• Title/Summary/Keyword: DNA repair

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DNA Repair Enhancement by Radioprotective Ginseng Protein Fraction (항 방사선 인삼단백분획의 DNA수복능력 증진효과)

  • Kim, Choon-Mi;Choi, Mi-Kyung
    • YAKHAK HOEJI
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    • v.36 no.5
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    • pp.449-454
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    • 1992
  • The effect of radioprotective ginseng protein fraction on DNA repair capacity was determined by measuring the amount of $^{3}H-thymidine$ incorporated into DNA in the process of repair synthesis for UV damaged DNA. CHO-Kl cells were prepared whose semiconservative replication was inhibited by trimethylpsoralen plus near-UV(PUVA) treatment. When the cells were exposed to UV light alone, the DNA repair capacity was increased at first and then decreased as UV dose increased. However, when the ginseng fraction was treated to the cells, the DNA repair capacity was kept increasing regardless of UV dose increment. When the concentration of protein contained in the added fraction was increased gradually, the repair capacity was also increased almost linearly showing dose-response relationship of the effect. These results suggest that the enhancement of DNA repair capacity of the cell can be one of the mechanisms of radioprotection by the ginseng fraction.

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Gamma-ray Induced DNA Repair Synthesis in Relation to Chromosome Exchanges in Mammalian Cells in Vitro (哺乳動物細胞에 있어 감마線에 의한 DNA 回復合成과 染色體交換과의 聯關性)

  • Park, Sang-Dai
    • The Korean Journal of Zoology
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    • v.18 no.1
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    • pp.41-49
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    • 1975
  • Dose response and time dependence of DNA repair synthesis were investigated to determine the possible relationship between DNA repair synthesis and chromosome exchanges in $\\gamma$-ray irradiated BHK-21 and KB cell lines. DNA repair synthesis induced by $\\gamma$-ray was dose dependent up to 5kR, then leveling off occurred until 50 kR was reached. Time dependence of DNA repair synthesis was continued for up to 1$\\sim$2 hours after irradiation although the initial dose responses were cell line specific. Chromosome exchanges induced by $\\gamma$-ray showed different radiosensitivities in these cell lines and did not show a correlation with the DNA repair synthesis.

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Revealing Regulatory Networks of DNA Repair Genes in S. Cerevisiae

  • Kim, Min-Sung;Lee, Do-Heon;Yi, Gwan-Su
    • Bioinformatics and Biosystems
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    • v.2 no.1
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    • pp.12-16
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    • 2007
  • DNA repair means a collection of processes that a cell identifies and corrects damage to genome sequence. The DNA repair processes are important because a genome would not be able to maintain its essential cellular functions without the processes. In this research, we make some gene regulatory networks of DNA repair in S. cerevisiae to know how each gene interacts with others. Two approaches are adapted to make the networks; Bayesian Network and ARACNE. After construction of gene regulatory networks based on the two approaches, the two networks are compared to each other to predict which genes have important roles in the DNA repair processes by finding conserved interactions and looking for hubs. In addition, each interaction between genes in the networks is validated with interaction information in S. cerevisiae genome database to support the meaning of predicted interactions in the networks.

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DNA Repair Gene Polymorphisms at XRCC1, XRCC3, XPD, and OGG1 Loci in the Hyderabad Population of India

  • Parine, Narasimha Reddy;Pathan, Akbar Ali Khan;Bobbarala, Varaprasad;Abduljaleel, Zainularifeen;Khan, Wajahatullah;Alanazi, Mohammed
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.12
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    • pp.6469-6474
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    • 2012
  • Background: DNA repair is one of the crucial defense mechanism against mutagenic exposure. Inherited SNPs of DNA repair genes may contribute to variation in DNA repair capacity and susceptibility to cancer. Due to the presence of these variants, inter-individual and ethnic differences in DNA repair capacity have been established in various populations. India harbors enormous genetic and cultural diversity. Materials and Methods: In the present study we aimed to determine the genotypes and allele frequencies of XRCC1 Arg399Gln (rs25487), XRCC3 Thr241Met (rs861539), XPD Lys751Gln (rs13181), and OGG1 Ser326Cys (rs1052133) gene polymorphisms in 186 healthy individuals residing in the Hyderabad region of India and to compare them with HapMap and other populations. Results and Conclusions: The genotype and allele frequency distribution at the four DNA repair gene loci among Hyderabad population of India revealed a characteristic pattern. Comparison of these gene polymorphisms with other populations revealed a distinctiveness of Hyderabad population from the Deccan region of India. To the best of our knowledge, this is the first report of such DNA repair gene polymorphisms in the Deccan Indian population.

Effect of 3-Aminobenzamide on DNA Repair Synthesis and Chromosome Aberrations Induced by Mutagens in Synchronized Mammalian Cells (동시화된 포유동물세포에서 돌연변이원에 의해 유발된 DNA 회복합성 및 염색체이상에 미치는 3-Aminobenzamide의 영향)

  • 신은주;강인영;엄경일
    • Environmental Mutagens and Carcinogens
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    • v.11 no.2
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    • pp.107-117
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    • 1991
  • The effect of 3-aminobenzamide (3AB), an inhibitor of poly (ADP-ribose) polymerase, on ethyl methanesulfonate (EMS)-or bleomycin (BLM)-induced DNA repair synthesis and chromosome aberrations was examined during the cell cycle of Chinese hamster ovary (CHO)-K$_1$ cells. The synchronized cells were obtained by using thymidine double block method and mitotic selection method. Three assays were employed in this study: unscheduled DNA synthesis, alkaline elution and chromosome aberrations. 3AB alone did not induce DNA repair and chromosome aberrations in all phases. The post-treatment with 3AB inhibited DNA repair synthesis induced by EMS or BLM in G$_2$ phase, whereas 3AB did not affect chromosome aberrations induced by EMS or BLM in all phases. These results suggest that 3AB aggravates the cell cycle disturbance which occur after DNA damage, and leads to an accumulation of cells at G$_2$ phase, and inhibits DNA repair synthesis, while the effect 3AB on chromosome aberrations may need reevaluated.

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Exploiting the Fanconi Anemia Pathway for Targeted Anti-Cancer Therapy

  • Jo, Ukhyun;Kim, Hyungjin
    • Molecules and Cells
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    • v.38 no.8
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    • pp.669-676
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    • 2015
  • Genome instability, primarily caused by faulty DNA repair mechanisms, drives tumorigenesis. Therapeutic interventions that exploit deregulated DNA repair in cancer have made considerable progress by targeting tumor-specific alterations of DNA repair factors, which either induces synthetic lethality or augments the efficacy of conventional chemotherapy and radiotherapy. The study of Fanconianemia (FA), a rare inherited blood disorder and cancer predisposition syndrome, has been instrumental in understanding the extent to which DNA repair defects contribute to tumorigenesis. The FA pathway functions to resolve blocked replication forks in response to DNA interstrand cross-links (ICLs), and accumulating knowledge of its activation by the ubiquitin-mediated signaling pathway has provided promising therapeutic opportunities for cancer treatment. Here, we discuss recent advances in our understanding of FA pathway regulation and its potential application for designing tailored therapeutics that take advantage of deregulated DNA ICL repair in cancer.

Environmental Toxic Agents on Genetic Material and Cellular Ativity V. The Roles of DNA Polymerases on Mutagen-Induced DNA Repair Synthesis in Relation to Cell Cycle in Chinese Hamster Ovary Cells (환경성 유해요인이 유전물질과 세포활성에 미치는 영향 V. CHO세포에서 세포주기에 따라 돌연변이원에 의해 유발된 DNA회복합성에 미치는 DNA중합효소의 역할)

  • 엄경일;김춘광;신은주;문용석;이천복
    • Environmental Mutagens and Carcinogens
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    • v.9 no.1
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    • pp.23-32
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    • 1989
  • Chinese hamster ovary (CHO)-K1 cells echibited a differential sensitivity in the process of DNA repair synthesis induced by ethyl methanesulfonate (EMS) or bleomycin (BLM) in relation to cell cycle. Two assays were employed in this study: alkaline elution and unscheduled DNA synthesis. The post-treat-ment with aphidicolin (APC), an inhibitor of DNA polymerase alpha, inhibited DNA repair synthesis induced by EMS in G2 phase, while APC did not show any effect on BLM-induced DNA repair synthesis in all phases. On the other hands, the 2', 3'-dideoxythymidine (ddTTP), an inhibitor of DNA polymerase beta, inhibited DNA repair synthesis induced by EMS or BLM in both of G1 and G2 phases. These results suggested that the involvement of DNA polymerase alpha and beta in DNA repair was dependent on cell stage or used chemical agent.

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Influence of Morinda citrifolia (Noni) on Expression of DNA Repair Genes in Cervical Cancer Cells

  • Gupta, Rakesh Kumar;Bajpai, Deepti;Singh, Neeta
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.8
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    • pp.3457-3461
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    • 2015
  • Background: Previous studies have suggested that Morinda citrifolia (Noni) has potential to reduce cancer risk. Objective: The purpose of this study was to investigate the effect of Noni, cisplatin, and their combination on DNA repair genes in the SiHa cervical cancer cell line. Materials and Methods: SiHa cells were cultured and treated with 10% Noni, $10{\mu}g/dl$ cisplatin or their combination for 24 hours. Post culturing, the cells were pelleted, RNA extracted, and processed for investigating DNA repair genes by real time PCR. Results: The expression of nucleotide excision repair genes ERCC1, ERCC2, and ERCC4 and base excision repair gene XRCC1 was increased 4 fold, 8.9 fold, 4 fold, and 5.5 fold, respectively, on treatment with Noni as compared to untreated controls (p<0.05). In contrast, expression was found to be decreased 22 fold, 13 fold, 16 fold, and 23 fold on treatment with cisplatin (p<0.05). However, the combination of Noni and cisplatin led to an increase of 2 fold, 1.6 fold, 3 fold, 1.2 fold, respectively (p<0.05). Conclusions: Noni enhanced the expression of DNA repair genes by itself and in combination with cisplatin. However, high expression of DNA repair genes at mRNA level only signifies efficient DNA transcription of the above mentioned genes; further investigations are needed to evaluate the DNA repair protein expression.

Genetic Variation in a DNA Double Strand Break Repair Gene in Saudi Population: A Comparative Study with Worldwide Ethnic Groups

  • Areeshi, Mohammed Yahya
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.12
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    • pp.7091-7094
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    • 2013
  • DNA repair capacity is crucial in maintaining cellular functions and homeostasis. However, it can be altered based on DNA sequence variations in DNA repair genes and this may lead to the development of many diseases including malignancies. Identification of genetic polymorphisms responsible for reduced DNA repair capacity is necessary for better prevention. Homologous recombination (HR), a major double strand break repair pathway, plays a critical role in maintaining the genome stability. The present study was performed to determine the frequency of the HR gene XRCC3 Exon 7 (C18067T, rs861539) polymorphisms in Saudi Arabian population in comparison with epidemiological studies by "MEDLINE" search to equate with global populations. The variant allelic (T) frequency of XRCC3 (C>T) was found to be 39%. Our results suggest that frequency of XRCC3 (C>T) DNA repair gene exhibits distinctive patterns compared with the Saudi Arabian population and this might be attributed to ethnic variation. The present findings may help in high-risk screening of humans exposed to environmental carcinogens and cancer predisposition in different ethnic groups.

DNA Repair Synthesis Induced by Bleomycin in HeLa $S_3$ Cells Pretreated with Base Analogs (鹽基相似體를 前處理한 HeLa $S_3$ 細胞에 있어 Bleomycin에 의한 DNA 回復合成)

  • Um, Kyung-Il;Park, Sang-Dai
    • The Korean Journal of Zoology
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    • v.20 no.1
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    • pp.41-48
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    • 1977
  • Dose response of DNA repair synthesis induced by bleomycin was dose-dependent in lower doses, and maximum rate of it at 5 $\\mu$g/ml represents about 15% of total cells analyzed. At higher doses DNA-repair synthesis was reduced and the rate of it remained unchanged even prolonged treatment. Pretreatment with BUdR or IUdR was found to enhance DNA repair synthesis and also to interfere with semiconservative DNA synthesis at higher doses. Time dependence study showed that DNA repair synthesis occurred as long as for 24 hours after removal of bleomycin. These results seem to suggest that bleomycin is not to be an effective chemical in inducing excision repair and that damages induced in DNA by this drug might include not only strand breaks but other types of DNA damage.

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