Relevant bibliographies by topics / Type II topoisomerase

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Type II topoisomerase'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Type II topoisomerase.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Type II topoisomerase"

1

Akasaka, Takaaki, Seiko Kurosaka, Yoko Uchida, Mayumi Tanaka, Kenichi Sato, and Isao Hayakawa. "Antibacterial Activities and Inhibitory Effects of Sitafloxacin (DU-6859a) and Its Optical Isomers against Type II Topoisomerases." Antimicrobial Agents and Chemotherapy 42, no. 5 (May 1, 1998): 1284–87. http://dx.doi.org/10.1128/aac.42.5.1284.

Full text
Abstract:
ABSTRACT The in vitro inhibitory effects of sitafloxacin (DU-6859a) and its three stereoisomers on bacterial DNA gyrase from Escherichia coli, topoisomerase IV from Staphylococcus aureus, and topoisomerase II from human placenta were compared. No correlation was observed between the inhibitory activities of quinolones against bacterial type II topoisomerases and those against human topoisomerase II. Sitafloxacin showed the most potent inhibitory activities against bacterial type II topoisomerases and the lowest activity against human type II topoisomerase.
APA, Harvard, Vancouver, ISO, and other styles
2

Takei, Masaya, Hideyuki Fukuda, Tokutaro Yasue, Masaki Hosaka, and Yasuo Oomori. "Inhibitory Activities of Gatifloxacin (AM-1155), a Newly Developed Fluoroquinolone, against Bacterial and Mammalian Type II Topoisomerases." Antimicrobial Agents and Chemotherapy 42, no. 10 (October 1, 1998): 2678–81. http://dx.doi.org/10.1128/aac.42.10.2678.

Full text
Abstract:
ABSTRACT We determined the inhibitory activities of gatifloxacin againstStaphylococcus aureus topoisomerase IV,Escherichia coli DNA gyrase, and HeLa cell topoisomerase II and compared them with those of several quinolones. The inhibitory activities of quinolones against these type II topoisomerases significantly correlated with their antibacterial activities or cytotoxicities (correlation coefficient [r] = 0.926 forS. aureus, r = 0.972 for E. coli, and r = 0.648 for HeLa cells). Gatifloxacin possessed potent inhibitory activities against bacterial type II topoisomerases (50% inhibitory concentration [IC50] = 13.8 μg/ml for S. aureustopoisomerase IV; IC50 = 0.109 μg/ml for E. coli DNA gyrase) but the lowest activity against HeLa cell topoisomerase II (IC50 = 265 μg/ml) among the quinolones tested. There was also a significant correlation between the inhibitory activities of quinolones against S. aureustopoisomerase IV and those against E. coli DNA gyrase (r = 0.969). However, the inhibitory activity against HeLa cell topoisomerase II did not correlate with that against either bacterial enzyme. The IC50 of gatifloxacin for HeLa cell topoisomerase II was 19 and was more than 2,400 times higher than that for S. aureus topoisomerase IV and that for E. coli DNA gyrase. These ratios were higher than those for other quinolones, indicating that gatifloxacin possesses a higher selectivity for bacterial type II topoisomerases.
APA, Harvard, Vancouver, ISO, and other styles
3

Garinther, W. I., and M. C. Schultz. "Topoisomerase function during replication-independent chromatin assembly in yeast." Molecular and Cellular Biology 17, no. 7 (July 1997): 3520–26. http://dx.doi.org/10.1128/mcb.17.7.3520.

Full text
Abstract:
DNA topoisomerases I and II are the two major nuclear enzymes capable of relieving torsional strain in DNA. Of these enzymes, topoisomerase I plays the dominant role in relieving torsional strain during chromatin assembly in cell extracts from oocytes, eggs, and early embryos. We tested if the topoisomerases are used differentially during chromatin assembly in Saccharomyces cerevisiae by a combined biochemical and pharmacological approach. As measured by plasmid supercoiling, nucleosome deposition is severely impaired in assembly extracts from a yeast mutant with no topoisomerase I and a temperature-sensitive form of topoisomerase II (strain top1-top2). Expression of wild-type topoisomerase II in strain top1-top2 fully restored assembly-driven supercoiling, and assembly was equally efficient in extracts from strains expressing either topoisomerase I or II alone. Supercoiling in top1-top2 extract was rescued by adding back either purified topoisomerase I or II. Using the topoisomerase II poison VP-16, we show that topoisomerase II activity during chromatin assembly is the same in the presence and absence of topoisomerase I. We conclude that both topoisomerases I and II can provide the DNA relaxation activity required for efficient chromatin assembly in mitotically cycling yeast cells.
APA, Harvard, Vancouver, ISO, and other styles
4

Forterre, Patrick, Christiane Eue, Mouldy Sioud, and Abdellah Hamal. "Studies on DNA polymerases and topoisomerases in archaebacteria." Canadian Journal of Microbiology 35, no. 1 (January 1, 1989): 228–33. http://dx.doi.org/10.1139/m89-035.

Full text
Abstract:
We have isolated DNA polymerases and topoisomerases from two thermoacidophilic archaebacteria: Sulfolobus acidocaldarius and Thermoplasma acidophilum. The DNA polymerases are composed of a single polypeptide with molecular masses of 100 and 85 kDa, respectively. Antibodies against Sulfolobus DNA polymerase did not cross react with Thermoplasma DNA polymerase. Whereas the major DNA topoisomerase activity in S. acidocaldarius is an ATP-dependent type I DNA topoisomerase with a reverse gyrase activity, the major DNA topoisomerase activity in T. acidophilum is a ATP-independent relaxing activity. Both enzymes resemble more the eubacterial than the eukaryotic type I DNA topoisomerase. We have found that small plasmids from halobacteria are negatively supercoiled and that DNA topoisomerase II inhibitors modify their topology. This suggests the existence of an archaebacterial type II DNA topoisomerase related to its eubacterial and eukaryotic counterparts. As in eubacteria, novobiocin induces positive supercoiling of halobacterial plasmids, indicating the absence of a eukaryotic-like type I DNA topoisomerase that relaxes positive superturns.Key words: archaebacteria, DNA topoisomerases, DNA polymerases, DNA topology, gyrase.
APA, Harvard, Vancouver, ISO, and other styles
5

Strumberg, Dirk, John L. Nitiss, Jiaowang Dong, Jerrylaine Walker, Marc C. Nicklaus, Kurt W. Kohn, Jonathan G. Heddle, Anthony Maxwell, Siegfried Seeber, and Yves Pommier. "Importance of the Fourth Alpha-Helix within the CAP Homology Domain of Type II Topoisomerase for DNA Cleavage Site Recognition and Quinolone Action." Antimicrobial Agents and Chemotherapy 46, no. 9 (September 2002): 2735–46. http://dx.doi.org/10.1128/aac.46.9.2735-2746.2002.

Full text
Abstract:
ABSTRACT We report that point mutations causing alteration of the fourth alpha-helix (α4-helix) of the CAP homology domain of eukaryotic (Saccharomyces cerevisiae) type II topoisomerases (Ser740Trp, Gln743Pro, and Thr744Pro) change the selection of type II topoisomerase-mediated DNA cleavage sites promoted by Ca2+ or produced by etoposide, the fluoroquinolone CP-115,953, or mitoxantrone. By contrast, Thr744Ala substitution had minimal effect on Ca2+- and drug-stimulated DNA cleavage sites, indicating the selectivity of single amino acid substitutions within the α4-helix on type II topoisomerase-mediated DNA cleavage. The equivalent mutation in the gene for Escherichia coli gyrase causing Ser83Trp also changed the DNA cleavage pattern generated by Ca2+ or quinolones. Finally, Thr744Pro substitution in the yeast type II topoisomerase rendered the enzyme sensitive to antibacterial quinolones. This study shows that the α4-helix within the conserved CAP homology domain of type II topoisomerases is critical for selecting the sites of DNA cleavage. It also demonstrates that selective amino acid residues in the α4-helix are important in determining the activity and possibly the binding of quinolones to the topoisomerase II-DNA complexes.
APA, Harvard, Vancouver, ISO, and other styles
6

Kaufmann, S. H., and R. Hancock. "Topoisomerase II as a target for anticancer chemotherapy." Acta Biochimica Polonica 42, no. 4 (December 31, 1995): 381–93. http://dx.doi.org/10.18388/abp.1995_4892.

Full text
Abstract:
Type II DNA topoisomerases are required for the segregation of genomic DNA at cell division in prokaryotic and eukaryotic cells, and inhibitors of these enzymes are potential cytotoxic agents in both prokaryotes and eukaryotes. The bacterial member of the topoisomerase II family, DNA gyrase, and the chemotherapeutic agents which target it are the subject of a recent review (Maxwell, A. et al., 1993, in Molecular Biology of DNA Topoisomerases, Andoh, T. et al., eds., pp. 21-30, CRC Press, Boca Raton). Here we present an overview of current knowledge of eukaryotic topoisomerase II and the anticancer agents which target this enzyme, focussing predominantly on new observations and recent reports and reviews.
APA, Harvard, Vancouver, ISO, and other styles
7

Blanche, F., B. Cameron, F. X. Bernard, L. Maton, B. Manse, L. Ferrero, N. Ratet, et al. "Differential behaviors of Staphylococcus aureus and Escherichia coli type II DNA topoisomerases." Antimicrobial Agents and Chemotherapy 40, no. 12 (December 1996): 2714–20. http://dx.doi.org/10.1128/aac.40.12.2714.

Full text
Abstract:
Staphylococcus aureus gyrA and gyrB genes encoding DNA gyrase subunits were cloned and coexpressed in Escherichia coli under the control of the T7 promoter-T7 RNA polymerase system, leading to soluble gyrase which was purified to homogeneity. Purified gyrase was catalytically indistinguishable from the gyrase purified from S. aureus and did not contain detectable amounts of topoisomerases from the E. coli host. Topoisomerase IV subunits GrlA and GrlB from S. aureus were also expressed in E. coli and were separately purified to apparent homogeneity. Topoisomerase IV, which was reconstituted by mixing equimolar amounts of GrlA and GrlB, had both ATP-dependent decatenation and DNA relaxation activities in vitro. This enzyme was more sensitive than gyrase to inhibition by typical fluoroquinolone antimicrobial agents such as ciprofloxacin or sparfloxacin, adding strong support to genetic studies which indicate that topoisomerase IV is the primary target of fluoroquinolones in S. aureus. The results obtained with ofloxacin suggest that this fluoroquinolone could also primarily target gyrase. No cleavable complex could be detected with S. aureus gyrase upon incubation with ciprofloxacin or sparfloxacin at concentrations which fully inhibit DNA supercoiling. This suggests that these drugs do not stabilize the open DNA-gyrase complex, at least under standard in vitro incubation conditions, but are more likely to interfere primarily with the DNA breakage step, contrary to what has been reported with E. coli gyrase. Both S. aureus gyrase-catalyzed DNA supercoiling and S. aureus topoisomerase IV-catalyzed decatenation were dramatically stimulated by potassium glutamate or aspartate (500- and 50-fold by 700 and 350 mM glutamate, respectively), whereas topoisomerase IV-dependent DNA relaxation was inhibited 3-fold by 350 mM glutamate. The relevance of the effect of dicarboxylic amino acids on the activities of type II topoisomerases is discussed with regard to the intracellular osmolite composition of S. aureus.
APA, Harvard, Vancouver, ISO, and other styles
8

Delgado, Justine L., Chao-Ming Hsieh, Nei-Li Chan, and Hiroshi Hiasa. "Topoisomerases as anticancer targets." Biochemical Journal 475, no. 2 (January 23, 2018): 373–98. http://dx.doi.org/10.1042/bcj20160583.

Full text
Abstract:
Many cancer type-specific anticancer agents have been developed and significant advances have been made toward precision medicine in cancer treatment. However, traditional or nonspecific anticancer drugs are still important for the treatment of many cancer patients whose cancers either do not respond to or have developed resistance to cancer-specific anticancer agents. DNA topoisomerases, especially type IIA topoisomerases, are proved therapeutic targets of anticancer and antibacterial drugs. Clinically successful topoisomerase-targeting anticancer drugs act through topoisomerase poisoning, which leads to replication fork arrest and double-strand break formation. Unfortunately, this unique mode of action is associated with the development of secondary cancers and cardiotoxicity. Structures of topoisomerase–drug–DNA ternary complexes have revealed the exact binding sites and mechanisms of topoisomerase poisons. Recent advances in the field have suggested a possibility of designing isoform-specific human topoisomerase II poisons, which may be developed as safer anticancer drugs. It may also be possible to design catalytic inhibitors of topoisomerases by targeting certain inactive conformations of these enzymes. Furthermore, identification of various new bacterial topoisomerase inhibitors and regulatory proteins may inspire the discovery of novel human topoisomerase inhibitors. Thus, topoisomerases remain as important therapeutic targets of anticancer agents.
APA, Harvard, Vancouver, ISO, and other styles
9

Snapka, R. M., M. A. Powelson, and J. M. Strayer. "Swiveling and decatenation of replicating simian virus 40 genomes in vivo." Molecular and Cellular Biology 8, no. 2 (February 1988): 515–21. http://dx.doi.org/10.1128/mcb.8.2.515.

Full text
Abstract:
We have found that type II topoisomerase inhibitors have two effects on replicating simian virus 40 genomes in vivo: production of catenated dimers and slowed replication of the last 5% of the genome. This suggests that type II topoisomerase simultaneously decatenates and facilitates replication fork movement at this stage of DNA replication. On the basis of this observation, a detailed model is proposed for the roles of topoisomerases I and II in simian virus 40 DNA replication.
APA, Harvard, Vancouver, ISO, and other styles
10

Snapka, R. M., M. A. Powelson, and J. M. Strayer. "Swiveling and decatenation of replicating simian virus 40 genomes in vivo." Molecular and Cellular Biology 8, no. 2 (February 1988): 515–21. http://dx.doi.org/10.1128/mcb.8.2.515-521.1988.

Full text
Abstract:
We have found that type II topoisomerase inhibitors have two effects on replicating simian virus 40 genomes in vivo: production of catenated dimers and slowed replication of the last 5% of the genome. This suggests that type II topoisomerase simultaneously decatenates and facilitates replication fork movement at this stage of DNA replication. On the basis of this observation, a detailed model is proposed for the roles of topoisomerases I and II in simian virus 40 DNA replication.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Type II topoisomerase"

1

Gupta, Ranjan Brockman Herman E. "Effect of DNA topoisomerase II-targeting antitumor drugs in Neurospora crassa similarities to prokaryotic type II DNA topoisomerases /." Normal, Ill. Illinois State University, 1990. http://wwwlib.umi.com/cr/ilstu/fullcit?p9115225.

Full text
Abstract:
Thesis (Ed. D.)--Illinois State University, 1990.
Title from title page screen, viewed November 28, 2005. Dissertation Committee: Herman E. Brockman (chair), Alan J. Katz, Lynne A. Lucher, Radheshyam K. Jayaswal, David F. Weber, Anthony E. Liberta. Includes bibliographical references (leaves 114-131) and abstract. Also available in print.
APA, Harvard, Vancouver, ISO, and other styles
2

Rance, Holly Ashlene. "Effect of quinolones which target bacterial gyrase and topoisomerase IV on mammalian type II topoisomerases." Thesis, University of Newcastle Upon Tyne, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627726.

Full text
Abstract:
uinolones are a family of drugs used to treat bacterial infections by targeting bacterial type II topoisomerases (TOP2s), DNA gyrase and topoisomerase IV. Recent studies have shown that quinolones can cause genotoxicity in mammalian cells. Genotoxicity occurs when an agent causes damage to the genetic apparatus of a cell. Due to the similarities between the mammalian and bacterial TOP2 enzymes it is thought that the quinolones are targeting mammalian TOP2 to produce their genotoxic response. The aim of this study was to investigate if quinolone genotoxicity involves mammalian TOP2. Using the micronucleus assay, the genotoxicity of two quinolones ciprofloxacin and gemifloxacin was tested in three Nalm-6 cell lines containing varying amounts of TOP2. With ciprofloxacin only the Nalm-6TOP2A+/- cells showed genotoxicity, whereas for gemifloxacin only the Nalm-6 WT cells showed genotoxicity, suggesting that for gemifloxacin the removal of TOP2A or TOP2B lowers the genotoxicity of the quinolone. A selection of quinolones were tested using the Trapped in AgaRose DNA ImmunoStaining (TARDIS) assay to determine whether they stabilise the TOP2-DNA complexes in mammalian cells as known TOP2 poisons do. The analysis showed that after three hours incubation the level of complexes increased, indicating that the quinolones are able to stabilise TOP2-DNA complexes. Taken together the micronucleus and TARDIS assay data show that the quinolones are targeting mammalian TOP2 at high concentrations.
APA, Harvard, Vancouver, ISO, and other styles
3

Chung, In Kwon. "Reactivity of eukaryotic type II topoisomerase with unusual DNA structures /." The Ohio State University, 1991. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487758178238665.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Tsai, Francis T. F. "Crystallographic studies of DNA gyrase B protein." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390473.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Soares, Bruno Marques. "Hellebrigenina, um BufodienolÃdeo com Potencial AÃÃo CompatÃvel de Inibidor CatalÃtico da Topoisomerase II." Universidade Federal do CearÃ, 2013. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=10367.

Full text
Abstract:
CoordenaÃÃo de AperfeiÃoamento de NÃvel Superior
Os bufodienolÃdeos sÃo esterÃides cardioativos de 24 carbonos, isolados originalmente de um extrato de pele de sapos da famÃlia Bufonidae utilizado na medicina chinesa. Os bufodienolÃdeos possuem grande variedade de atividades biolÃgicas, incluindo atividades antineoplÃsicas. Em relaÃÃo à atividade antitumoral, os bufodienolÃdeos tem demonstrado inibir o crescimento de vÃrias linhagens de cÃlulas cancerÃgenas humanas por induzir apoptose e parada do ciclo celular. O presente estudo avaliou o potencial citotÃxico e genetÃxico de seis bufodienolÃdeos em seis linhagens tumorais humanos, trÃs linhagens murinas normais e cÃlulas mononucleadas do sangue perifÃrico (CMSP) humano. Todos os seis bufodienolÃdeos foram citotÃxicos para todas as linhagens tumorais e CMSP com valores de IC50 variando entre 0,002 e 3,17 ÂM. Os bufodienolÃdeos testados nÃo apresentaram citotoxicidade para linhagens murinas normais. Desta forma, o composto hellebrigenina foi escolhido para se determinar o mecanismo de aÃÃo envolvido. Uma sequÃncia de experimentos in vitro foram realizados utilizando-se a linhagem leucÃmica HL-60. As cÃlulas foram tratadas em diferentes concentraÃÃes da amostra hellebrigenina (0,03, 0,06 e 0,12 ÂM) por 24 horas. A viabilidade das cÃlulas (nÃmero de cÃlulas viÃveis e integridade de membrana) HL-60 avaliada por citometria de fluxo, mostrou que o nÃmero de cÃlulas reduziu a partir da menor concentraÃÃo (0,03 ÂM) testada e a porcentagem de cÃlulas com membrana integra reduziu a partir da concentraÃÃo 0,06 ÂM. A anÃlise morfolÃgica por citometria de fluxo revelou aumento de cÃlulas com padrÃo apoptÃtico a partir da concentraÃÃo de 0,06 ÂM. Jà a anÃlise do conteÃdo nuclear, nos mostrou aumento de fragmentaÃÃo de DNA sub-G1 indicativo de apoptose e acÃmulo de cÃlulas na fase G2/M a partir das concentraÃÃes de 0,03 e 0,06 ÂM, respectivamente. Outros testes por citometria de fluxo revelaram que houve externalizaÃÃo da fosfatidilserina, despolarizaÃÃo mitocondrial, ativaÃÃo da caspase iniciadora 8 e consequente ativaÃÃo das caspases efetoras 3 e 7. Estes dados indicam um mecanismo citotÃxico por induÃÃo de mais de uma via apoptÃtica. Hellebrigenina nÃo foi capaz de causar danos ao DNA de HL-60 e de CMSP e nem o surgimento de aberraÃÃes cromossÃmicas em CMSP. Por meio dos estudos de docking molecular foi possÃvel predizer a ligaÃÃo entre hellebrigenina e topoisomeraseIIα humana, resultado compatÃvel com a possÃvel inibiÃÃo dessa enzima. De forma geral, os resultados apontam o potencial citotÃxico do bufodienolÃdeo hellebrigenina
Bufodienolides are cardioactive steroids of 24 carbons, originally isolated from a frogâs skin extract of the family Bufonidae used in Chinese medicine. Bufodienolides shows many biological activities, including anticancer activities. Related to antitumor activity, the bufodienolÃdeos has been shown to inhibit the growth of several human cancer cell lines by inducing apoptosis and cell cycle arrest. This study evaluated the potential cytotoxicity and genotoxicity of six bufodienolides, in six human tumor cell lines, three normal murine lineages and PBMC (peripheral blood mononuclear cells). All six bufodienolides were cytotoxic to all cell lines and tumor PBMC with IC50 values ranging from 0.002 to 3.17 ÂM. Bufodienolides showed no cytotoxicity for normal murine strains. Thus, the compound hellebrigenin was chosen to determine the action mechanism involved, a sequence of in vitro experiments were performed using HL-60 leukemia cell line. Cells were treated at different concentrations of hellebrigenin (0.03, 0.06 and 0.12 ÂM) for 24 hours. Cell viability (viable cell number and membrane integrity) HL-60 assessed by flow cytometry showed that the number of cells decreased from the lower concentration (0.03 ÂM) tested and the percentage of cells with reduced membrane integrity from 0.06 ÂM concentration. Morphological analysis by flow cytometry revealed increased apoptotic cells starting at concentrations of 0.06 ÂM. The analysis of nuclear content, showed an increase in DNA fragmentation indicative of sub-G1 apoptosis and accumulation of cells in G2 / M phase from the concentrations of 0.03 and 0.06 ÂM, respectively. Other tests by flow cytometry revealed that there was an externalization of phosphatidylserine, mitochondrial depolarization, activation of caspase 8 and initiating subsequent activation of effector caspases 3 and 7. These data indicate a cytotoxic mechanism induced by over an apoptotic pathway. Hellebrigenin was not able to cause DNA damage in HL-60 and PBMC nor the emergence of chromosomal aberrations in PBMC. Through the studies of molecular docking was possible to predict the connection between hellebrigenina and human topoisomeraseIIα, showing a result that is compatible with a possible inhibition of this enzyme. Overall, the results indicate the potential cytotoxicity of hellebrigenin
APA, Harvard, Vancouver, ISO, and other styles
6

Coelho, Raquel Autran [UNIFESP]. "Expressão de topoisomerase II alfa e de caspase-3 ativada em lesão intra-epitelial cervical escamosa de baixo grau." Universidade Federal de São Paulo (UNIFESP), 2008. http://repositorio.unifesp.br/handle/11600/9620.

Full text
Abstract:
Made available in DSpace on 2015-07-22T20:50:13Z (GMT). No. of bitstreams: 0 Previous issue date: 2008-03-26. Added 1 bitstream(s) on 2015-08-11T03:25:45Z : No. of bitstreams: 1 Publico-10807.pdf: 786945 bytes, checksum: a640250d88b5bd045dc6f2f53834bd45 (MD5)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Objetivos: Estudar a expressao imuno-histoquimica de topoisomerase IIƒ¿ e de caspase-3 ativada, marcadores de proliferacao e de apoptose, respectivamente, a deteccao de DNA HPV e a evolucao da lesao cervical em mulheres portadoras de lesao intra-epitelial escamosa de baixo grau (LBG). Metodos: Foram avaliadas 40 mulheres portadoras de LBG e 32 sem neoplasia cervical, diagnosticadas por exame cito-colpo-histopatologico, quanto a imunoexpressao de topoisomerase IIƒ¿ e de caspase-3 ativada e quanto a deteccao de DNA HPV por PCR consensual (GP5+/GP6+) em material de esfregaco cervico-vaginal. Os achados foram relacionados as variaveis clinicas das pacientes e a evolucao clinica das lesoes cervicais em 12 meses. As pacientes assinaram termo de consentimento livre e esclarecido. Resultados: A media percentual de celulas imunomarcadas por topoisomerase foi de 11,71% e 4,13%, no grupo com LBG e controle, respectivamente, com diferenca estatisticamente significante. Observou-se que houve expressao de caspase-3 em 17 (42,5%) e em 5 (15,63%) pacientes com e sem LBG, respectivamente, com diferenca estatisticamente significante. Foi detectado HPV DNA em 65% das pacientes com LBG e em 59,4% das pacientes sem lesao cervical, sem relacao com a expressao de topoisomerase IIƒ¿ ou caspase-3. Na presenca de DNA-HPV, a expressao de topoisomerase IIƒ¿ no grupo com LBG foi significativamente maior do que em fragmentos sem lesao. Nao foi observada diferenca quanto a evolucao da lesao cervical em 12 meses de acordo com a imunoexpressao de topoisomerase IIƒ¿. Com relacao a caspase-3 ativada, a maioria das pacientes com imuno-histoquimica negativa teve regressao da lesao cervical. Conclusoes: A imunoexpressao de topoisomerase IIƒ¿ e de caspase-3 ativada podem ser considerados marcadores de proliferacao e de apoptose em lesao cervical de baixo grau, sem relacao com a presenca de DNA-HPV.
Purpose: To evaluate the correlation between the expression of topoisomerase II alpha, active caspase-3 and infection with human papillomavirus in low-grade cervical intraepithelial lesion and in the normal cervix, and whether they might influence susceptibility to, or evolution of, cervical lesion. Patients and methods: Forty cervical biopsies patients with low-grade cervical intraepithelial lesion and thirty-two with normal cervix were stained by immunohistochemistry for topoisomerase IIá and active caspase-3 and were investigated for the presence of HPV on exfoliated cells by general primer GP5+/6+ PCR amplification of DNA. These findings were correlated with clinicopathological features of the patients including their clinical outcome after twelve months. Subjects provided written informed consent. Results: Low-grade CIN patients as a group had a significantly higher expression of topoisomerase II alpha compared to controls, without correlation to disease outcome at 12 months. Caspase-3 was expressed in 42.5% of CIN patients and in 15.63% without disease, and most of women without caspase-3 receded cervical lesion. HPV DNA testing was positive in 65% of the patients with cervical lesion, and in 59.4% of the control group and was not associated to the expression of topoisomerase IIá or active caspase-3. In the presence of a positive HPV DNA testing, women with cervical lesion had a significantly higher expression of topoisomerase II alpha compared to controls. Conclusion: Topoisomerase II alpha and active caspase-3 might be useful diagnostic and prognostic markers in low-grade cervical lesions, delaying a better follow-up.
CNPq: 134106/2005-9
TEDE
BV UNIFESP: Teses e dissertações
APA, Harvard, Vancouver, ISO, and other styles
7

Bassi, Marco Antonio. "Cinética celular na endometriose profunda infiltrativa de reto-sigmoide: estudo anátomo-clínico." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5139/tde-23112011-191633/.

Full text
Abstract:
INTRODUÇÃO: A endometriose, uma doença benigna, tem características invasivas com potencial proliferativo. O desenvolvimento das lesões pode ocorrer em decorrência de crescimento celular glandular e/ou estromal ou de alterações na cinética celular. Cinética celular refere-se ao equilíbrio entre a morte celular, ou apoptose, e a proliferação celular, que pode ser avaliada pela expressão de fatores de crescimento como, por exemplo, a topoisomerase 2-alfa (TOP2A). Também influenciam a cinética celular oncoproteínas como p53 e c-erB2, conhecidas por interferir na apoptose, podendo resultar em oncogênese. OBJETIVOS: O objetivo principal deste estudo foi comparar a cinética celular da endometriose infiltrativa de retosigmoide com a do endométrio eutópico de pacientes sem endometriose. Para tanto, foi avaliada a expressão de apoptose e de TOP2A bem como das oncoproteínas p53 e c-erB2. MÉTODOS: Foram obtidas amostras de lesões de endometriose envolvendo o reto-sigmoide de 60 mulheres com a doença e amostras de endométrio eutópico de 20 mulheres sem endometriose. A expressão de TOP2A e das proteínas p53 e c-erB2 foram quantificadas por técnica imuno-histoquímica. Método TUNEL foi utilizado para analisar os padrões de apoptose, que resultaram em índice de apoptose (IA). Índice de proliferação celular (IP) foi determinado a partir do nível de expressão de TOP2A. Índice de renovação celular (IRC) foi calculado pela razão entre IP e IA. As análises imuno-histoquímicas foram realizadas tanto no tecido endometrial como um todo, quanto nos componentes estromal e glandular separadamente. Coeficiente de Correlação de Spearman foi aplicado para identificar eventuais correlações entre variáveis clínicas, morfológicas (tamanho, quantidade e nível de invasão das lesões) e experimentais. RESULTADOS: Na análise da amostra do tecido como um todo, não foram evidenciadas diferenças entre os grupos experimental e controle em relação ao IA (p = 0,389). Por outro lado, o IP foi significativamente maior nas amostras-controle (p < 0,001). Na avaliação em que se sepaxii raram as células estromais dos componentes glandulares, tanto o IP quanto o IRC foram significativamente maiores no grupo-controle em comparação com o grupo experimental (IP estromal: p = 0,006; IP glandular: p = 0,001; IRC estromal: p =0,032; IRC glandular: p = 0,007). Nas pacientes com endometriose, foi encontrada correlação entre IP e IRC glandular e o número de lesões (p = 0,003). Também foi observada correlação entre o IRC glandular e o tamanho das lesões (p = 0,006). Não houve diferença entre os grupos no que se refere à expressão de p53 e cerB2. CONCLUSÕES: A cinética celular se mostrou alterada em pacientes com endometriose do reto-sigmoide, conforme demonstrado pela redução nos níveis e na frequência de TOP2A, e pelos IP e IRC mais baixos; entretanto, apoptose e as expressões de p53 e c-erB2 se mostraram inalteradas
BACKGROUND: Endometriosis, a benign disease, has invasive features with its proliferative potential. Development of lesions may occur due to stromal and/or glandular cell growth and to alterations in cellular kinetics. Cellular kinetics involves a balance between the regulation of cell death, or apoptosis, and cell growth, that can be evaluated by the expression of growth factors, such as topoisomerase 2- alpha (TOP2A). Oncoproteins, such as p53 and c-erB2, known to affect apoptosis resulting in oncogenesis, also influence cellular kinetics. OBJECTIVES: The main objective of this study was to compare the cellular kinetics in deep endometriosis involving the recto-sigmoid to eutopic endometrium from patients without endometriosis. Apoptosis and TOP2A expression were primarily evaluated, as well as p53 and c-erB2 expression. METHODS: Study samples were obtained from endometriosis lesions involving the recto-sigmoid in 60 women, and control samples were obtained from eutopic endometrium from 20 women without endometriosis. The expression of TOP-2A, p53 and c-erB2 proteins were quantified using immuno-histochemistry. TUNEL method was used in the analysis of apoptosis patterns, and the apoptosis index (AI) was derived. The proliferation index (PI) was derived from the level of expression of TOP-2A. Cellular renew index (CRI) was calculated from the ratio of the PI and AI. Immunohistochemical analyses were performed in two ways: on the tissue collectively, and on the stromal and glandular components separately. Spearmans correlation coefficient was used to identify the correlation between clinical, morphological (size, number and level of invasion of lesions) and the study variables. RESULTS: When looked at collectively, there was no difference in the AI between study and control groups (p = 0.389). PI, however, was noted to be significantly higher in the control samples (p < 0.001). When evaluating the stromal cells separately from the glandular components, the PI and CRI were both significantly xiv higher in the control group compared to the study group (Study stromal PI vs control stromal PI; p = 0.006; Study glandular PI vs study glandular PI; p = 0.001; Study stromal CRI vs control stromal CRI; p = 0.032; study glandular CRI vs control glandular CRI; p = 0.007). In patients with endometriosis, a correlation was found between glandular PI, CRI and number of lesions (p = 0.003). The same result was observed in the analysis of stromal CRI and lesion size (p = 0.006). There was no difference in expression of p53 and c-erB2 between groups. CONCLUSIONS: Cellular kinetics is altered in endometriosis of the recto-sigmoid, as shown by the decrease in the levels and frequency of TOP2A expression, and lower PI and CRI; however, apoptosis and p53 and c-erB2 expression were unaffected
APA, Harvard, Vancouver, ISO, and other styles
8

McNamara, Suzan. "Topoisomerase II beta negatively modulates retinoic acid receptor alpha function : a novel mechanism of retinoic acid resistance in acute promyelocytic leukemia." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115693.

Full text
Abstract:
Interactions between the retinoic acid receptor alpha (RARalpha) and coregulators play a key role in coordinating gene transcription and myeloid differentiation. In acute promyelocytic leukemia (APL), RARalpha is fused with the promyelocytic leukemia (PML) gene, resulting in the expression of the fusion protein PML/RARalpha. Here, I report that topoisomerase II beta (topoIIbeta) associates with and negatively modulates PML/RARalpha and RARalpha transcriptional activity, and increased levels and association of topoIIbeta cause resistance to retinoic acid (RA) in APL cell lines. Knock down of topoIIbeta was able to overcome resistance by permitting RA-induced differentiation and increased RA-gene expression. Overexpression of topoIIbeta, in clones from an RA-sensitive cell line, conferred resistance by a reduction in RA-induced expression of target genes and differentiation. Chromatin immunoprecipitation assays indicate that topoIIbeta is bound to an RA-response element, and inhibition of topoIIbeta causes hyper-acetylation of histone 3 at lysine 9 and activation of transcription. These results identify a novel mechanism of resistance in APL and provide further insights to the role of topoIIbeta in gene regulation and differentiation.
Studies to determine the mechanism by which topoIIbeta protein is regulated found that levels of protein kinase C delta (PKCdelta) correlated with topoIIbeta protein expression. Moreover, activation of PKCdelta, by RA or PMA, led to an increase of topoIIbeta protein levels. Most notably, in NB4-MR2 cells, we observed increased phosphorylation levels of threonine 505 on PKCdelta, a marker of activation. Inhibition of PKCdelta was able to overcome the topoIIbeta repressive effects on RA-target genes. In addition, the combination of RA and PKCdelta inhibition led to increased expression of the granulocytic marker, CD11c, in NB4 and NB4-MR2 cells. These results suggest that PKCdelta regulates topoIIbeta expression, and a constitutively active PKCdelta in the NB4-MR2 cell line leads to overexpression of topoIIbeta.
In conclusion, these studies demonstrate that topoIIbeta associates with RARalpha, binds to RAREs and plays a critical role in RA dependent transcriptional regulation and granulocytic differentiation. In addition, I show that topoIIbeta overexpression leads to RA resistance and provide evidence that topoIIbeta protein levels are regulated via a mechanism involving the PKCdelta pathway. This work has contributed to an enhanced understanding of the role of topoIIbeta in gene regulation and brings novel perspectives in the treatment of RA-resistance in APL.
APA, Harvard, Vancouver, ISO, and other styles
9

Azrak, Sami. "Type II DNA topoisomerases in zebrafish development." Thesis, University of Newcastle Upon Tyne, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493231.

Full text
Abstract:
DNA topoisomerases are vital enzymes for major cellular processes like replication, transcription, and chromosome segregation. They play an essential role in solving DNA topological problems by catalysing the passage of DNA strands through each other via introducing transient single or double strand breaks. Type IIA DNA topoisomerases members introduce double strand breaks via an ATP-dependent strand passage reaction. This study aimed to investigate the roles of topo Ila and topo Iip in zebrafish development.
APA, Harvard, Vancouver, ISO, and other styles
10

Engel, Roxane. "The nuclear export of DNA topoisomerase iialpha in hematological myeloma cell lines as a function of drug sensitivity : clinical implications and a theoretical approach for overcoming the observed drug resistance /." [Tampa, Fla.] : University of South Florida, 2005. http://purl.fcla.edu/fcla/etd/SFE0001358.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Type II topoisomerase"

1

Pommier, Yves. DNA Topoisomerases and Cancer. New York, NY: Springer Science+Business Media, LLC, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

(Editor), Leroy F. Liu, J. Thomas August (Series Editor), M. W. Anders (Series Editor), Ferid Murad (Series Editor), and Joseph T. Coyle (Series Editor), eds. DNA Topoisomearases: Biochemistry and Molecular Biology, Volume 29A (Advances in Pharmacology). Academic Press, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Milan, Potmesil, and Kohn Kurt W, eds. DNA topoisomerases in cancer. New York: Oxford University Press, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Pommier, Yves. DNA Topoisomerases and Cancer. Humana, 2013.

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Type II topoisomerase"

1

East, Stephen P., Lloyd G. Czaplewski, and David J. Haydon. "Chapter 20. Ethyl Urea Inhibitors of the Bacterial Type II Topoisomerases DNA Gyrase (GyrB) and Topoisomerase IV (ParE)." In Drug Discovery, 335–52. Cambridge: Royal Society of Chemistry, 2012. http://dx.doi.org/10.1039/9781849734912-00335.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Gibson, Elizabeth G., Rachel E. Ashley, Robert J. Kerns, and Neil Osheroff. "Bacterial Type II Topoisomerases and Target-Mediated Drug Resistance." In Antimicrobial Resistance in the 21st Century, 507–29. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78538-7_16.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Huang, Wai Mun. "Type II DNA Topoisomerase Genes." In DNA Topoisomerases: Biochemistry and Molecular Biology, 201–25. Elsevier, 1994. http://dx.doi.org/10.1016/s1054-3589(08)60547-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Mitton-Fry, Mark Joseph. "Novel Bacterial Type II Topoisomerase Inhibitors." In 2017 Medicinal Chemistry Reviews, 281–302. Medicinal Chemistry Division of the American Chemical Society, 2017. http://dx.doi.org/10.29200/acsmedchemrev-v52.ch15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Shirude, Pravin S., and Shahul Hameed. "Nonfluoroquinolone-Based Inhibitors of Mycobacterial Type II Topoisomerase as Potential Therapeutic Agents for TB." In Annual Reports in Medicinal Chemistry Volume 47, 319–30. Elsevier, 2012. http://dx.doi.org/10.1016/b978-0-12-396492-2.00021-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Goodenow, Donna, Kiran Lalwani, and Christine Richardson. "DNA Damage and Repair Mechanisms Triggered by Exposure to Bioflavonoids and Natural Compounds." In DNA - Damages and Repair Mechanisms. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95453.

Full text
Abstract:
Eukaryotic cells use homologous recombination (HR), classical end-joining (C-NHEJ), and alternative end-joining (Alt-EJ) to repair DNA double-strand breaks (DSBs). Repair pathway choice is controlled by the activation and activity of pathways specific proteins in eukaryotes. Activity may be regulated by cell cycle stage, tissue type, and differentiation status. Bioflavonoids and other environmental agents such as pesticides have been shown to biochemically act as inhibitors of topoisomerase II (Top2). In cells, bioflavonoids directly lead to DNA double-strand breaks through both Top2-dependent and independent mechanisms, as well as induce DNA damage response (DDR) signaling, and promote alternative end-joining and chromosome alterations. This chapter will present differences in expression and activity of proteins in major DNA repair pathways, findings of Top2 inhibition by bioflavonoids and cellular response, discuss how these compounds trigger alternative end-joining, and conclude with implications for genome instability and human disease.
APA, Harvard, Vancouver, ISO, and other styles
7

Bensimon, David, Vincent Croquette, Jean-François Allemand, Xavier Michalet, and Terence Strick. "Topoisomerases." In Single-Molecule Studies of Nucleic Acids and Their Proteins, 177–98. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198530923.003.0009.

Full text
Abstract:
This chapter discusses single-molecule approaches in the study of topoisomerases. After introducing the problem posed by DNA entanglement, it describes type I and type II topoisomerases, which solve that issue. Single-molecule assays have nailed down the different mechanisms of bacterial and eukaryotic type I topoisomerases. The properties of type II topoisomerases are then described. Single-molecule experiments have shown that they relax DNA torsion by two units, passing one dsDNA segment through a break in another segment. However, while topoII relaxes positive and negative supercoils similarly, topoIV relaxes positive supercoils quickly and processively, but negative ones slowly and distributively. This chiral discrimination is compared with the activity of the enzyme on two catenated DNA molecules. After describing single-molecule assays of the activity of gyrases, in-vivo investigations of single fluorescently labelled topoIV units in single E.coli are discussed, with concluding remarks on the future of single-molecule DNA/protein studies.
APA, Harvard, Vancouver, ISO, and other styles
8

Gentry, A. C., and N. Osheroff. "DNA Topoisomerases: Type II." In Encyclopedia of Biological Chemistry, 163–68. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-378630-2.00246-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Dalvie, Esha D., and Neil Osheroff. "DNA Topoisomerases: Type II." In Reference Module in Life Sciences. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-809633-8.21378-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Vélez-Cruz, Renier, and Neil Osheroff. "DNA Topoisomerases: Type II." In Encyclopedia of Biological Chemistry, 806–11. Elsevier, 2004. http://dx.doi.org/10.1016/b0-12-443710-9/00680-3.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Type II topoisomerase"

1

Ketron, Adam, David E. Graves, and Neil Osheroff. "Abstract 2529: Structure-activity relationship studies of the type II topoisomerase poison amsacrine." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2529.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Vologodskii, Alexander. "Maxwell demon and topology simplification by type II topoisomerases." In the second annual international conference. New York, New York, USA: ACM Press, 1998. http://dx.doi.org/10.1145/279069.279129.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Topcu, Zeki, Isa Unlukurt, and Sevil Zencir. "Abstract 1688: Effect of Gefitinib on the reactions of mammalian type I and type II DNA topoisomerases." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1688.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Johnson, Amanda M., Lokha Ranjani A. Boopathy, Raveena Gupta, Hannah N. Miles, Matthew Gilbertson, Karin C. Nitiss, and John L. Nitiss. "Abstract 1742: Modulation of genotoxic DNA damage by the ATPase domain of type II topoisomerases." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1742.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Johnson, Amanda M., Lokha Ranjani A. Boopathy, Raveena Gupta, Hannah N. Miles, Matthew Gilbertson, Karin C. Nitiss, and John L. Nitiss. "Abstract 1742: Modulation of genotoxic DNA damage by the ATPase domain of type II topoisomerases." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1742.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Li, Tsai-Kun, Yu-Chen Yang, and Tang-Long Shen. "Abstract LB-394: Type II topoisomerases contribute to nitric oxide-induced DNA breakage during cancer-related inflammation." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-394.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Type II topoisomerase' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography