Relevant bibliographies by topics / Transcription; Drug effects

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

Academic literature on the topic 'Transcription; Drug effects'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Transcription; Drug effects"

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MARÍN, Silvia, Sylvia MANSILLA, Natàlia GARCÍA-REYERO, Marta ROJAS, José PORTUGAL, and Benjamin PIÑA. "Promoter-specific inhibition of transcription by daunorubicin in Saccharomyces cerevisiae." Biochemical Journal 368, no. 1 (2002): 131–36. http://dx.doi.org/10.1042/bj20020724.

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Several anti-tumour drugs exert some of their cytotoxic effects by direct binding to DNA, thus inhibiting the transcription of certain genes. We analysed the influence of the anti-tumour antibiotic daunorubicin on the transcription of different genes in vivo using the budding yeast Saccharomyces cerevisiae. Daunorubicin only affected wild-type yeast strains at very high concentrations; however, erg6 mutant strains (but not pdr1, pdr3 or pdr5 strains) were sensitive to daunorubicin at low micromolar concentrations. In Δerg6 strains, daunorubicin inhibited the galactose-induced transcription by
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Nawrocki, Arkadiusz, Stephen J. Fey, Peter Mose Larsen, André Goffeau, and Peter Roepstorff. "The Effects of Transcription Regulating GenesPDR1, pdr1-3andPDR3in Pleiotropic Drug Resistance." European Journal of Mass Spectrometry 7, no. 2 (2001): 195–205. http://dx.doi.org/10.1255/ejms.403.

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Wilmańska, Dorota, Malgorzata Czyz, Kazimierz Studzian, Mariola K. Piestrzeniewicz, and Marek Gniazdowski. "Effects of Anticancer Drugs on Transcription in vitro." Zeitschrift für Naturforschung C 56, no. 9-10 (2001): 886–91. http://dx.doi.org/10.1515/znc-2001-9-1034.

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AbstractThe effects of DNA interacting drugs on: (1) total RNA synthesis catalyzed by E.coli and T7 RNA polymerase; (2) synthesis of the initiating dinucleotide (pppApU) by E .coli RNA polymerase (“abortive initiation“); (3) elongation of RNA chains synthesized by T7 RNA polymerase on pT7-7 plasmid DNA bearing T7 RNA polymerase promoter ϕ 10 with human Cu/Zn superoxide dismutase coding sequence, (4) interaction of transcription factor Sp1 and its binding site were studied. Intercalating ligands which form quickly dissociating complexes with DNA (anthracyclines, proflavine, ethidium bromide) ar
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Takeshita, Akira, Junko Igarashi-Migitaka, Noriyuki Koibuchi, and Yasuhiro Takeuchi. "Mitotane induces CYP3A4 expression via activation of the steroid and xenobiotic receptor." Journal of Endocrinology 216, no. 3 (2012): 297–305. http://dx.doi.org/10.1530/joe-12-0297.

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Adrenocortical carcinoma (ACC) is a rare disease with an extremely poor prognosis. Mitotane alone or in combination with other cytotoxic drugs is a common therapeutic option for ACC. In addition to its adrenolytic function, mitotane has been known for decades to increase the metabolic clearance of glucocorticoids. It was recently shown that the tyrosine kinase inhibitor sunitinib is also rapidly metabolized in patients treated with mitotane, indicating that mitotane engages in clinically relevant drug interactions. Although the precise mechanism of these interactions is not well understood, cy
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Gniazdowski, Marek, William A. Denny, Stephanie M. Nelson, and Malgorzata Czyz. "Effects of anticancer drugs on transcription factor–DNA interactions." Expert Opinion on Therapeutic Targets 9, no. 3 (2005): 471–89. http://dx.doi.org/10.1517/14728222.9.3.471.

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Wang, Fu-Zhang, Debasmita Roy, Edward Gershburg, Christopher B. Whitehurst, Dirk P. Dittmer, and Joseph S. Pagano. "Maribavir Inhibits Epstein-Barr Virus Transcription in Addition to Viral DNA Replication." Journal of Virology 83, no. 23 (2009): 12108–17. http://dx.doi.org/10.1128/jvi.01575-09.

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ABSTRACT Although many drugs inhibit the replication of Epstein-Barr virus (EBV) in cell culture systems, there is still no drug that is effective and approved for use in primary EBV infection. More recently, maribavir (MBV), an l-ribofuranoside benzimidazole, has been shown to be a potent and nontoxic inhibitor of EBV replication and to have a mode of action quite distinct from that of acyclic nucleoside analogs such as acyclovir (ACV) that is based primarily on MBV's ability to block the phosphorylation of target proteins by EBV and human cytomegalovirus protein kinases. However, since the a
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Tepperman, Katherine, Pamela W. Roy, Brian F. Moloney, and R. C. Elder. "Dicyanogold Effects on Lymphokine Production." Metal-Based Drugs 6, no. 4-5 (1999): 301–9. http://dx.doi.org/10.1155/mbd.1999.301.

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Having identified dicyanogold(I) as a common metabolite of gold-based antiarthritis drugs, we are investigating the effects of the compound on the production of lymphokines. Handel, et al. 1 suggested that the transcription factor AP-1, critical to the production of a number of cytokines, might be the target for gold compounds because of a critical cysteine within its DNA binding region. Using Jurkat cells, an established cell line as a model for CD4+ lymphocytes, we have shown that dicyanogold inhibits the binding of AP-1 to DNA and inhibits the synthesis of IL-2 mRNA and protein. In a macrop
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Heinbockel, Thomas, and Antonei Csoka. "Epigenetic Effects of Drugs of Abuse." International Journal of Environmental Research and Public Health 15, no. 10 (2018): 2098. http://dx.doi.org/10.3390/ijerph15102098.

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Drug addiction affects a large extent of young people and disadvantaged populations. Drugs of abuse impede brain circuits or affect the functionality of brain circuits and interfere with bodily functions. Cannabinoids (Δ9-tetrahydrocannabinol) form key constituents of marijuana derived from the cannabis plant. Marijuana is a frequently used illegal drug in the USA. Here, we review the effects of cannabinoids at the epigenetic level and the potential role of these epigenetic effects in health and disease. Epigenetics is the study of alterations in gene expression that are transmitted across gen
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Escoter-Torres, Laura, Franziska Greulich, Fabiana Quagliarini, Michael Wierer, and Nina Henriette Uhlenhaut. "Anti-inflammatory functions of the glucocorticoid receptor require DNA binding." Nucleic Acids Research 48, no. 15 (2020): 8393–407. http://dx.doi.org/10.1093/nar/gkaa565.

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Abstract The glucocorticoid receptor is an important immunosuppressive drug target and metabolic regulator that acts as a ligand-gated transcription factor. Generally, GR’s anti-inflammatory effects are attributed to the silencing of inflammatory genes, while its adverse effects are ascribed to the upregulation of metabolic targets. GR binding directly to DNA is proposed to activate, whereas GR tethering to pro-inflammatory transcription factors is thought to repress transcription. Using mice with a point mutation in GR’s zinc finger, that still tether via protein–protein interactions while be
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Nawrocki, Arkadiusz, Stephen J. Fey, André Goffeau, Peter Roepstorff, and Peter Mose Larsen. "The effects of transcription regulating genesPDR1,pdr1-3 andPDR3 in pleiotropic drug resistance." PROTEOMICS 1, no. 8 (2001): 1022–32. http://dx.doi.org/10.1002/1615-9861(200108)1:8<1022::aid-prot1022>3.0.co;2-7.

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Dissertations / Theses on the topic "Transcription; Drug effects"

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Cowie, Philip David. "Analysis of the effects of disease-associated variation within a cis-regulatory element of the CNR1 locus on CNR1 promoter dynamics." Thesis, University of Aberdeen, 2014. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=225652.

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Genetic variation within the cannabinoid 1 receptor (CB1R) locus (CNR1) has been repeatedly associated with drug addiction pathologies. Genomic annotation of CNR1 indicates the vast majority of this genetic variation likely results in altered transcriptional regulation of the CNR1 gene as a mechanistic link to the disease phenotype. There is a lack of information describing the regulation of CNR1 transcription and the potential impact of disease-associated variation within the CNR1 locus on its transcriptional regulation. This study investigates the impact of an evolutionary conserved regulato
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Yan, Jin 1972. "The mechanisms of hydroxyurea induced developmental toxicity in the organogenesis stage mouse embryo /." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115897.

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Hydroxyurea was used as a model teratogen to investigate the role of oxidative stress and stress-response pathways in mediating developmental toxicity. When administered to pregnant mice during early organogenesis, hydroxyurea induced fetal death and growth retardation, as well as external and skeletal malformations. The malformed fetuses displayed hindlimb, vertebral column, and tail defects. Hydroxyurea treatment enhanced the production of 4-hydroxynonenal, a lipid peroxidation end product, in malformation sensitive regions of the embryo. Depletion of glutathione, a major cellular antioxidan
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Varandas, Edna Soraia Gregório Ribeiro Varandas. "Low-dose effects of Bisphenol A on human primary vascular endothelial cells and colon cancer cells." Doctoral thesis, ISA/UL, 2014. http://hdl.handle.net/10400.5/7338.

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Doutoramento em Biologia - Instituto Superior de Agronomia<br>Bisphenol A (BPA) is an extensively utilized endocrine disruptor for which human exposure is considered generalized through ingestion. Information regarding BPA effects on vascular and digestive tract tissues is scarce. Therefore, in this work primary Human Umbilical Vein Endothelial Cells (HUVEC) and human colon adenocarcinona cell line HT29 were used to evaluate BPA effects at two distinct low-dose concentrations relevant in terms of human health risk assessment. BPA differentially affects the cell types studied, with more
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Gnanabakthan, Naveen. "Understanding the basis of 5-Bromo-2'-deoxuridine teratogen specificity in organogenesis stage mouse embryos." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112624.

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5-Bromo-2'-deoxyuridine (BrdU), a thymidine analogue, is genotoxic and teratogenic. The exposure of mouse embryos to BrdU at doses that cause malformations induces oxidative stress and an embryonic stress response characterized by an increase in c-Fos dependent AP-1 DNA binding. The goal of this thesis was to test the hypothesis that development is disturbed at sites where BrdU is incorporated into DNA, triggering oxidative stress and c-Fos induction. Gestation day 9 CD-1 mice were treated with BrdU and embryos were obtained for immunolocalization of BrdU, 8-oxoguanine, a biomarker for oxidati
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Feuerhahn, Sascha. "Mechanistic insights into the effect of oxidative lesions and anticancer drugs on RNA pol II transcription and transcription coupled repair." Université Louis Pasteur (Strasbourg) (1971-2008), 2008. https://publication-theses.unistra.fr/restreint/theses_doctorat/2008/FEUERHAHN_Sascha_2008.pdf.

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Le processus vital d’expression des gènes par l’ARN polymérase II (ARN pol II) peut être perturbé par les lésions portées par l’ADN. Une ARN pol II bloquée peut déclencher la réparation couplée à la transcription (TCR). Un acteur central de la TCR est la protéine du syndrome de Cockayne du groupe B (CSB), qui, quand elle est mutée, peut donner naissance au syndrome de Cockayne (CS). Dans cette thèse, l’effet de trois lésions oxydatives abondantes a été étudié en utilisant un système de transcription in vitro bien défini. Les lésions oxydatives peuvent bloquer la progression de l’ARN pol II qui
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Fappi, Alan. "Efeitos do ácido graxo ômega-3 na prevenção da atrofia muscular induzida pela dexametasona." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5138/tde-13012014-114428/.

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Várias condições podem estar associadas com a atrofia muscular, tais como inatividade, envelhecimento, septicemia, diabetes, câncer e uso de glicocorticoides. Todas estas condições levam a atrofia muscular através de mecanismos que incluem aumento da degradação proteica e/ou redução na síntese proteica, envolvendo pelo menos cinco sistemas: lisossomal, da calpaína, das caspases, metaloproteinases e o sistema ubiquitina-proteasoma (SUP). Glicocorticoides, tais como a dexametasona, acarretam atrofia muscular atuando em quase todos esses sistemas, com significante ativação do SUP e lisossomal, af
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"Screening of factors that affect GSK-3[beta] expression and study of tau phosphorylation by GSK-3[beta] in cultured cell lines." 2001. http://library.cuhk.edu.hk/record=b6073389.

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by Lee Wing-cheung.<br>"November 2001."<br>Thesis (Ph.D.)--Chinese University of Hong Kong, 2001.<br>Includes bibliographical references (p. 152-169).<br>Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.<br>Mode of access: World Wide Web.<br>Abstracts in English and Chinese.
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Mardaryev, Andrei N., N. Meier, Krzysztof Poterlowicz, et al. "Lhx2 differentially regulates Sox9, Tcf4 and Lgr5 in hair follicle stem cells to promote epidermal regeneration after injury." 2011. http://hdl.handle.net/10454/6079.

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The Lhx2 transcription factor plays essential roles in morphogenesis and patterning of ectodermal derivatives as well as in controlling stem cell activity. Here, we show that during murine skin morphogenesis, Lhx2 is expressed in the hair follicle (HF) buds, whereas in postnatal telogen HFs Lhx2(+) cells reside in the stem cell-enriched epithelial compartments (bulge, secondary hair germ) and co-express selected stem cell markers (Sox9, Tcf4 and Lgr5). Remarkably, Lhx2(+) cells represent the vast majority of cells in the bulge and secondary hair germ that proliferate in response to skin injury
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"Flavonoids display differential actions on er transactivation and apoptosis in MCF-7 cells." 2002. http://library.cuhk.edu.hk/record=b5896009.

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Po Lai See.<br>Thesis (M.Phil.)--Chinese University of Hong Kong, 2002.<br>Includes bibliographical references (leaves 142-152).<br>Abstracts in English and Chinese.<br>TITLE PAGE --- p.p.1<br>ACKNOWLEGDEMENTS --- p.p.2<br>ABSTRACT --- p.p.3<br>摘要 --- p.p.6<br>TABLE OF CONTENTS --- p.p.9<br>LIST OF FIGURES AND TABLES --- p.p.16<br>Chapter CHAPTER 1 --- GENERAL INTRODUCTION<br>Chapter 1.1 --- Estrogen and Estrogen Receptors and its Action --- p.p.18<br>Chapter 1.1.1 --- Estrogen --- p.p.19<br>Chapter 1.1.2 --- Estrogen Receptors --- p.p.19<br>Chapter 1.1.3 --- Structural Diff
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Shakibaei, M., C. Buhrmann, and A. Mobasheri. "Resveratrol-mediated SIRT-1 interactions with p300 modulate receptor activator of NF-kappaB ligand (RANKL) activation of NF-kappaB signaling and inhibit osteoclastogenesis in bone-derived cells." 2011. http://hdl.handle.net/10454/6182.

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Resveratrol is a polyphenolic phytoestrogen that has been shown to exhibit potent anti-oxidant, anti-inflammatory, and anti-catabolic properties. Increased osteoclastic and decreased osteoblastic activities result in bone resorption and loss of bone mass. These changes have been implicated in pathological processes in rheumatoid arthritis and osteoporosis. Receptor activator of NF-kappaB ligand (RANKL), a member of the TNF superfamily, is a major mediator of bone loss. In this study, we investigated the effects of resveratrol on RANKL during bone morphogenesis in high density bone cultures in
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Books on the topic "Transcription; Drug effects"

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Reinhard, Grzanna, Brown Roger M, and National Institute on Drug Abuse., eds. Activation of immediate early genes by drugs of abuse. U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Institute on Drug Abuse, 1993.

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Histone deacetylases: Transcriptional regulation and other cellular functions. Humana Press, 2006.

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Verdin, Eric. Histone Deacetylases: Transcriptional Regulation and Other Cellular Functions (Cancer Drug Discovery and Development). Humana Press, 2006.

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Eric, Verdin, ed. Histone deacetylases: Transcriptional regulation and other cellular functions. Humana Press, 2006.

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Verdin, Eric. Histone Deacetylases: Transcriptional Regulation and Other Cellular Functions. Humana Press, 2010.

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Verdin, Eric. Histone Deacetylases: Transcriptional Regulation and Other Cellular Functions. Humana Press, 2007.

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Book chapters on the topic "Transcription; Drug effects"

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Shandilya, Manish, Shrutika Sharma, Prabhu Prasad Das, and Sonika Charak. "Molecular-Level Understanding of the Anticancer Action Mechanism of Anthracyclines." In Overview of Doxorubicin - Clinical Use, Resistance, Side Effects, and Palliative Care [Working Title]. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.94180.

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Anthracyclines drugs are used as a treatment regime to combat cancer owing to their great chemotherapeutic potential. They are characterized by the presence of a wide range of derivatives, the most famous are doxorubicin and daunorubicin. The proposed action mechanism of anthracyclines and their derivatives to exert cytotoxic effect involves the intercalation of the drug molecule into nucleic acid and inhibition of the activity of topoisomerases. These events consequences in halting DNA replication and transcription mechanisms of the cell. Understanding of the structural and conformational changes associated with nucleic acid after binding with drugs provides significant knowledge for the development of more effective drugs. A comprehensive elucidation of the molecular mechanism(s) of action of anthracyclines drugs plays a significant role in the rational drug designing to obtain an effective, selective, and safe anti-cancer drugs.
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McCarty, Richard. "Stress and Depression." In Stress and Mental Disorders: Insights from Animal Models. Oxford University Press, 2020. http://dx.doi.org/10.1093/med-psych/9780190697266.003.0013.

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This chapter on animal models of depression includes a summary of additional approaches to modeling a depression-like phenotype in animals. Several risk genes have been evaluated, including genes involved in dopamine, serotonin, and corticotropin-releasing factor signaling. Using a two-hit model, some investigators have examined the effects of early life stress combined with stress in adulthood to unmask the risk for a depression-like phenotype. Female mice were more sensitive than male mice to a sub-chronic paradigm of chronic variable stress and displayed depression-like behavioral changes. A naturally occurring depression-like phenotype has also been documented in captive social groups of cynomolgous monkeys. Three additional approaches to study mechanisms involved in the onset of depression have included stress and neurogenesis, stress and epigenetic alterations in gene transcription, and stress and immune signaling through proinflammatory cytokines. Taken together, these experiments have identified multiple potential targets for future drug development.
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Przewlocki, Ryszard, Michal Korostynski, and Marcin Piechota. "Transcriptional Effects of Heroin and Methamphetamine in the Striatum." In Neuropathology of Drug Addictions and Substance Misuse. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-800213-1.00087-0.

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Basu, Anamika, Piyali Basak, and Anasua Sarkar. "Molecular-Docking-Based Anti-Allergic Drug Design." In Pharmaceutical Sciences. IGI Global, 2017. http://dx.doi.org/10.4018/978-1-5225-1762-7.ch027.

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Allergens are foreign proteins that when come in contact of part(s) of human body stimulate the production of immunoglobulin types of proteins (antibodies). These allergens react with antibodies (immunoglobulin type E or IgE) produces allergic reactions, also known as immediate-type hypersensitivity reactions. As much as 20% of the general population may be affected by grass pollen as a major cause of allergic disease. EXPB class of proteins are known in the immunological literature as group-1 grass pollen allergens Molecular docking method can be used to identify the predicated the interaction of pollen allergen EXPB1 (Zea m 1), a beta-expansin and group-1 pollen allergen from maize with IgE molecules of human. The World Health Organization recognised allergen immunotherapy, as therapeutics for allergic diseases. RNA Interference (RNAi) is a biological process in which RNA molecules e.g. Small Interfering RNAs (siRNAs) inhibit gene expression, by cleavage and destruction of specific mRNA molecules. Use of Small Interfering RNA (siRNA) is a novel method in the induction of RNA Interference (RNAi), which is a potent method for therapeutics of allergic reactions. Due to various effects of STAT 6 proteins during hypersensitivity reactions caused by pollen allergens, mRNA of STAT6 gene is selected as target gene for allergy therapeutics via Post-Transcriptional Gene Silencing (PTGS). Using molecular docking study a specific sense siRNA is identified as anti allergic drug to treat allergic asthma during immediate type of hypersensitivity reaction, caused by Zea m 1 pollen allergen.
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Basu, Anamika, Piyali Basak, and Anasua Sarkar. "Molecular-Docking-Based Anti-Allergic Drug Design." In Advances in Medical Technologies and Clinical Practice. IGI Global, 2016. http://dx.doi.org/10.4018/978-1-5225-0362-0.ch009.

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Allergens are foreign proteins that when come in contact of part(s) of human body stimulate the production of immunoglobulin types of proteins (antibodies). These allergens react with antibodies (immunoglobulin type E or IgE) produces allergic reactions, also known as immediate-type hypersensitivity reactions. As much as 20% of the general population may be affected by grass pollen as a major cause of allergic disease. EXPB class of proteins are known in the immunological literature as group-1 grass pollen allergens Molecular docking method can be used to identify the predicated the interaction of pollen allergen EXPB1 (Zea m 1), a beta-expansin and group-1 pollen allergen from maize with IgE molecules of human. The World Health Organization recognised allergen immunotherapy, as therapeutics for allergic diseases. RNA Interference (RNAi) is a biological process in which RNA molecules e.g. Small Interfering RNAs (siRNAs) inhibit gene expression, by cleavage and destruction of specific mRNA molecules. Use of Small Interfering RNA (siRNA) is a novel method in the induction of RNA Interference (RNAi), which is a potent method for therapeutics of allergic reactions. Due to various effects of STAT 6 proteins during hypersensitivity reactions caused by pollen allergens, mRNA of STAT6 gene is selected as target gene for allergy therapeutics via Post-Transcriptional Gene Silencing (PTGS). Using molecular docking study a specific sense siRNA is identified as anti allergic drug to treat allergic asthma during immediate type of hypersensitivity reaction, caused by Zea m 1 pollen allergen.
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Halene, Tobias B., Gregor Hasler, Amanda Mitchell, and Schahram Akbarian. "Epigenomic Exploration of the Human Brain." In Psychiatric Genetics. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190221973.003.0010.

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The exploration of the epigenome has become a flourishing area in the neurosciences. Scientists increasingly appreciate that even the position of genetic material within the nucleus is purposeful, and its spatial orientation conveys information with critical influence on transcription, genome integrity, and stability. Together, epigenetic and three-dimensional genome data hold promise to reveal how DNA variants and mutations come into play in brain disease. Powerful new technologies can now map transcriptome, DNA-methylome, and other epigenetic regulators on the level of single brain cells. Many of these findings are limited to preclinical studies. Nevertheless, the advent of chromatin-modifying drugs in cancer therapy and the discovery that approved medications such as valproic acid and lithium have a chromatin-modifying effect have spurred hopes for improved biological therapies. Here we summarize current concepts and emerging insights into epigenetic regulation, with a focus on human brain and the neurobiology and pharmacology of psychiatric disorders.
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Evans Adunyah, Samuel, Richard Akomeah, Fareed K.N. Arthur, Roland S. Cooper, and Joshua C.M. Williams. "IL-17 Biological Effects and Signaling Mechanisms in Human Leukemia U937 Cells." In Interleukins - The Immune and Non-Immune Systems’ Related Cytokines. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96422.

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Human Interlekin-17 is produced by memory activated CD4+ T cells and other cells. It was initially considered unique in that its specific receptor is distinct from other cytokine receptors. IL-17 receptor is ubiquitously expressed by different cells including T cells. IL-17 plays a role in regulating growth, immune response and pro-inflammatory responses. It regulates differentiation of a subset of Th0 cells into Th-17 cells, which produce IL-17-induced cytokines. The IL-17R belongs to type 1 cytokine receptors. IL-17 belongs to a superfamily of its own, which includes IL-17A, IL-17B, IL-17C, IL-17E and IL-17F. These members of IL-17 superfamily have some sequence homology but bind to different receptors. Prior to this investigation, limited information existed on the effects of IL-17A in human leukemia cell lines. Our results show that IL-17A promotes growth, anti-apoptotic effects, chemotaxis, cytokine expression and transcriptional factor activation in leukemia cells. IL-17A activates multiple signaling pathways including PI-3 K, Jak–STAT, Raf-ERK1/2 and SRC kinase pathways, which mediate different biological effects of IL-17A in leukemia cells. Our findings implicate IL-17A in leukemia cell growth and survival, supporting potential leukemia therapy via development of anti-IL-17A drugs. This chapter focuses on IL-17A, herein referred to as IL-17.
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Schlotzig, Vanessa, Kevin Kornrumpf, Alexander König, et al. "Predicting the Effect of Variants of Unknown Significance in Molecular Tumor Boards with the VUS-Predict Pipeline." In Studies in Health Technology and Informatics. IOS Press, 2021. http://dx.doi.org/10.3233/shti210562.

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Precision oncology utilizing molecular biomarkers for targeted therapies is one of the hopes to treat cancer. The availability of patient specific molecular profiling through next-generation sequencing, though, increases the amount of available data per patient to an extent that computational support is required to identify potential driver alterations for targeted therapies and rational decision-making in molecular tumor boards (MTBs). For some genetic variants evidence-based drug recommendations are available in public databases, but for the majority, the variants of unknown significance (VUS), this clinical information is missing. Additionally, for most of these variants no information about the functional impact on the protein is accessible. To acquire maximal functional evidence for VUS, the VUS-Predict pipeline collects estimations about the effect of a VUS by integrating multiple pre-existing tools. Pre-existing tools implement different approaches for their predictions, which are summarized by our newly developed tool with a common score and classification in neutral or deleterious variants. The primary tools are chosen based on their sensitivity and specificity on well-known variants of the transcription factor TP53. Resulting negative and positive predictive values are used to calibrate the VUS-Predict pipeline. Further, the pipeline is evaluated using data from public cancer databases and cases of the MTB in Göttingen, both also in comparison with the ensemble method REVEL. The results show that VUS-Predict has clear advantages in a clinical setting due to clear and traceable predictions. In particular, VUS outperforms REVEL in the real-life setting of a MTB. Likewise, an evaluation on variants of public cancer databases confirms the good results of VUS-Predict and shows the need for a reliable gold standard and unambiguous results of the tools under test.
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Buchanan, Ruaridh, and Armine Sefton. "Mechanism of Action of Antimicrobial Agents." In Tutorial Topics in Infection for the Combined Infection Training Programme. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198801740.003.0053.

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Antibacterial and antifungal agents aim to kill pathogens, or at the very least incapacitate them. To achieve this aim these agents must have a reasonable degree of toxicity at the cellular level. If this toxicity was equally manifest against all cell types then the drugs would be unusable in patients as the side effect profile would be unacceptably severe. Selective toxicity, whereby the agents are orders of magnitude more toxic to bacteria or fungi than human cells, allows for the safe and effective administration of these agents to patients. There are a number of different mechanisms by which an antimicrobial agent can yield selective toxicity: ● Target a cellular structure that exists only in bacteria/fungi—e.g. the cell wall; ● Target a cellular structure that has a significantly different structure in bacteria/ fungi— e.g. the ribosome; the fungal cell membrane; ● Target cellular enzymes that are significantly different in bacteria/fungi e.g. topoisomerase; ● Target a synthetic pathway that exists only in bacteria e.g. folate synthesis. Broadly, antibacterial drugs can be divided into the following categories: ● Agents that target the cell wall; ● Agents that target the cell membrane; ● Agents that inhibit protein synthesis; ● Agents that inhibit DNA replication/ transcription of RNA; ● Agents that target folate synthesis; ● Agents that directly damage intracellular structures. The cell wall is unique to bacteria, and therefore an ideal target. Disrupting the complex cross-linking process required to produce the cell wall leads to loss of bacterial cell integrity and therefore to cell death. The following classes of antibiotics target the cell wall: The first class to be discovered, and still in many cases the most effective, incorporates the four-membered beta-lactam ring—its homology to d-alanyl-d-alanine allows beta-lactam-containing compounds to bind to cell wall peptidoglycans and act as chain terminators. The beta-lactam ring is fused to a five-membered sulphur-containing ring. Variations in side chains account for the differing pharmacokinetics and spectra of action of the different compounds—for example, the addition of an amino group to benzylpenicillin produces ampicillin.
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10

Shaw, James A. M., and Kevin Docherty. "Gene therapy in diabetes mellitus." In Oxford Textbook of Endocrinology and Diabetes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.1603.

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The distinctions between what has previously been termed cell therapy and gene therapy have become blurred. Cell therapy traditionally implied the in vitro expansion of cells that could subsequently be engrafted into patients to elicit a therapeutic effect, while gene therapy was a term applied to the genetic manipulation of tissues or cells in vivo or ex vivo. With the amazing advances that have been achieved using transcription factors to reprogramme cells, this distinction, at least for regenerative medicine applications, no longer exists. In this chapter, following the statement of the unmet clinical need, we review potential sources of new β‎ cells and approaches to β‎ cell replacement therapy; discuss how recent advances in safety and efficacy of gene transfer technology can augment cellular therapeutic approaches, and summarize pure gene therapy approaches dependent on expression of genes encoding insulin and other glucose-lowering hormones in the recipient’s own cells. Since both type 1 and type 2 diabetes are associated with a decline in β‎ cell mass, cell and gene therapy targeted at the β‎ cell and insulin replacement have potential applications for both forms of the disease. In type 1 diabetes, uninterrupted compliance with insulin injection therapy is necessary to prevent potentially fatal ketoacidosis. The landmark Diabetes Control and Complications Trial and Epidemiology of Diabetes Interventions and Complications follow-up study have confirmed that chronic hyperglycaemic microvascular and macrovascular complications can be prevented by tight glycaemic control, but this was at the expense of a threefold increase in severe hypoglycaemia—one of the greatest fears of those living with daily insulin injections. Overall, the health implications and economic costs of type 1 diabetes are massive, and increasing annually. There is, therefore, an unquestionable clinical need for new therapeutic options. While transplantation of whole pancreas together with its blood supply can entirely normalize blood glucose levels, the major surgery required is associated with 5% mortality in the first year, even in the most experienced centres. Isolation and transplantation of purified insulin-secreting islets of Langerhans from a donor pancreas requires only minimally invasive cannulation of the portal vein transhepatically under X-ray guidance. This offers the promise of more widespread implementation restoring excellent control, preventing both long-term complications and severe hypoglycaemia. Capacity will, however, be severely limited by the scarcity of deceased donor organs: currently sufficient for fewer than 1% of those who might benefit from this form of treatment. This has provided impetus to efforts to produce a replenishable supply of glucose-responsive insulin-secreting cells that could be used in transplantation. One potential source might involve the in vitro differentiation of stem cells derived from embryonic and adult tissue. Type 2 diabetes is marked by both a resistance of target tissue to the effects of insulin and impaired function of the β‎ cell. The major β‎-cell defects relate to an impaired secretory response to glucose, altered kinetics of secretion including pulsatility, accumulation of islet amyloid polypeptide, an increase in glucagon-secreting α‎ cells, and a decline in β‎-cell mass. Current therapy for type 2 diabetes involves a combination of drugs directed at improvements in both insulin sensitivity and β‎-cell function, together with management of associated cardiovascular risk factors. Conventional treatment modalities have not been able to prevent the inexorable progressive loss of β‎-cell function necessitating insulin replacement in the majority over time, but this is often insufficient to sustainably achieve target glucose levels outwith intensive clinical trials. It is envisaged that novel cell therapy approaches will enable restoration of β‎-cell mass.
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Conference papers on the topic "Transcription; Drug effects"

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Shen, Yao, Mariano Alvarez, Sergey Pampou, Jorida Coku, and Andrea Califano. "Abstract A35: Predicting drugs effect on transcription factor activity by regulatory network analysis of drug perturbed cellular states." In Proceedings: AACR Special Conference on Chemical Systems Biology: Assembling and Interrogating Computational Models of the Cancer Cell by Chemical Perturbations--Jun 27-30, 2012; Boston, MA. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.csb12-a36.

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Uddin, Sardar M. Zia, and Yi-Xian Qin. "Anabolic Effects of Ultrasound as Countermeasures of Simulated Microgravity in In-Vitro and In-Vivo Functional Disuse Models." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53796.

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Microgravity (MG) during space flight has been known to cause adverse effect on bone quality. Data collected from studies done on spaceflights show loss of 1–1.6% bone mineral density (BMD) per space-flight-month[1]. Most BMD has been recorded in load-bearing bones [2]. Some studies has considered using drugs and different growth factors to maintain bone mass in microgravity conditions but it can be too expensive to maintain over longer periods of time besides the systematic effects of such treatments [3]. Considering the effects of microgravity are partially attributed to lack of mechanical f
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Chen, Kok Hao, and Jong Hyun Choi. "Nanoparticle-Aptamer: An Effective Growth Inhibitor for Human Cancer Cells." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-11966.

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Semiconductor nanocrystals have unique optical properties due to quantum confinement effects, and a variety of promising approaches have been devised to interface the nanomaterials with biomolecules for bioimaging and therapeutic applications. Such bio-interface can be facilitated via a DNA template for nanoparticles as oligonucleotides can mediate the aqueous-phase nucleation and capping of semiconductor nanocrystals.[1,2] Here, we report a novel scheme of synthesizing fluorescent nanocrystal quantum dots (NQDs) using DNA aptamers and the use of this biotic/abiotic nanoparticle system for gro
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Reports on the topic "Transcription; Drug effects"

1

Leslie, Stephanie J. Evaluation of DNA Binding Drugs as Inhibitors of ESX, an ETS Domain Transcription Factor Associated with Breast Cancer: Effects of ESX/DNA Complex Disruption. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada401300.

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