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Mutation research. Fundamental and molecular mecha... 13건

  1. [해외논문]   Editorial Board   SCI SCIE


    Mutation research. Fundamental and molecular mechanisms of mutagenesis v.808 ,pp. ii - ii , 2018 , 0027-5107 ,

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  2. [해외논문]   Quantification of DNA damage products by gas chromatography tandem mass spectrometry in lung cell lines and prevention effect of thyme antioxidants on oxidative induced DNA damage   SCI SCIE

    Aybastıer, Ö (University of Uludag, Faculty of Science and Arts, Department of Chemistry, 16059 Bursa, Turkey ) , nder (University of Uludag, Faculty of Science and Arts, Department of Chemistry, 16059 Bursa, Turkey ) , Dawbaa, Sam (University of Uludag, Faculty of Science and Arts, Department of Chemistry, 16059 Bursa, Turkey ) , Demir, Cevdet (University of Uludag, Faculty of Science and Arts, Department of Biology, 16059 Bursa, Turkey ) , Akgü (University of İstinye, Faculty of Medicine, Department of Medical Biochemistry, İstanbul, Turkey ) , n, Oğ (University of Uludag, Faculty of Science and Arts, Department of Biology, 16059 Bursa, Turkey) , uzhan , Ulukaya, Engin , Arı, Ferda
    Mutation research. Fundamental and molecular mechanisms of mutagenesis v.808 ,pp. 1 - 9 , 2018 , 0027-5107 ,

    초록

    Abstract Lung cancer has a high treatment cost and poor prognosis in comparison to other types of cancers. This work was involved in studying oxidative DNA base damage inhibition. Accordingly, standard carvacrol, thymol, thymoquinone with water and water-methanol extract of thyme ( Origanum vulgare L. subsp . hirtum (link.) Ietswaart), thyme oil and thyme water were prepared and investigated for their efficacy to inhibit DNA oxidative damage formed by H 2 O 2 in malignant lung cells (A549). The antioxidant capacity by ABTS assay was 271.73 ± 11.45 mg trolox equivalent/mL for thyme oil. HPLC analysis was carried out to determine the contents of different thyme extracts, results showing the presence of carvacrol, thymol, protocatechuic acid, caffeic acid, epicatechin and rosmarinic acid in water and water-methanol extracts while only carvacrol and thymol were found in thyme oil and thyme water. After DNA isolation from the cultured cells, the formed oxidative induced DNA damage products were analysed using GC–MS/MS. It was proven that the antioxidants in the cell culture media have succeeded to inhibit oxidative DNA base damage. Thymoquinone was shown to be the best protectant antioxidant among other antioxidants against the formation of oxidative DNA damage, whereas water-methanol extract of thyme was the best among the plant-sourced samples. Thymoquinone and thyme water-methanol extract were investigated for their efficacy on cultured healthy lung cells (BEAS-2B), and it was proven that they are efficient in protection against the oxidation of DNA of healthy lung cells too. Highlights Antioxidants and plant extracts were investigated for preventing DNA damage. Oxidative damage to DNA was studied in healthy and malignant lung cells. Carvacrol, thymol, thymoquinone and thyme extracts were the targeted objects. Antioxidants particularly thymoquinone impeded the DNA damage products formation. Thyme extracts particularly water-methanol extract impeded the damage too. Graphical abstract [DISPLAY OMISSION]

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  3. [해외논문]   The roles of human MTH1, MTH2 and MTH3 proteins in maintaining genome stability under oxidative stress   SCI SCIE

    Hashiguchi, Kazunari (Department of Biochemistry, Fukuoka Dental College, Fukuoka 814-0193, Japan ) , Hayashi, Michio (Department of Biochemistry, Fukuoka Dental College, Fukuoka 814-0193, Japan ) , Sekiguchi, Mutsuo (Frontier Research Center, Fukuoka Dental College, Fukuoka 814-0193, Japan ) , Umezu, Keiko (Department of Biochemistry, Fukuoka Dental College, Fukuoka 814-0193, Japan)
    Mutation research. Fundamental and molecular mechanisms of mutagenesis v.808 ,pp. 10 - 19 , 2018 , 0027-5107 ,

    초록

    Abstract The hydrolysis of nucleotides containing 8-oxo-7,8-dihydroguanine (8-oxoG) is important in the maintenance of genome stability. Human cells possess three types of proteins, MTH1 (NUDT1), MTH2 (NUDT15) and MTH3 (NUDT18), which have the potential to hydrolyze deoxyribonucleoside di- and triphosphates containing 8-oxoG to the monophosphate, the form of which is unusable for DNA synthesis. To elucidate the physiological roles of these enzymes, we constructed single knockout (KO) cell lines for each of the MTH1 , MTH2 and MTH3 genes and MTH1 and MTH2 -double KO cell lines from the human HeLa S3 line using CRISPR/Cas9. With the exception of MTH3 -KO, all of the KO cell lines showed similar proliferation rates to the parental line, HeLa S3, indicating that the MTH1 and MTH2 functions are dispensable for cell growth. On the other hand, the MTH3 -KO cells showed a significantly slower growth rate, suggesting that MTH3 has a definite role in cell growth in addition to the cleavage of 8-oxoG-containing deoxyribonucleotide. MTH1 -KO, MTH2 -KO and MTH1 - MTH2 -KO cells exhibited increased sensitivity to hydrogen peroxide, whereas MTH3 -KO did not. MTH1 -KO cells showed only a slight increase in mutant frequency in comparison to the parental HeLa S3 line. The overproduction of MTH1 and MTH2 suppressed the mutator phenotype of mutT -deficient E. coli cells, whereas the overproduction of MTH3 did not show such a suppressive effect. Our findings suggest that both MTH1 and MTH2 are involved in the maintaining genome stability in human cells against oxidative stress, while MTH3 may play some other role(s). Highlights MTH1-KO cells shows only a slight increase in mutant frequency. Both MTH1-KO and MTH2-KO are sensitive to hydrogen peroxide. MTH3 cannot substitute the E. coli MutT activity. MTH3 may possess another function besides the degradation of oxidized nucleotides.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  4. [해외논문]   NOTCH1 modulates activity of DNA-PKcs   SCI SCIE

    Adamowicz, Marek (IFOM Foundation –) , d'Adda di Fagagna, Fabrizio (FIRC Institute of Molecular Oncology Foundation, 20139 Milan, Italy ) , Vermezovic, Jelena (IFOM Foundation –)
    Mutation research. Fundamental and molecular mechanisms of mutagenesis v.808 ,pp. 20 - 27 , 2018 , 0027-5107 ,

    초록

    Abstract DNA-dependent protein kinase catalytic subunit (DNA-PKcs) controls one of the most frequently used DNA repair pathways in a cell, the non-homologous end joining (NHEJ) pathway. However, the exact role of DNA-PKcs in NHEJ remains poorly defined. Here we show that NOTCH1 attenuates DNA-PKcs-mediated autophosphorylation, as well as the phosphorylation of its specific substrate XRCC4. Surprisingly, NOTCH1-expressing cells do not display any significant impairment in the DNA damage repair, nor cellular survival, and remain sensitive to small molecule DNA-PKcs inhibitor. Additionally, in vitro DNA-PKcs kinase assay shows that NOTCH1 does not inhibit DNA-PKcs kinase activity, implying that NOTCH1 acts on DNA-PKcs through a different mechanism. Together, our set of results suggests that NOTCH1 is a physiological modulator of DNA-PKcs, and that it can be a useful tool to clarify the mechanisms by which DNA-PKcs governs NHEJ DNA repair. Highlights DNA-PKcs-mediated phosphorylations are attenuated by NOTCH1. NOTCH1 interacts with DNA-PKcs and ATR kinases. NOTCH1-expressing cells are repair proficient. NOTCH1-expressing cells are sensitive to DNA-PKcs inhibitor.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  5. [해외논문]   A change in structural integrity of c-Kit mutant D816V causes constitutive signaling   SCI SCIE

    Raghav, Pawan Kumar (Corresponding author.) , Singh, Ajay Kumar , Gangenahalli, Gurudutta
    Mutation research. Fundamental and molecular mechanisms of mutagenesis v.808 ,pp. 28 - 38 , 2018 , 0027-5107 ,

    초록

    Abstract Several signaling pathways, ligands, and genes that regulate proliferative and self-renewal properties of the Hematopoietic Stem Cells (HSCs) have been studied meticulously. One of the signaling pathways that play a crucial role in the process of hematopoiesis is the Stem Cell Factor (SCF) mediated c-Kit pathway. The c-Kit is a Receptor Tyrosine Kinase (RTK), which is expressed in the cells including HSCs. It undergoes dimerization upon binding with its cognate ligand SCF. As a result, phosphorylation of the Juxtamembrane (JM) domain of c-Kit takes place at Tyr568 and Tyr570 residues. These phosphorylated residues become the docking sites for protein tyrosine phosphatases (PTPs) namely SHP-1 and SHP-2, which in turn cause dephosphorylation and negative regulation of the downstream signaling responsible for the cell proliferation. Interestingly, it has been reported that the mutation of c-Kit at D816V makes it independent of SCF stimulation and SHP-1/SHP-2 inhibition, thereby, causing its constitutive activation. The present study was commenced to elucidate the structural behavior of this mutation in the JM and A-loop region of c-Kit using Molecular Dynamics (MD) simulations of the wild-type and mutant c-Kit in unphosphorylated and phosphorylated states. The energy difference computed between the wild type and mutant (D816V) c-Kit, and protein–protein docking and complex analysis revealed the impact of this single residue mutation on the integrity dynamics of c-Kit that makes it independent of SHP-1/SHP-2 negative regulation. Highlights Elucidation of the molecular mechanism underlying the independence and self-reliance of c-Kit mutation (D816V). Presence of additional intramolecular hydrogen bonds in D816V c-Kit mutant. Integrity dynamics of the Mutant D816V structure affects the binding site of the negative regulators. Graphical abstract [DISPLAY OMISSION]

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  6. [해외논문]   Drosophila bendless catalyzes K63-linked polyubiquitination and is involved in the response to DNA damage   SCI SCIE

    Bai, Zhiqiang (Beijing Key Laboratory of DNA Damage Responses and College of Life Sciences, Capital Normal University, Beijing 100048, China ) , Li, Zhouhua (Beijing Key Laboratory of DNA Damage Responses and College of Life Sciences, Capital Normal University, Beijing 100048, China ) , Xiao, Wei (Beijing Key Laboratory of DNA Damage Responses and College of Life Sciences, Capital Normal University, Beijing 100048, China)
    Mutation research. Fundamental and molecular mechanisms of mutagenesis v.808 ,pp. 39 - 47 , 2018 , 0027-5107 ,

    초록

    Abstract In this study, we report the identification and functional characterization of the Drosophila ben/ubc13 gene, encoding a unique ubiquitin-conjugating enzyme (Ubc or E2), in DNA-damage response. Ben forms a heterodimer with DmUev1a, the only Ubc/E2 variant (Uev) in Drosophila . Ben and DmUev1a act together to catalyze K63-linked polyubiquitination in vitro . ben can functionally rescue the yeast ubc13 null mutant from killing by DNA-damaging agents. We also find that Ben P97S , which was previously described to affect the connectivity between the giant fiber and the tergotrochanter motor neuron, fails to interact with the RING protein Chfr but retains interaction with DmUev1a as well as Uevs from other species. The corresponding yeast Ubc13 P97S interacts with Mms2 but fails to bind Rad5. Consequently, neither ben P97S nor ubc13 P97S is able to complement the yeast ubc13 mutant defective in error-free DNA-damage tolerance. More importantly, the ben P97S mutant flies are more sensitive to a DNA-damaging agent, suggesting that Ben functions in a manner similar to its yeast and mammalian counterparts. Collectively, our observations imply that Ben-DmUev1a-promoted K63-linked polyubiquitination and involvement in DNA-damage response are highly conserved in eukaryotes including flies. Highlights Ben interacts with Uev1a and mediates K63-linked polyubiquitination. Ben is able to functionally complement the yeast ubc13 mutant. The ben 1 mutation is identified and characterized. The budding yeast Ubc13-P97S substitution fails to interact with Rad5 and confer DDT activity. Ben is involved in DNA-damage response in vivo .

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  7. [해외논문]   Is inflammation a direct response to dsDNA breaks?   SCI SCIE

    Chaudhary, Shahid (Corresponding author.) , Raghuram, Gorantla Venkata , Mittra, Indraneel
    Mutation research. Fundamental and molecular mechanisms of mutagenesis v.808 ,pp. 48 - 52 , 2018 , 0027-5107 ,

    초록

    Abstract Recent research shows that extra-nuclear cell-free chromatin (cfCh) released from dying cells can freely enter into healthy cells and integrate into their genomes. Genomic integration of cfCh leads to dsDNA breaks and activation of inflammatory cytokines both of which occur concurrently with similar kinetics and that induction of inflammation can be abrogated by preventing DNA breaks with the use of cfCh inactivating agents. The proposal is put forward that inflammatory cytokines are a new family of DDR proteins that are activated following dsDNA breaks inflicted by genomic integration of cfCh.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  8. [해외논문]   Special section: Replication stress, a threat to the nuclear and mitochondrial genome   SCI SCIE

    Wiesmü (Corresponding author.) , ller, Lisa , Scharffetter-Kochanek, Karin , Geiger, Hartmut
    Mutation research. Fundamental and molecular mechanisms of mutagenesis v.808 ,pp. 53 - 55 , 2018 , 0027-5107 ,

    초록

    Abstract Recent research shows that extra-nuclear cell-free chromatin (cfCh) released from dying cells can freely enter into healthy cells and integrate into their genomes. Genomic integration of cfCh leads to dsDNA breaks and activation of inflammatory cytokines both of which occur concurrently with similar kinetics and that induction of inflammation can be abrogated by preventing DNA breaks with the use of cfCh inactivating agents. The proposal is put forward that inflammatory cytokines are a new family of DDR proteins that are activated following dsDNA breaks inflicted by genomic integration of cfCh.

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    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  9. [해외논문]   DNA replication stress drives fragile site instability   SCI SCIE

    Irony-Tur Sinai, Michal (Corresponding author at: Department of Genetics, The Life Sciences Institute, The Hebrew University, Edmond J Safra Campus, Givat Ram, Jerusalem, 91904, Israel.) , Kerem, Batsheva
    Mutation research. Fundamental and molecular mechanisms of mutagenesis v.808 ,pp. 56 - 61 , 2018 , 0027-5107 ,

    초록

    Abstract DNA replication stress is one of the early drivers enabling the ongoing acquisition of genetic changes arising during tumorigenesis. As such, it is a feature of most pre-malignant and malignant cells. In this review article, we focus on the early events initiating DNA replication stress and the preferential sensitivity of common fragile sites (CFSs) to this stress. CFSs are specific genomic regions within the normal chromosomal structure, which appear as gaps and breaks in the metaphase chromosomes of cells grown under mild replication stress conditions. The main characteristics predisposing CFSs to instability include late replication timing, delayed replication completion, failure to activate additional origins, origin paucity along large genomic regions, collision between replication and transcription complexes along large genes, and the presence of AT-dinucleotide rich sequences. The contribution of these features to instability at CFSs during early cancer development is discussed. Highlights DNA replication stress drives genome instability and initiates tumorigenicity. Nucleotide deficiency and deregulated origin firing lead to replication stress. CFSs exhibit intrinsic sensitivity to replication stress conditions. Under stress the replication along CFSs is delayed and even uncompleted. CFSs are preferentially unstable in pre-cancerous lesions and during cancer development.

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    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  10. [해외논문]   Role of specialized DNA polymerases in the limitation of replicative stress and DNA damage transmission   SCI SCIE

    Bournique, Elodie (Corresponding author.) , Dall'Osto, Marina , Hoffmann, Jean-Sé , bastien , Bergoglio, Valé , rie
    Mutation research. Fundamental and molecular mechanisms of mutagenesis v.808 ,pp. 62 - 73 , 2018 , 0027-5107 ,

    초록

    Abstract Replication stress is a strong and early driving force for genomic instability and tumor development. Beside replicative DNA polymerases, an emerging group of specialized DNA polymerases is involved in the technical assistance of the replication machinery in order to prevent replicative stress and its deleterious consequences. During S-phase, altered progression of the replication fork by endogenous or exogenous impediments induces replicative stress, causing cells to reach mitosis with genomic regions not fully duplicated. Recently, specific mechanisms to resolve replication intermediates during mitosis with the aim of limiting DNA damage transmission to daughter cells have been identified. In this review, we detail the two major actions of specialized DNA polymerases that limit DNA damage transmission: the prevention of replicative stress by non-B DNA replication and the recovery of stalled replication forks.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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