc Natl Acad Sci U S A. 2014;111:409-14 pubmed publisher
    ..In patients with glioblastoma, MGMT promoter methylation in tumor tissue was not more predictive for response to alkylating chemotherapy in patients who received concomitant corticosteroids. ..
  24. Tashiro S, Walter J, Shinohara A, Kamada N, Cremer T. Rad51 accumulation at sites of DNA damage and in postreplicative chromatin. J Cell Biol. 2000;150:283-91 pubmed
    ..This finding supports a role of Rad51 in recombinational repair processes of DNA damage present in postreplicative chromatin. ..
  25. Fritz G, Kaina B. Phosphorylation of the DNA repair protein APE/REF-1 by CKII affects redox regulation of AP-1. Oncogene. 1999;18:1033-40 pubmed
  26. Speit G, Schutz P, Merk O. Induction and repair of formaldehyde-induced DNA-protein crosslinks in repair-deficient human cell lines. Mutagenesis. 2000;15:85-90 pubmed
  27. Bock N, Meden H, Regenbrecht M, Jünemann B, Wangerin J, Marx D. Expression of the mismatch repair protein hMSH2 in carcinoma in situ and invasive cancer of the breast. Anticancer Res. 2000;20:119-24 pubmed
    ..However, in invasive cancer, hMSH2 expression seems to be associated with tumor progression. This could be explained by the fact that enhanced proliferation of tumor cells results in increased mistakes within DNA replication procedures. ..
  28. Purschke M, Kasten Pisula U, Brammer I, Dikomey E. Human and rodent cell lines showing no differences in the induction but differing in the repair kinetics of radiation-induced DNA base damage. Int J Radiat Biol. 2004;80:29-38 pubmed
    ..Repair of radiation-induced Fpg-sensitive sites was much faster in rodent than in human cells, which might result from the higher level of polymerase ss found in rodent cells. ..
  29. Greubel C, Hable V, Drexler G, Hauptner A, Dietzel S, Strickfaden H, et al. Competition effect in DNA damage response. Radiat Environ Biophys. 2008;47:423-9 pubmed publisher
    ..The observed effects suggest that DNA damage response at individual nuclear sites depends on the time course of damage load. This may have implications for therapeutic radiation treatments. ..
  30. Schmitz K, Schmitt N, Hoffmann Rohrer U, Schäfer A, Grummt I, Mayer C. TAF12 recruits Gadd45a and the nucleotide excision repair complex to the promoter of rRNA genes leading to active DNA demethylation. Mol Cell. 2009;33:344-53 pubmed publisher
    ..The results reveal a mechanism that recruits the DNA repair machinery to the promoter of active genes, keeping them in a hypomethylated state. ..
  31. Ahmed E, Agay D, Schrock G, Drouet M, Meineke V, Scherthan H. Persistent DNA damage after high dose in vivo gamma exposure of minipig skin. PLoS ONE. 2012;7:e39521 pubmed publisher
    ..An elevated frequency of keratinocytes with persistent RIFs may thus serve as indicator of previous acute radiation exposure, which may be useful in the follow up of nuclear or radiological accident scenarios. ..
  32. Hackenberg S, Scherzed A, Zapp A, Radeloff K, Ginzkey C, Gehrke T, et al. Genotoxic effects of zinc oxide nanoparticles in nasal mucosa cells are antagonized by titanium dioxide nanoparticles. Mutat Res Genet Toxicol Environ Mutagen. 2017;816-817:32-37 pubmed publisher
    ..The combination of both metal oxide nanoparticles interferes with the genotoxicity of ZnO-NPs and should be discussed as a reasonable and safe alternative to the sole use of ZnO-NPs in consumer products. ..
  33. Osterod M, Larsen E, Le Page F, Hengstler J, van der Horst G, Boiteux S, et al. A global DNA repair mechanism involving the Cockayne syndrome B (CSB) gene product can prevent the in vivo accumulation of endogenous oxidative DNA base damage. Oncogene. 2002;21:8232-9 pubmed
    ..The data indicate a role for Csb in the removal of 8-oxoG from the overall genome that is independent of both Ogg1-mediated base excision repair and regular transcription. ..
  34. Toulany M, Dittmann K, Fehrenbacher B, Schaller M, Baumann M, Rodemann H. PI3K-Akt signaling regulates basal, but MAP-kinase signaling regulates radiation-induced XRCC1 expression in human tumor cells in vitro. DNA Repair (Amst). 2008;7:1746-56 pubmed publisher
    ..Likewise, potential of IR-induced XRCC1 expression depends on its basal expression level. ..
  35. Hennecke F, Kolmar H, Bründl K, Fritz H. The vsr gene product of E. coli K-12 is a strand- and sequence-specific DNA mismatch endonuclease. Nature. 1991;353:776-8 pubmed
    ..The incision is mismatch-dependent and strand-specific. These results illustrate how Vsr endonuclease initiates VSP mismatch repair. ..
  36. Norgauer J, Idzko M, Panther E, Hellstern O, Herouy Y. Xeroderma pigmentosum. Eur J Dermatol. 2003;13:4-9 pubmed
    ..In future, causal therapy could be based on gene therapy. The introduction of an intact repair gene which specifically codes the repair protein, could open new possibilities in the treatment of xeroderma pigmentosum. ..
  37. Christmann M, Tomicic M, Gestrich C, Roos W, Bohr V, Kaina B. WRN protects against topo I but not topo II inhibitors by preventing DNA break formation. DNA Repair (Amst). 2008;7:1999-2009 pubmed publisher
    ..We suggest that the WRN status of tumor cells impacts anticancer therapy with topoisomerase I, but not topoisomerase II inhibitors. ..
  38. Nollen M, Ebert F, Moser J, Mullenders L, Hartwig A, Schwerdtle T. Impact of arsenic on nucleotide excision repair: XPC function, protein level, and gene expression. Mol Nutr Food Res. 2009;53:572-82 pubmed publisher
    ..In summary, our data demonstrate that in human skin fibroblasts arsenite and even more pronounced MMA(III) interact with XPC expression, resulting in decreased XPC protein level and diminished assembly of the NER machinery. ..
  39. Boeckmann L, Schirmer M, Rosenberger A, Struever D, Thoms K, Gutzmer R, et al. Effect of DNA repair host factors on temozolomide or dacarbazine melanoma treatment in Caucasians. Pharmacogenet Genomics. 2009;19:760-9 pubmed publisher
    ..The genetic variant rs2303428 (MSH2) might serve as a predictive marker for hematologic side effects and treatment response. ..
  40. Lage H, Christmann M, Kern M, Dietel M, Pick M, Kaina B, et al. Expression of DNA repair proteins hMSH2, hMSH6, hMLH1, O6-methylguanine-DNA methyltransferase and N-methylpurine-DNA glycosylase in melanoma cells with acquired drug resistance. Int J Cancer. 1999;80:744-50 pubmed
    ..Our data indicate that modulation of both MMR components and MGMT expression level may contribute to the drug-resistant phenotype of melanoma cells. ..
  41. Muyrers J, Zhang Y, Buchholz F, Stewart A. RecE/RecT and Redalpha/Redbeta initiate double-stranded break repair by specifically interacting with their respective partners. Genes Dev. 2000;14:1971-82 pubmed
    ..The DSB repair reactions studied here are reminiscent of the RecBCD/RecA reaction and suggest a general mechanism that is likely to be relevant to other systems, including RAD52 mediated recombination. ..
  42. Grummt I. Life on a planet of its own: regulation of RNA polymerase I transcription in the nucleolus. Genes Dev. 2003;17:1691-702 pubmed
  43. Adelfalk C, Kontou M, Hirsch Kauffmann M, Schweiger M. Physical and functional interaction of the Werner syndrome protein with poly-ADP ribosyl transferase. FEBS Lett. 2003;554:55-8 pubmed
    ..Here we demonstrate an interaction of these two proteins resulting in ADP-ribosylation of the WRN protein. These results imply that WRN is involved in DNA replication and in DNA repair. ..
  44. Kruse R, Ruzicka T. DNA mismatch repair and the significance of a sebaceous skin tumor for visceral cancer prevention. Trends Mol Med. 2004;10:136-41 pubmed
  45. Goekkurt E, Hoehn S, Wolschke C, Wittmer C, Stueber C, Hossfeld D, et al. Polymorphisms of glutathione S-transferases (GST) and thymidylate synthase (TS)--novel predictors for response and survival in gastric cancer patients. Br J Cancer. 2006;94:281-6 pubmed
    ..044). Testing for TS and GSTP1 polymorphisms may allow identification of gastric cancer patients who will benefit from 5-FU/cisplatin chemotherapy, sparing others the side effects of this chemotherapy. ..
  46. Deckbar D, Birraux J, Krempler A, Tchouandong L, Beucher A, Walker S, et al. Chromosome breakage after G2 checkpoint release. J Cell Biol. 2007;176:749-55 pubmed
    ..Strikingly, we show that checkpoint release occurs at a point when approximately three to four premature chromosome condensation breaks and approximately 20 gammaH2AX foci remain. ..
  47. Kirik V, Schrader A, Uhrig J, Hulskamp M. MIDGET unravels functions of the Arabidopsis topoisomerase VI complex in DNA endoreduplication, chromatin condensation, and transcriptional silencing. Plant Cell. 2007;19:3100-10 pubmed
  48. Briggs A, Stenzel U, Meyer M, Krause J, Kircher M, Paabo S. Removal of deaminated cytosines and detection of in vivo methylation in ancient DNA. Nucleic Acids Res. 2010;38:e87 pubmed publisher
    ..In addition, our results demonstrate that Neandertal DNA retains in vivo patterns of CpG methylation, potentially allowing future studies of gene inactivation and imprinting in ancient organisms...
  49. Steininger S, Ahne F, Winkler K, Kleinschmidt A, Eckardt Schupp F, Moertl S. A novel function for the Mre11-Rad50-Xrs2 complex in base excision repair. Nucleic Acids Res. 2010;38:1853-65 pubmed publisher
    ..Reduced gap-filling activity and the missing effect of aphidicoline treatment, an inhibitor for polymerases, on the BER efficiency indicate an involvement of the MRX complex in providing efficient polymerase activity. ..
  50. Zhang S, Hemmerich P, Grosse F. Werner syndrome helicase (WRN), nuclear DNA helicase II (NDH II) and histone gammaH2AX are localized to the centrosome. Cell Biol Int. 2007;31:1109-21 pubmed
  51. Fritz G. Human APE/Ref-1 protein. Int J Biochem Cell Biol. 2000;32:925-9 pubmed
    ..Thus, specific downmodulation of APE/Ref-1 activity in tumors might be considered as a novel therapeutic approach in tumor therapy. ..
  52. Alpi A, Pasierbek P, Gartner A, Loidl J. Genetic and cytological characterization of the recombination protein RAD-51 in Caenorhabditis elegans. Chromosoma. 2003;112:6-16 pubmed
  53. Kidane D, Sanchez H, Alonso J, Graumann P. Visualization of DNA double-strand break repair in live bacteria reveals dynamic recruitment of Bacillus subtilis RecF, RecO and RecN proteins to distinct sites on the nucleoids. Mol Microbiol. 2004;52:1627-39 pubmed
  54. Rennicke A, Voigt W, Mueller T, Fruehauf A, Schmoll H, Beyer C, et al. Resistance mechanisms following cisplatin and oxaliplatin treatment of the human teratocarcinoma cell line 2102EP. Anticancer Res. 2005;25:1147-55 pubmed
    ..Oxaliplatin and cisplatin are widely used in cancer chemotherapy, however, their clinical efficiency is often limited by the development of resistance...
  55. Lubomierski N, Plotz G, Wormek M, Engels K, Kriener S, Trojan J, et al. BRAF mutations in colorectal carcinoma suggest two entities of microsatellite-unstable tumors. Cancer. 2005;104:952-61 pubmed
  56. Essen L, Klar T. Light-driven DNA repair by photolyases. Cell Mol Life Sci. 2006;63:1266-77 pubmed
    ..Apart from these mechanistic aspects, the potential of DNA photolyases for the generation of highly UV-resistant organisms, or for skin cancer prevention by ectopical application is increasingly recognized. ..
  57. Pacher M, Schmidt Puchta W, Puchta H. Two unlinked double-strand breaks can induce reciprocal exchanges in plant genomes via homologous recombination and nonhomologous end joining. Genetics. 2007;175:21-9 pubmed
    ..Thus, DSB-induced reciprocal exchanges might play a significant role in plant genome evolution. The technique applied in this study may also be useful for the controlled exchange of unlinked sequences in plant genomes. ..
  58. Gatz S, Keimling M, Baumann C, Dork T, Debatin K, Fulda S, et al. Resveratrol modulates DNA double-strand break repair pathways in an ATM/ATR-p53- and -Nbs1-dependent manner. Carcinogenesis. 2008;29:519-27 pubmed publisher
    ..Repression of error-prone recombination subpathways could at least partially explain the chemopreventive effects of this natural plant constituent in animal cancer models. ..
  59. Emmert S, Ueda T, Zumsteg U, Weber P, Khan S, Oh K, et al. Strict sun protection results in minimal skin changes in a patient with xeroderma pigmentosum and a novel c.2009delG mutation in XPD (ERCC2). Exp Dermatol. 2009;18:64-8 pubmed publisher
    ..Gly670Alafs*39). The latter mutation potentially behaves as a null allele. While not preventing neurological degeneration, early diagnosis and rigorous sun protection can result in minimal skin disease without cancer in XP patients. ..
  60. Schomacher L, Schürer K, Ciirdaeva E, McDermott P, Chong J, Kramer W, et al. Archaeal DNA uracil repair via direct strand incision: A minimal system reconstituted from purified components. DNA Repair (Amst). 2010;9:438-47 pubmed publisher
    ..Finally, DNA ligase seals the resulting nick. This defines mechanism and minimal enzymatic requirements of DNA-U repair in this organism. ..
  61. Becker K, Thomas A, Kaina B. Does increase in DNA repair allow "tolerance-to-insult" in chemical carcinogenesis? Skin tumor experiments with MGMT-overexpressing mice. Environ Mol Mutagen. 2014;55:145-50 pubmed publisher
    ..It is shown here that MGMT overexpression significantly protects against, but does not completely nullify, the effect of MNU in tumor initiation. The possible mechanisms involved have also been discussed. ..
  62. Stopper H, Full M, Helbig R, Speit G. Micronucleus induction by neocarzinostatin and methyl methanesulfonate in ionizing radiation--sensitive Chinese hamster V79 cell mutants. Mutat Res. 1997;383:107-12 pubmed
    ..Thus, defects in cellular responses to DNA damage are modulating factors in micronucleus formation. ..
  63. Starkuviene V, Fritz H. A novel type of uracil-DNA glycosylase mediating repair of hydrolytic DNA damage in the extremely thermophilic eubacterium Thermus thermophilus. Nucleic Acids Res. 2002;30:2097-102 pubmed
    ..Together, the characteristics of TTUDGB and its homologs in other organisms define a novel family of UDG repair enzymes...
  64. Justenhoven C, Hamann U, Pesch B, Harth V, Rabstein S, Baisch C, et al. ERCC2 genotypes and a corresponding haplotype are linked with breast cancer risk in a German population. Cancer Epidemiol Biomarkers Prev. 2004;13:2059-64 pubmed
    ..49; 95% CI, 2.30-5.28). To our knowledge, this is the first study assigning breast cancer risk to both the ERCC2 genotype encoding Asp(312)Asp and the haplotype encoding Asp(312)/Gln(751). ..
  65. Baumann C, Boehden G, Burkle A, Wiesmuller L. Poly(ADP-RIBOSE) polymerase-1 (Parp-1) antagonizes topoisomerase I-dependent recombination stimulation by P53. Nucleic Acids Res. 2006;34:1036-49 pubmed
    ..Our data further indicate that PARP-1, probably through topoisomerase I interactions rather than poly(ADP-ribosyl)ation, prevents p53 from stimulating spontaneous HR on chromosomes via topoisomerase I activity. ..
  66. Mortusewicz O, Ame J, Schreiber V, Leonhardt H. Feedback-regulated poly(ADP-ribosyl)ation by PARP-1 is required for rapid response to DNA damage in living cells. Nucleic Acids Res. 2007;35:7665-75 pubmed
    ..We conclude that feedback regulated recruitment of PARP-1 and concomitant local poly(ADP-ribosyl)ation at DNA lesions amplifies a signal for rapid recruitment of repair factors enabling efficient restoration of genome integrity. ..
  67. Ragg H. Intron creation and DNA repair. Cell Mol Life Sci. 2011;68:235-42 pubmed publisher
    ..Some implications on our perception of the mosaic structure of eukaryotic genes are also discussed. ..
  68. Chanarat S, Burkert Kautzsch C, Meinel D, Sträßer K. Prp19C and TREX: interacting to promote transcription elongation?and mRNA export. Transcription. 2012;3:8-12 pubmed publisher
    ..We recently identified Prp19C to be essential for a second step in gene expression namely TREX occupancy at transcribed genes, answering this long-standing question but also raising new ones. ..
  69. Deshmukh J, Pofahl R, Haase I. Epidermal Rac1 regulates the DNA damage response and protects from UV-light-induced keratinocyte apoptosis and skin carcinogenesis. Cell Death Dis. 2017;8:e2664 pubmed publisher
    ..Taken together, our data provide direct evidence for a protective role of Rac1 in UV-light-induced skin carcinogenesis and keratinocyte apoptosis probably through regulating mechanisms of the DNA damage response and repair pathways. ..
  70. Ziegler Skylakakis K, Nill S, Pan J, Andrae U. S-oxygenation of thiourea results in the formation of genotoxic products. Environ Mol Mutagen. 1998;31:362-73 pubmed
    ..The finding that FASA, a product of both the nonenzymatic and the enzymatic S-oxygenation of TU, is genotoxic in cultured mammalian cells provides for the first time a hypothesis to explain the genotoxicity of TU...
  71. Michl P, Downward J. Mechanisms of disease: PI3K/AKT signaling in gastrointestinal cancers. Z Gastroenterol. 2005;43:1133-9 pubmed
    ..In addition, activation of PI3K/Akt by various growth factors, the modulation of downstream targets by Akt-induced phosphorylation as well as novel treatment strategies targeting this pathway in gastrointestinal tumors are discussed. ..
  72. Weichart D, Gobom J, Klopfleisch S, Häsler R, Gustavsson N, Billmann S, et al. Analysis of NOD2-mediated proteome response to muramyl dipeptide in HEK293 cells. J Biol Chem. 2006;281:2380-9 pubmed
  73. Rass K, Reichrath J. UV damage and DNA repair in malignant melanoma and nonmelanoma skin cancer. Adv Exp Med Biol. 2008;624:162-78 pubmed publisher
  74. Mortusewicz O, Roth W, Li N, Cardoso M, Meisterernst M, Leonhardt H. Recruitment of RNA polymerase II cofactor PC4 to DNA damage sites. J Cell Biol. 2008;183:769-76 pubmed publisher
    ..We propose that PC4 plays a role in the early response to DNA damage by recognizing single-stranded DNA and may thus initiate or facilitate the subsequent steps of DNA repair. ..
  75. Rübe C, Fricke A, Wendorf J, Stützel A, Kühne M, Ong M, et al. Accumulation of DNA double-strand breaks in normal tissues after fractionated irradiation. Int J Radiat Oncol Biol Phys. 2010;76:1206-13 pubmed publisher
    ..Moreover, our data indicate that even minor impairments in DSB repair lead to exceeding DNA damage accumulation during fractionated irradiation and thus may have a significant impact on normal tissue responses in clinical radiotherapy. ..
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