Relevant bibliographies by topics / DNA modifying agent

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

Academic literature on the topic 'DNA modifying agent'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 February 2022

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Journal articles on the topic "DNA modifying agent"

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Trus, Michael, Ying Lin, Gurmit Singh, and Mark D. Minden. "Combinations of Epigenetic Modifying Agents Accentuate Retinoid-Mediated Gene Expression Over Single Agent Therapies In Acute Myelogenous Leukemia Cells." Blood 116, no. 21 (2010): 2497. http://dx.doi.org/10.1182/blood.v116.21.2497.2497.

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Abstract Abstract 2497 Background. High cure rates seen in acute promyelocytic leukemia (APL) result from adding the retinoid all trans retinoic acid (ATRA) to chemotherapy. The addition of ATRA to chemotherapy has not consistently improved survival for other acute myelogenous leukemia (AML) subtypes. This likely reflects differences in the degree ATRA overcomes transcriptional repression imposed by the epigenetic mechanisms of histone acetylation and DNA methylation between AML and APL. Purpose To determine if differences in induction of retinoic acid receptor (RAR) β2 accounts for variations
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McKeating, Kristy S., Jennifer A. Dougan, and Karen Faulds. "Nanoparticle assembly for sensitive DNA detection using SERRS." Biochemical Society Transactions 40, no. 4 (2012): 597–602. http://dx.doi.org/10.1042/bst20120007.

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SERRS (surface-enhanced resonance Raman scattering) is a vibrational technique, whereby a relatively weak Raman scattering effect is enhanced through the use of a visible chromophore and a roughened metal surface. The direct analysis of DNA by SERRS requires the modification of a nucleic acid sequence to incorporate a chromophore, and adsorption of the modified sequence on to a roughened metal surface. Aggregated metallic nanoparticles are commonly used in the analysis of dye-labelled DNA by SERRS, allowing for detection levels that rival those gained from standard fluorescence-based technique
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Kwa, Faith A. A., Merrole F. Cole-Sinclair, and Miroslav K. Kapuscinski. "Combination Treatment of p53-Null HL-60 cells with Histone Deacetylase Inhibitors and Chlorambucil Augments Apoptosis and Increases BCL6 and p21 Gene Expression." Current Molecular Pharmacology 12, no. 1 (2019): 72–81. http://dx.doi.org/10.2174/1874467211666181010161836.

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Background:Treatment of hematological malignancies with conventional DNA-damaging drugs, such as chlorambucil (CLB), commonly results in p53-dependent chemo-resistance. Chromatin modifying agents, such as histone deacetylase inhibitors (HDACIs), sodium butyrate (NaBu) and trichostatin A (TSA), may reverse chemo-resistance by modulating the activity of chromatin remodeling enzymes and/or genes that control cell proliferation, differentiation and survival.Objective:This study examined the potential use of HDACIs and CLB combination therapies in an in vitro chemo-resistant leukemia model.Methods:
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Parekh, Hemant, Surendra Chavan, and Manik Chitnis. "Antiproliferative Effects of Mitoxantrone in Adr-Sensitive and Adr-Resistant P388 Leukemia Cells Enhanced by Vitamin K3." Tumori Journal 77, no. 6 (1991): 484–90. http://dx.doi.org/10.1177/030089169107700607.

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Vitamin K3 was employed as a resistance-modifying agent to Investigate its activity in enhancing mitoxantrone (MITO)-induced cytotoxicity in parental (P388/S) and multidrug resistant (P388/ADR) P388 leukemia cells. Vitamin K3 potentiated the antitumor effects of MITO in P388/S and P388/ ADR tumor cells as monitored by inhibition of tumor cell survival (MTT assay). MITO and vitamin K3 in combination effected an enhanced inhibition of [3H]thymidine (DNA synthesis) and [3H]uridine (RNA synthesis) and also Increased the life span of the sensitive and resistant tumor-bearing animals. The effect of
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Zhang, W. W., and M. Yaneva. "Reduced sulphydryl groups are required for DNA binding of Ku protein." Biochemical Journal 293, no. 3 (1993): 769–74. http://dx.doi.org/10.1042/bj2930769.

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The Ku protein, a DNA-binding complex that is composed of two subunits of 70 kDa and of 86 kDa, has been suggested to play a role in gene transcription. The dependence of the in vitro DNA-binding activity of affinity-purified Ku protein on reduced cysteine residues has been studied using sulphydryl-modifying agents. Inhibition of the DNA-binding activity was caused by alkylation with N-ethylmaleimide and by crosslinking with azadicarboxylic acid bis(dimethylamide). Treatment of the protein with a large excess of N-ethylmaleimide after it had bound to DNA did not completely dissociate the compl
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Ustyugov, Aleksey, Elena Shevtsova, Ghulam Md Ashraf, Vadim V. Tarasov, Sergey O. Bachurin, and Gjumrakch Aliev. "New Therapeutic Property of Dimebon as a Neuroprotective Agent." Current Medicinal Chemistry 25, no. 39 (2019): 5315–26. http://dx.doi.org/10.2174/0929867323666160804122746.

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Dimebon (or Latrepirdine) was initially used as an anti-histamergic drug but later new therapeutic properties were rediscovered, adding to a growing body of “old” agents with prominent neuroprotective effects. In the present manuscript, we are focusing on our latest study on Dimebon with regard to brain’s pathological processes using in vivo proteinopathy models. In the study, neurodegenerative pathology has been attributed to a group of aggregate-prone proteins: hyperphosphorylated tau, fused in sarcoma and γ-synuclein , which are involved in a number of neurological disorders. We have also p
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Ghisletti, Serena, Clara Meda, Adriana Maggi та Elisabetta Vegeto. "17β-Estradiol Inhibits Inflammatory Gene Expression by Controlling NF-κB Intracellular Localization". Molecular and Cellular Biology 25, № 8 (2005): 2957–68. http://dx.doi.org/10.1128/mcb.25.8.2957-2968.2005.

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ABSTRACT Estrogen is an immunoregulatory agent, in that hormone deprivation increases while 17β-estradiol (E2) administration blocks the inflammatory response; however, the underlying mechanism is still unknown. The transcription factor p65/relA, a member of the nuclear factor κB (NF-κB) family, plays a major role in inflammation and drives the expression of proinflammatory mediators. Here we report a novel mechanism of action of E2 in inflammation. We observe that in macrophages E2 blocks lipopolysaccharide-induced DNA binding and transcriptional activity of p65 by preventing its nuclear tran
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O’Hara, Bethany A., Gretchen V. Gee, Sheila A. Haley, et al. "Teriflunomide Inhibits JCPyV Infection and Spread in Glial Cells and Choroid Plexus Epithelial Cells." International Journal of Molecular Sciences 22, no. 18 (2021): 9809. http://dx.doi.org/10.3390/ijms22189809.

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Several classes of immunomodulators are used for treating relapsing-remitting multiple sclerosis (RRMS). Most of these disease-modifying therapies, except teriflunomide, carry the risk of progressive multifocal leukoencephalopathy (PML), a severely debilitating, often fatal virus-induced demyelinating disease. Because teriflunomide has been shown to have antiviral activity against DNA viruses, we investigated whether treatment of cells with teriflunomide inhibits infection and spread of JC polyomavirus (JCPyV), the causative agent of PML. Treatment of choroid plexus epithelial cells and astroc
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Klaus, Christine R., Scott R. Daigle, Dorothy Iwanowics, et al. "DOT1L Inhibitor EPZ-5676 Displays Synergistic Antiproliferative Activity in Combination with Standard of Care Drugs or DNA Hypomethylating Agents in MLL-Rearranged Leukemia Cells." Blood 122, no. 21 (2013): 3930. http://dx.doi.org/10.1182/blood.v122.21.3930.3930.

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Abstract EPZ-5676 is a small molecule inhibitor of the histone methyltransferase DOT1L that is currently under clinical investigation as a potential therapy for acute leukemias bearing MLL-rearrangements. Gene knockout and small molecule inhibitor studies have demonstrated that DOT1L is required for MLL-fusion protein–mediated leukemogenesis in model systems. In preclinical studies EPZ-5676 promoted cell killing of acute leukemia lines bearing MLL translocations in vitro while sparing those without MLL gene translocations and also caused sustained tumor regressions in a rat xenograft model of
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Reu, Frederic J., Soo In Bae, Leonid Cherkassky, et al. "Overcoming Resistance to Interferon-Induced Apoptosis of Renal Carcinoma and Melanoma Cells by DNA Demethylation." Journal of Clinical Oncology 24, no. 23 (2006): 3771–79. http://dx.doi.org/10.1200/jco.2005.03.4074.

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Epigenetic editing of gene expression by aberrant methylation of DNA may help tumor cells escape attack from the innate and acquired immune systems. Resistance to antiproliferative effects and apoptosis induction by interferons (IFNs) was postulated to result from silencing of IFN response genes by promoter hypermethylation. Treatment of human ACHN renal cell carcinoma (RCC) and A375 melanoma cells with the DNA demethylating nucleoside analog 5-AZA-2′-deoxycytidine (5-AZA-dC) synergistically augmented antiproliferative effects of IFN- alpha (α) 2 and IFN-beta (β). Either 5-AZA-dC or an antisen
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Dissertations / Theses on the topic "DNA modifying agent"

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Jones, Amy R. "Using Drosophila melanogaster as a Whole-Model Animal System to Elucidate the Mechanism of Action of Novel Anticancer Agents." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1353153948.

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Subramanian, Deepa. "Characterization of topoisomerase I as a target for chemotherapy: Effect of topoisomerase I poisons and DNA-modifying agents on enzyme activity /." The Ohio State University, 1997. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487943610783598.

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Srinivasan, Sheila. "The design and synthesis of novel heterocyclic inhibitors of the DNA-repair enzyme, poly(ADP-ribose) polymerase, as potential resistance-modifying agents." Thesis, University of Newcastle Upon Tyne, 1997. http://hdl.handle.net/10443/1022.

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The abundant nuclear enzyme, poly(ADP-ribose) polymerase (PARP) is activated by DNA strand breaks and catalyses the transfer of ADP-ribose moieties from its substrate, nicotinamide adenine dinucleotide (NAD), to various histone- or non-histone nuclear acceptor proteins. The net result is the formation of long, homopolymeric chains, the exact purpose of which is not clearly understood. Since this process is thought to facilitate DNA repair, the PARP enzyme represents a possible therapeutic target. A well known mechanism by which tumours become resistant to anticancer treatments is increased DNA
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Book chapters on the topic "DNA modifying agent"

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Niangoran, Koissi, Neuvonen Kari, and Lönnberg Harri. "Reaction of Nucleic Acids with Triformylmethane; A Novel Dna-Modifying Agent." In Advances in Experimental Medicine and Biology. Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-0667-6_58.

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Miki, Brian L. A., Terry J. Reich, and V. N. Iyer. "Microinjection: An Experimental Tool for Studying and Modifying Plant Cells." In Plant DNA Infectious Agents. Springer Vienna, 1987. http://dx.doi.org/10.1007/978-3-7091-6977-3_10.

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Conference papers on the topic "DNA modifying agent"

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Biton, Adva, Aviva Ezra, Jana Kasparkova, Victor Brabec, and Eylon Yavin. "DNA/LNA and PNA conjugates as gene modifying agents." In XVth Symposium on Chemistry of Nucleic Acid Components. Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2011. http://dx.doi.org/10.1135/css201112140.

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