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1

Sharma, Kaushal K., Brijendra Singh, Somdutt Mujwar та Prakash S. Bisen. "Molecular Docking Based Analysis to Elucidate the DNA Topoisomerase IIβ as the Potential Target for the Ganoderic Acid; A Natural Therapeutic Agent in Cancer Therapy". Current Computer-Aided Drug Design 16, № 2 (2020): 176–89. http://dx.doi.org/10.2174/1573409915666190820144759.

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Introduction: Intermediate covalent complex of DNA-Topoisomerase II enzyme is the most promising target of the anticancer drugs to induce apoptosis in cancer cells. Currently, anticancer drug and chemotherapy are facing major challenges i.e., drug resistance, chemical instability and, dose-limiting side effect. Therefore, in this study, natural therapeutic agents (series of Ganoderic acids) were used for the molecular docking simulation against Human DNATopoisomerase II beta complex (PDB ID:3QX3). Methods: Molecular docking studies were performed on a 50 series of ganoderic acids reported in t
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2

Bernard, F. X., S. Sablé, B. Cameron, et al. "Glycosylated flavones as selective inhibitors of topoisomerase IV." Antimicrobial Agents and Chemotherapy 41, no. 5 (1997): 992–98. http://dx.doi.org/10.1128/aac.41.5.992.

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Three flavonoids which promoted Escherichia coli topoisomerase IV-dependent DNA cleavage were isolated from cottonseed flour and identified as quercetin 3-O-beta-D-glucose-[1,6]-O-alpha-L-rhamnose (rutin), quercetin 3-O-beta-D-galactose-[1,6]-O-alpha-L-rhamnose, and quercetin 3-O-beta-D-glucose (isoquercitrin). The most active one (rutin) also inhibited topoisomerase IV-dependent decatenation activity (50% inhibitory concentration, 64 microg/ml) and induced the SOS response of a permeable E. coli strain. Derivatives of quercetin glycosylated at position C-3 were shown to induce two site-specif
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3

Strehl, Sabine, Karin Nebral, Helmut H. Schmidt, and Oskar A. Haas. "Topoisomerase (DNA) II Beta 180 kDa TOP2B) - A New NUP98 Fusion Partner." Blood 106, no. 11 (2005): 2849. http://dx.doi.org/10.1182/blood.v106.11.2849.2849.

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Abstract The nucleoporin 98 kDa (NUP98) gene has been reported to be fused to 18 different partner genes in various hematological malignancies with 11p15 aberrations. The most frequently observed fusion partners of NUP98 belong to the homeobox family of transcription factors, whereas the non-HOX NUP98 fusion partners comprise a heterogeneous group of genes that are associated with a wide range of biological functions. Cytogenetic analysis of an adult de novo acute myeloid leukemia (AML-M5a) revealed a t(3;11)(p24;p15) indicating fusion of NUP98 with a novel partner gene. Fluorescence in situ h
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4

Biersack, H., S. Jensen, I. Gromova, I. S. Nielsen, O. Westergaard, and A. H. Andersen. "Active heterodimers are formed from human DNA topoisomerase II alpha and II beta isoforms." Proceedings of the National Academy of Sciences 93, no. 16 (1996): 8288–93. http://dx.doi.org/10.1073/pnas.93.16.8288.

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5

Jenkins, J. R., M. J. Pocklington, and E. Orr. "The F1 ATP synthetase beta-subunit: a major yeast novobiocin binding protein." Journal of Cell Science 96, no. 4 (1990): 675–82. http://dx.doi.org/10.1242/jcs.96.4.675.

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Novobiocin affects DNA metabolism in both prokaryotes and eukaryotes, resulting in cell death. In prokaryotes, the drug is a specific inhibitor of DNA gyrase, a type II topoisomerase that can be purified on a novobiocin-Sepharose column. The yeast type II topoisomerase is neither the biochemical, nor the genetic target of the antibiotic. We have purified the major yeast novobiocin binding proteins and identified one of them as the beta-subunit of the yeast mitochondrial F1 ATP synthetase, a protein highly conserved throughout evolution. The inactivation of this protein might explain the toxic
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6

LONN, Ulf, and Sigrid LONN. "5,6-Dichloro-1-beta-O-ribofuranosylbenzimidazole induces DNA damage by interfering with DNA topoisomerase II." European Journal of Biochemistry 164, no. 3 (1987): 541–45. http://dx.doi.org/10.1111/j.1432-1033.1987.tb11160.x.

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7

Khazeem, Mushtaq M., Ian G. Cowell, Lauren F. Harkin, John W. Casement, and Caroline A. Austin. "Transcription of carbonyl reductase 1 is regulated by DNA topoisomerase II beta." FEBS Letters 594, no. 20 (2020): 3395–405. http://dx.doi.org/10.1002/1873-3468.13904.

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8

Vassetzky, Y. S., Q. Dang, P. Benedetti, and S. M. Gasser. "Topoisomerase II forms multimers in vitro: effects of metals, beta-glycerophosphate, and phosphorylation of its C-terminal domain." Molecular and Cellular Biology 14, no. 10 (1994): 6962–74. http://dx.doi.org/10.1128/mcb.14.10.6962.

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We present a novel assay for the study of protein-protein interactions involving DNA topoisomerase II. Under various conditions of incubation we observe that topoisomerase II forms complexes at least tetrameric in size, which can be sedimented by centrifugation through glycerol. The multimers are enzymatically active and can be visualized by electron microscopy. Dephosphorylation of topoisomerase II inhibits its multimerization, which can be restored at least partially by rephosphorylation of multiple sites within its 200 C-terminal amino acids by casein kinase II. Truncation of topoisomerase
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9

Vassetzky, Y. S., Q. Dang, P. Benedetti, and S. M. Gasser. "Topoisomerase II forms multimers in vitro: effects of metals, beta-glycerophosphate, and phosphorylation of its C-terminal domain." Molecular and Cellular Biology 14, no. 10 (1994): 6962–74. http://dx.doi.org/10.1128/mcb.14.10.6962-6974.1994.

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We present a novel assay for the study of protein-protein interactions involving DNA topoisomerase II. Under various conditions of incubation we observe that topoisomerase II forms complexes at least tetrameric in size, which can be sedimented by centrifugation through glycerol. The multimers are enzymatically active and can be visualized by electron microscopy. Dephosphorylation of topoisomerase II inhibits its multimerization, which can be restored at least partially by rephosphorylation of multiple sites within its 200 C-terminal amino acids by casein kinase II. Truncation of topoisomerase
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10

Muller, M. T., and V. B. Mehta. "DNase I hypersensitivity is independent of endogenous topoisomerase II activity during chicken erythrocyte differentiation." Molecular and Cellular Biology 8, no. 9 (1988): 3661–69. http://dx.doi.org/10.1128/mcb.8.9.3661.

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Endogenous topoisomerase II cleavage sites were mapped in the chicken beta A-globin gene of 12- to 14-day embryonic erythrocytes. A major topoisomerase II catalytic site was mapped to the 5' end of the globin gene which contained a nucleosome-free and DNase I-hypersensitive site and additional but minor sites were mapped to the second intron and 3' of the gene to a tissue-specific enhancer. Cleavage sites, mapped in situ by indirect end labeling, were aligned to single-base-pair resolution by comparison to a consensus sequence derived for vertebrate topoisomerase II catalytic sites. In contras
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11

Muller, M. T., and V. B. Mehta. "DNase I hypersensitivity is independent of endogenous topoisomerase II activity during chicken erythrocyte differentiation." Molecular and Cellular Biology 8, no. 9 (1988): 3661–69. http://dx.doi.org/10.1128/mcb.8.9.3661-3669.1988.

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Endogenous topoisomerase II cleavage sites were mapped in the chicken beta A-globin gene of 12- to 14-day embryonic erythrocytes. A major topoisomerase II catalytic site was mapped to the 5' end of the globin gene which contained a nucleosome-free and DNase I-hypersensitive site and additional but minor sites were mapped to the second intron and 3' of the gene to a tissue-specific enhancer. Cleavage sites, mapped in situ by indirect end labeling, were aligned to single-base-pair resolution by comparison to a consensus sequence derived for vertebrate topoisomerase II catalytic sites. In contras
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12

Burden, D. A., L. J. Goldsmith, and D. M. Sullivan. "Cell-cycle-dependent phosphorylation and activity of Chinese-hamster ovary topoisomerase II." Biochemical Journal 293, no. 1 (1993): 297–304. http://dx.doi.org/10.1042/bj2930297.

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Cell-cycle-dependent protein levels and phosphorylation of DNA topoisomerase II in relation to its catalytic and cleavage activities were studied in Chinese-hamster ovary cells. Immunoreactive topoisomerase II protein levels were maximal in G2-phase cells, intermediate in S- and M-phase cells, and minimal in a predominantly G1-phase population. When the phosphorylation of topoisomerase II in vivo was corrected for differences in specific radioactivity of intracellular ATP, the apparent phosphorylation of S- and M-phase topoisomerase II was altered significantly. Relative phosphorylation in viv
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13

Reitman, M., and G. Felsenfeld. "Developmental regulation of topoisomerase II sites and DNase I-hypersensitive sites in the chicken beta-globin locus." Molecular and Cellular Biology 10, no. 6 (1990): 2774–86. http://dx.doi.org/10.1128/mcb.10.6.2774.

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We have mapped DNase I-hypersensitive sites and topoisomerase II (topo II) sites in the chicken beta-globin locus, which contains four globin genes (5'-rho-beta H-beta A-epsilon-3'). In the 65 kilobases (kb) mapped, 12 strong hypersensitive sites were found clustered within the 25-kb region from 10 kb upstream of rho to just downstream of epsilon. The strong sites were grouped into several classes based on their tissue distribution, developmental pattern, and location. (i) One site was present in all cells examined, both erythroid and nonerythroid. (ii) Three sites, located upstream of the rho
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14

Reitman, M., and G. Felsenfeld. "Developmental regulation of topoisomerase II sites and DNase I-hypersensitive sites in the chicken beta-globin locus." Molecular and Cellular Biology 10, no. 6 (1990): 2774–86. http://dx.doi.org/10.1128/mcb.10.6.2774-2786.1990.

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We have mapped DNase I-hypersensitive sites and topoisomerase II (topo II) sites in the chicken beta-globin locus, which contains four globin genes (5'-rho-beta H-beta A-epsilon-3'). In the 65 kilobases (kb) mapped, 12 strong hypersensitive sites were found clustered within the 25-kb region from 10 kb upstream of rho to just downstream of epsilon. The strong sites were grouped into several classes based on their tissue distribution, developmental pattern, and location. (i) One site was present in all cells examined, both erythroid and nonerythroid. (ii) Three sites, located upstream of the rho
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15

OGAWA, Makoto. "Expression of DNA topoisomerase I and II β in the developing cerebellar plate in rat embryos." Okayama Igakkai Zasshi (Journal of Okayama Medical Association) 111, no. 3-8 (1999): 105–14. http://dx.doi.org/10.4044/joma1947.111.3-8_105.

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16

Ng, Shu-Wing, Yan Liu, and Lowell E. Schnipper. "Cloning and characterization of the 5′-flanking sequence for the human DNA topoisomerase II beta gene." Gene 203, no. 2 (1997): 113–19. http://dx.doi.org/10.1016/s0378-1119(97)00500-3.

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17

Emmons, M., D. Boulware, D. M. Sullivan, and L. A. Hazlehurst. "Topoisomerase II beta levels are a determinant of melphalan-induced DNA crosslinks and sensitivity to cell death." Biochemical Pharmacology 72, no. 1 (2006): 11–18. http://dx.doi.org/10.1016/j.bcp.2006.03.017.

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18

Morse-Gaudio, M., and M. S. Risley. "Topoisomerase II expression and VM-26 induction of DNA breaks during spermatogenesis in Xenopus laevis." Journal of Cell Science 107, no. 10 (1994): 2887–98. http://dx.doi.org/10.1242/jcs.107.10.2887.

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The relative content of topoisomerase II (topo II) and the induction of topo-II-mediated DNA damage and cellular abnormalities have been characterized in developing spermatogenic cells of Xenopus laevis to gain an insight into the role of topo II during spermatogenesis. Decatenation assays identified topo II activity in nuclear extracts from spermatocytes and pre-elongate spermatids, but not in extracts from elongate spermatids or sperm. Extracts from early-mid spermatids contained 14% (per cell) of the decatenation activity found in spermatocyte extracts. Immunoblots of SDS extracts from whol
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19

Calderón-Montaño, José Manuel, Estefanía Burgos-Morón, Manuel Luis Orta, et al. "Alpha, beta-unsaturated lactones 2-furanone and 2-pyrone induce cellular DNA damage, formation of topoisomerase I- and II-DNA complexes and cancer cell death." Toxicology Letters 222, no. 1 (2013): 64–71. http://dx.doi.org/10.1016/j.toxlet.2013.07.007.

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20

Harker, W. Graydon, D. Lynn Slade, Fred H. Drake, and Ryan L. Parr. "Mitoxantrone resistance in HL-60 leukemia cells: reduced nuclear topoisomerase II catalytic activity and drug-induced DNA cleavage in association with reduced expression of the topoisomerase II .beta. isoform." Biochemistry 30, no. 41 (1991): 9953–61. http://dx.doi.org/10.1021/bi00105a020.

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21

Broyles, S. S., and B. Moss. "Sedimentation of an RNA polymerase complex from vaccinia virus that specifically initiates and terminates transcription." Molecular and Cellular Biology 7, no. 1 (1987): 7–14. http://dx.doi.org/10.1128/mcb.7.1.7.

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A high-molecular-weight protein complex that is capable of accurate transcription initiation and termination of vaccinia virus early genes without additional factors was demonstrated. The complex was solubilized by disruption of purified virions, freed of DNA by passage through a DEAE-cellulose column, and isolated by glycerol gradient sedimentation. All detectable RNA polymerase activity was associated with the transcription complex, whereas the majority of enzymes released from virus cores including mRNA (nucleoside-2'-O)methyltransferase, poly(A) polymerase, topoisomerase, nucleoside tripho
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22

Broyles, S. S., and B. Moss. "Sedimentation of an RNA polymerase complex from vaccinia virus that specifically initiates and terminates transcription." Molecular and Cellular Biology 7, no. 1 (1987): 7–14. http://dx.doi.org/10.1128/mcb.7.1.7-14.1987.

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A high-molecular-weight protein complex that is capable of accurate transcription initiation and termination of vaccinia virus early genes without additional factors was demonstrated. The complex was solubilized by disruption of purified virions, freed of DNA by passage through a DEAE-cellulose column, and isolated by glycerol gradient sedimentation. All detectable RNA polymerase activity was associated with the transcription complex, whereas the majority of enzymes released from virus cores including mRNA (nucleoside-2'-O)methyltransferase, poly(A) polymerase, topoisomerase, nucleoside tripho
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23

Tomkins, C. E., S. N. Edwards, and A. M. Tolkovsky. "Apoptosis is induced in post-mitotic rat sympathetic neurons by arabinosides and topoisomerase II inhibitors in the presence of NGF." Journal of Cell Science 107, no. 6 (1994): 1499–507. http://dx.doi.org/10.1242/jcs.107.6.1499.

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Sympathetic neurons depend on nerve growth factor (NGF) for their survival and die by apoptosis when NGF is withdrawn, despite their post-mitotic state. Martin et al. (1990, J. Neurosci. 10, 184–193) showed that cytosine arabinoside, but no other arabinofuranosyl nucleoside, could induce cell death in the presence of NGF and they suggested that it may block a critical step in the NGF-signalling pathway. We show that cytosine arabinoside is not the only nucleoside capable of inducing apoptosis in sympathetic neurons in the presence of NGF. In newly isolated neurons from P0 rat pups cultured in
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24

Fleenor, DE, and RE Kaufman. "Characterization of the DNase I hypersensitive site 3' of the human beta globin gene domain." Blood 81, no. 10 (1993): 2781–90. http://dx.doi.org/10.1182/blood.v81.10.2781.2781.

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Abstract The members of the human beta globin gene family are flanked by strong DNase I hypersensitive sites. The collection of sites 5' to the epsilon globin gene is able to confer high levels of expression of linked globin genes, but a function has not been assigned to the site 3' to the beta globin gene (3'HS1). Our analysis of this DNase I super hypersensitive site shows that the region is composed of multiple DNase I sites. By examination of the DNA sequence, we have determined that the region is very A/T-rich and contains topoisomerase II recognition sequences, as well as several consens
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Fleenor, DE, and RE Kaufman. "Characterization of the DNase I hypersensitive site 3' of the human beta globin gene domain." Blood 81, no. 10 (1993): 2781–90. http://dx.doi.org/10.1182/blood.v81.10.2781.bloodjournal81102781.

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The members of the human beta globin gene family are flanked by strong DNase I hypersensitive sites. The collection of sites 5' to the epsilon globin gene is able to confer high levels of expression of linked globin genes, but a function has not been assigned to the site 3' to the beta globin gene (3'HS1). Our analysis of this DNase I super hypersensitive site shows that the region is composed of multiple DNase I sites. By examination of the DNA sequence, we have determined that the region is very A/T-rich and contains topoisomerase II recognition sequences, as well as several consensus bindin
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26

Burden, D. Andrew, and Daniel M. Sullivan. "Phosphorylation of the .alpha.- and .beta.-Isoforms of DNA Topoisomerase II Is Qualitatively Different in Interphase and Mitosis in Chinese Hamster Ovary Cells." Biochemistry 33, no. 49 (1994): 14651–55. http://dx.doi.org/10.1021/bi00253a001.

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27

Wang, Zhe Qing, Yao Haur Kuo, Dora Schnur, et al. "Antitumor agents. 113. New 4.beta.-arylamino derivatives of 4'-O-demethylepipodophyllotoxin and related compounds as potent inhibitors of human DNA topoisomerase II." Journal of Medicinal Chemistry 33, no. 9 (1990): 2660–66. http://dx.doi.org/10.1021/jm00171a050.

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28

Hu, Hong, Su Ying Liu, Yung Chi Cheng, Kuo Hsiung Lee, and Zhe Qing Wang. "Antitumor agents. 123. Synthesis and human DNA topoisomerase II inhibitory activity of 2'-chloro derivatives of etoposide and 4.beta.-(arylamino)-4'-O-demethylpodophyllotoxins." Journal of Medicinal Chemistry 35, no. 5 (1992): 866–71. http://dx.doi.org/10.1021/jm00083a009.

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29

Jazwinski, S. M. "Participation of ATP in the binding of a yeast replicative complex to DNA." Biochemical Journal 246, no. 1 (1987): 213–19. http://dx.doi.org/10.1042/bj2460213.

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The activity that replicates yeast DNA in vitro can be isolated from cells of the budding yeast Saccharomyces in a high-Mr (approximately 2 × 10(6] form. Several lines of evidence indicate that this fraction contains a multiprotein replicative complex. A functional assay has been developed for the analysis of the interaction of the replicating activity with DNA. Binding of the activity required Mg2+, but did not require the addition of ATP or the other ribo- or deoxynucleoside triphosphates. However, the ATP analogues adenosine 5′-[gamma-thio]triphosphate and adenosine 5′-[beta gamma-imido]tri
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30

Kimura, K., N. Nozaki, M. Saijo, A. Kikuchi, M. Ui, and T. Enomoto. "Identification of the nature of modification that causes the shift of DNA topoisomerase II beta to apparent higher molecular weight forms in the M phase." Journal of Biological Chemistry 269, no. 40 (1994): 24523–26. http://dx.doi.org/10.1016/s0021-9258(17)31419-9.

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31

Charron, Martin, and Ronald Hancock. "DNA topoisomerase II is required for formation of mitotic chromosomes in Chinese hamster ovary cells: studies using the inhibitor 4'-demethylepipodophyllotoxin 9-(4,6-O-thenylidene-.beta.-D-glucopyranoside)." Biochemistry 29, no. 41 (1990): 9531–37. http://dx.doi.org/10.1021/bi00493a006.

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32

Wang, Zhe-Qing, Hong Hu, Hong-Xin Chen, Yung-Chi Cheng, and Kuo Hsiung Lee. "Antitumor agents. 124. New 4.beta.-substituted aniline derivatives of 6,7-O,O-demethylene-4'-O-demethylpodophyllotoxin and related compounds as potent inhibitors of human DNA topoisomerase II." Journal of Medicinal Chemistry 35, no. 5 (1992): 871–77. http://dx.doi.org/10.1021/jm00083a010.

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33

Renzi, L., M. S. Gersch, M. S. Campbell, L. Wu, S. A. Osmani, and G. J. Gorbsky. "MPM-2 antibody-reactive phosphorylations can be created in detergent-extracted cells by kinetochore-bound and soluble kinases." Journal of Cell Science 110, no. 17 (1997): 2013–25. http://dx.doi.org/10.1242/jcs.110.17.2013.

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The MPM-2 antibody labels mitosis-specific and cell cycle-regulated phosphoproteins. The major phosphoproteins of mitotic chromosomes recognized by the MPM-2 antibody are DNA topoisomerase II (topoII) alpha and beta. In immunofluorescence studies of PtK1 cytoskeletons, prepared by detergent lysis in the presence of potent phosphatase inhibitors, the MPM-2 antibody labels phosphoproteins found at kinetochores, chromosome arms, midbody and spindle poles of mitotic cells. In cells extracted without phosphatase inhibitors, labeling of the MPM-2 antibodies at kinetochores is greatly diminished. How
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34

Celada, A., S. McKercher, and R. A. Maki. "Repression of major histocompatibility complex IA expression by glucocorticoids: the glucocorticoid receptor inhibits the DNA binding of the X box DNA binding protein." Journal of Experimental Medicine 177, no. 3 (1993): 691–98. http://dx.doi.org/10.1084/jem.177.3.691.

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Glucocorticoids are effective repressors of major histocompatibility complex (MHC) class II gene expression. The repression occurs in B cells, which constitutively express MHC class II, as well as in macrophages, which only express MHC class II after the cells are treated with interferon gamma. For the MHC class II gene IA beta, this negative regulation has been linked to the X box DNA sequence, located with the IA beta promoter. The addition of the glucocorticoid receptor was shown to inhibit the DNA binding of the X box DNA binding protein to the X box. The DNA binding of two other DNA bindi
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35

Hagiwara, Kazumi, Hiromi Ito, Takashi Murate, Yasuhiko Miyata, Haruhiko Ohashi, and Hirokazu Nagai. "PROX1 overexpression inhibits protein kinase C beta II transcription through promoter DNA methylation." Genes, Chromosomes and Cancer 51, no. 11 (2012): 1024–36. http://dx.doi.org/10.1002/gcc.21985.

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36

Lin, G. C., J. Jaeger, and J. B. Sweasy. "Loop II of DNA polymerase beta is important for polymerization activity and fidelity." Nucleic Acids Research 35, no. 9 (2007): 2924–35. http://dx.doi.org/10.1093/nar/gkm126.

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37

Lin, George C., Joachim Jaeger, Kristin A. Eckert, and Joann B. Sweasy. "Loop II of DNA polymerase beta is important for discrimination during substrate binding." DNA Repair 8, no. 2 (2009): 182–89. http://dx.doi.org/10.1016/j.dnarep.2008.10.006.

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38

Moi, P., G. Loudianos, J. Lavinha, et al. "Delta-thalassemia due to a mutation in an erythroid-specific binding protein sequence 3' to the delta-globin gene." Blood 79, no. 2 (1992): 512–16. http://dx.doi.org/10.1182/blood.v79.2.512.bloodjournal792512.

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We have previously described a family of Northern Sardinian descent in which the propositus was affected by thalassemia major resulting from compound heterozygosity for codon 39 nonsense mutation and the beta +IVS II nt 745 mutation and in which all heterozygotes for the beta +IVS II nt 745 mutation had normal hemoglobin (Hb) A2 levels. To define the reasons for normal HbA2 levels in otherwise typical beta- thalassemia heterozygotes, we cloned and sequenced the delta- thalassemia gene in cis to the beta +IVS II nt 745 mutation. The sequence analysis showed a single nucleotide substitution (G--
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Wade, W. F., J. H. Freed, and M. Edidin. "Translational diffusion of class II major histocompatibility complex molecules is constrained by their cytoplasmic domains." Journal of Cell Biology 109, no. 6 (1989): 3325–31. http://dx.doi.org/10.1083/jcb.109.6.3325.

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Site-directed mutagenesis in vitro was used to introduce stop codons in the genomic DNA of the alpha and beta chains of the murine class II major histocompatibility complex antigen, I-Ak. Mutated DNA was transfected into B lymphoma cells that were then selected by neomycin resistance and for their ability to express I-Ak molecules on their plasma membrane. The translational diffusion coefficient (Dlat) of I-Ak molecules composed of a wild-type beta chain paired with an alpha chain missing either 6 or 12 amino acids from the cytoplasmic domain is on the average threefold higher than the Dlat of
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40

Khalil, N., R. N. O'Connor, K. C. Flanders, W. Shing, and C. I. Whitman. "Regulation of type II alveolar epithelial cell proliferation by TGF-beta during bleomycin-induced lung injury in rats." American Journal of Physiology-Lung Cellular and Molecular Physiology 267, no. 5 (1994): L498—L507. http://dx.doi.org/10.1152/ajplung.1994.267.5.l498.

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Three isoforms of transforming growth factor-beta (TGF-beta) are found in mammalian cells and are potent regulators of inflammation, connective tissue synthesis, cellular proliferation, and differentiation. To determine the distribution and regulation of TGF-beta isoforms during pulmonary injury, a rat model of bleomycin-induced lung inflammation and repair was used. Using immunohistochemistry, we demonstrate that TGF-beta 2 and TGF-beta 3 were localized to alveolar macrophages as well as epithelial and smooth muscle cells of both normal rat lungs and rat lungs obtained at all time intervals a
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41

German, M. S., L. G. Moss, J. Wang, and W. J. Rutter. "The insulin and islet amyloid polypeptide genes contain similar cell-specific promoter elements that bind identical beta-cell nuclear complexes." Molecular and Cellular Biology 12, no. 4 (1992): 1777–88. http://dx.doi.org/10.1128/mcb.12.4.1777.

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The pancreatic beta cell makes several unique gene products, including insulin, islet amyloid polypeptide (IAPP), and beta-cell-specific glucokinase (beta GK). The functions of isolated portions of the insulin, IAPP, and beta GK promoters were studied by using transient expression and DNA binding assays. A short portion (-247 to -197 bp) of the rat insulin I gene, the FF minienhancer, contains three interacting transcriptional regulatory elements. The FF minienhancer binds at least two nuclear complexes with limited tissue distribution. Sequences similar to that of the FF minienhancer are pres
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42

German, M. S., L. G. Moss, J. Wang, and W. J. Rutter. "The insulin and islet amyloid polypeptide genes contain similar cell-specific promoter elements that bind identical beta-cell nuclear complexes." Molecular and Cellular Biology 12, no. 4 (1992): 1777–88. http://dx.doi.org/10.1128/mcb.12.4.1777-1788.1992.

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The pancreatic beta cell makes several unique gene products, including insulin, islet amyloid polypeptide (IAPP), and beta-cell-specific glucokinase (beta GK). The functions of isolated portions of the insulin, IAPP, and beta GK promoters were studied by using transient expression and DNA binding assays. A short portion (-247 to -197 bp) of the rat insulin I gene, the FF minienhancer, contains three interacting transcriptional regulatory elements. The FF minienhancer binds at least two nuclear complexes with limited tissue distribution. Sequences similar to that of the FF minienhancer are pres
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43

Hansmann, Paul. "Daffodil Chromoplast DNA: Comparison with Chloroplast DNA, Physical Map, and Gene Localization." Zeitschrift für Naturforschung C 42, no. 1-2 (1987): 118–22. http://dx.doi.org/10.1515/znc-1987-1-219.

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Abstract In daffodil, development of chloroplasts or chromoplasts is not accompanied by plastid DNA modification. This has been shown by comparing the fragment pattern of different restriction endonucleases, and by the lack of methylation of CCGG sequences. A physical map has been constructed for the plastome using the restriction endonucleases Sal I, Pst I, and Bgl I. The fragments containing the genes for the large subunit of ribulose bisphosphate carboxylase/oxygenase (rbcL), the alpha, beta, and epsilon subunits of the ATP synthase complex (atpA , atpB, atpE ), cytochrome f(petA ), and for
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44

Rohrbaugh, M. L., J. E. Johnson, M. D. James, and R. C. Hardison. "Transcription unit of the rabbit beta 1 globin gene." Molecular and Cellular Biology 5, no. 1 (1985): 147–60. http://dx.doi.org/10.1128/mcb.5.1.147.

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We have hybridized pulse-labeled nuclear transcripts to cloned DNA fragments from the rabbit beta-like globin genes to determine the developmental timing, extent, and asymmetry of their transcription. The fetal-adult gene beta 1 was transcribed in fetal liver but not embryonic nuclei, whereas genes beta 3 and beta 4, which encode embryonic globin polypeptides, were transcribed only in embryonic nuclei. This shows that the switch from embryonic to fetal-adult globin production in rabbits is accomplished primarily by differential transcription of the beta-like globin genes. Gene beta 1 was subdi
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45

Rohrbaugh, M. L., J. E. Johnson, M. D. James, and R. C. Hardison. "Transcription unit of the rabbit beta 1 globin gene." Molecular and Cellular Biology 5, no. 1 (1985): 147–60. http://dx.doi.org/10.1128/mcb.5.1.147-160.1985.

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We have hybridized pulse-labeled nuclear transcripts to cloned DNA fragments from the rabbit beta-like globin genes to determine the developmental timing, extent, and asymmetry of their transcription. The fetal-adult gene beta 1 was transcribed in fetal liver but not embryonic nuclei, whereas genes beta 3 and beta 4, which encode embryonic globin polypeptides, were transcribed only in embryonic nuclei. This shows that the switch from embryonic to fetal-adult globin production in rabbits is accomplished primarily by differential transcription of the beta-like globin genes. Gene beta 1 was subdi
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46

Moi, P., G. Loudianos, J. Lavinha, et al. "Delta-thalassemia due to a mutation in an erythroid-specific binding protein sequence 3' to the delta-globin gene." Blood 79, no. 2 (1992): 512–16. http://dx.doi.org/10.1182/blood.v79.2.512.512.

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Abstract We have previously described a family of Northern Sardinian descent in which the propositus was affected by thalassemia major resulting from compound heterozygosity for codon 39 nonsense mutation and the beta +IVS II nt 745 mutation and in which all heterozygotes for the beta +IVS II nt 745 mutation had normal hemoglobin (Hb) A2 levels. To define the reasons for normal HbA2 levels in otherwise typical beta- thalassemia heterozygotes, we cloned and sequenced the delta- thalassemia gene in cis to the beta +IVS II nt 745 mutation. The sequence analysis showed a single nucleotide substitu
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Schmidt, T., and J. S. Heslop-Harrison. "Variability and evolution of highly repeated DNA sequences in the genus Beta." Genome 36, no. 6 (1993): 1074–79. http://dx.doi.org/10.1139/g93-142.

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Satellite DNA from wild beet species was separated from restriction endonuclease digested genomic DNA by polyacrylamide gel electrophoresis. Two nonhomologous HaeIII satellite DNA repeats were cloned from the wild beet Beta trigyna. The type I repeat is 140–149 bp long and AT rich, while the type II is 162 bp in size and GC rich. A third repetitive HaeIII element cloned from the related wild beet B. corolliflora was shown to be organized as a HinfI satellite DNA family in the cultivated beet B. vulgaris ssp. vulgaris and the wild beet B. vulgaris ssp. maritima. This type III satellite monomer
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48

Lu, H. T., J. L. Riley, G. T. Babcock, et al. "Interferon (IFN) beta acts downstream of IFN-gamma-induced class II transactivator messenger RNA accumulation to block major histocompatibility complex class II gene expression and requires the 48-kD DNA-binding protein, ISGF3-gamma." Journal of Experimental Medicine 182, no. 5 (1995): 1517–25. http://dx.doi.org/10.1084/jem.182.5.1517.

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Interferon (IFN) gamma, a cardinal proinflammatory cytokine, induces expression of the gene products of the class II locus of the major histocompatibility complex (MHC), whereas IFN-alpha or -beta suppresses MHC class II expression. The mechanism of IFN-beta-mediated MHC class II inhibition has been unclear. Recently, a novel factor termed class II transactivator (CIITA) has been identified as essential for IFN-gamma-induced MHC class II transcription. We studied the status of IFN-gamma-induced CIITA messenger RNA (mRNA) accumulation and CIITA-driven transactivation in IFN-beta-treated cells a
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49

Embury, SH, GL Kropp, TS Stanton, TC Warren, PA Cornett, and FF Chehab. "Detection of the hemoglobin E mutation using the color complementation assay: application to complex genotyping." Blood 76, no. 3 (1990): 619–23. http://dx.doi.org/10.1182/blood.v76.3.619.619.

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Abstract The color complementation assay (CCA) is a method of allele-specific DNA amplification by which competitive priming and extension of fluorescently labeled oligonucleotide primers determine the color of DNA amplification product. This diagnostic method precludes the need for radioisotopes, electrophoresis, and multiple high-stringency reaction conditions. The multiplicity of mutant globin genes present in Southeast Asians complicates clinical diagnosis and underscores the importance of DNA-based diagnostic methods. We have applied CCA to distinguish beta A and beta E alleles. Competing
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50

Embury, SH, GL Kropp, TS Stanton, TC Warren, PA Cornett, and FF Chehab. "Detection of the hemoglobin E mutation using the color complementation assay: application to complex genotyping." Blood 76, no. 3 (1990): 619–23. http://dx.doi.org/10.1182/blood.v76.3.619.bloodjournal763619.

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The color complementation assay (CCA) is a method of allele-specific DNA amplification by which competitive priming and extension of fluorescently labeled oligonucleotide primers determine the color of DNA amplification product. This diagnostic method precludes the need for radioisotopes, electrophoresis, and multiple high-stringency reaction conditions. The multiplicity of mutant globin genes present in Southeast Asians complicates clinical diagnosis and underscores the importance of DNA-based diagnostic methods. We have applied CCA to distinguish beta A and beta E alleles. Competing 15mer pr
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