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Journal articles on the topic 'Transcription; Drug effects'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

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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3

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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Liu, Fang, Wenyan Jiang, Yi Sui, et al. "CDK7 inhibition suppresses aberrant hedgehog pathway and overcomes resistance to smoothened antagonists." Proceedings of the National Academy of Sciences 116, no. 26 (2019): 12986–95. http://dx.doi.org/10.1073/pnas.1815780116.

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The aberrant hedgehog (Hh) pathway plays important roles in multiple cancer types, therefore serving as a promising drug target. Current clinically available hedgehog-targeted drugs act mostly by antagonizing the upstream component smoothened; however, both primary and acquired resistance to FDA-approved smoothened inhibitor (SMOi) drugs have been described. We have recently demonstrated that the BET inhibitor effectively suppresses SMOi-resistant Hh-driven cancers through antagonizing transcription of GLI1 and GLI2, the core transcriptional factors of Hh pathway, suggesting epigenetic or tran

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Rokudai, Susumu, Naoya Fujita, Osamu Kitahara, Yusuke Nakamura, and Takashi Tsuruo. "Involvement of FKHR-Dependent TRADD Expression in Chemotherapeutic Drug-Induced Apoptosis." Molecular and Cellular Biology 22, no. 24 (2002): 8695–708. http://dx.doi.org/10.1128/mcb.22.24.8695-8708.2002.

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ABSTRACT Chemotherapeutic drugs exhibit their cytotoxic effect by inducing apoptosis in tumor cells. Because the serine/threonine kinase Akt is involved in apoptosis suppression, we investigated the relationship between Akt activity and drug sensitivity. We discovered that certain chemotherapeutic drugs induced apoptosis with caspase activation only when Akt was inactivated after drug treatment, while inactivation of Akt was not observed when tumor cells showed resistance to the drug-induced caspase activation. So, turn-off of the Akt-mediated survival signal is correlated with the sensitivity

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Chen, Duchu, Huiping Wang, Jude Juventus Aweya та ін. "HMBA Enhances Prostratin-Induced Activation of Latent HIV-1 via Suppressing the Expression of Negative Feedback Regulator A20/TNFAIP3 in NF-κB Signaling". BioMed Research International 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/5173205.

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In the past decade, much emphasis has been put on the transcriptional activation of HIV-1, which is proposed as a promised strategy for eradicating latent HIV-1 provirus. Two drugs, prostratin and hexamethylene bisacetamide (HMBA), have shown potent effects as inducers for releasing HIV-1 latency when used alone or in combination, although their cellular target(s) are currently not well understood, especially under drug combination. Here, we have shown that HMBA and prostratin synergistically release HIV-1 latency via different mechanisms. While prostratin strongly stimulates HMBA-induced HIV-

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Yao, Liangliang, Muhammad Farrukh Nisar, Tingdong Yan, and Chunpeng (Craig) Wan. "Potential Effects of Dietary Isoflavones on Drug-Induced Liver Injury." Journal of Food Quality 2021 (August 30, 2021): 1–10. http://dx.doi.org/10.1155/2021/2870969.

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Numerous prescribed drugs and herbal and dietary supplements have been reported to cause drug-induced acute liver injury, which is a frequent cause of acute liver failure (ALF). It is a tremendous challenge with ever-increasing drug application in the medication system for huge populations. Drug-induced acute liver injury can lead to diverse pathologies similar to acute and chronic hepatitis, acute liver failure, biliary obstruction, fatty liver disease, and so on. Recently, extensive work demonstrated that isoflavones play an essential and protecting role in drug-induced liver injury (DILI).

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Özenver, Nadire, Joelle C. Boulos, and Thomas Efferth. "Activity of Cordycepin From Cordyceps sinensis Against Drug-Resistant Tumor Cells as Determined by Gene Expression and Drug Sensitivity Profiling." Natural Product Communications 16, no. 2 (2021): 1934578X2199335. http://dx.doi.org/10.1177/1934578x21993350.

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Cordycepin is one of the substantial components of the parasitic fungus Cordyceps sinensis as well as other Cordyceps species. It exerts various effects such as antimetastatic, antiinflammatory, antioxidant, and neuroprotective activities. Assorted studies revealed in vitro and in vivo anticancer influence of cordycepin and put forward its potential for cancer therapy. However, the role of multidrug resistance-associated mechanisms for the antitumor effect of cordycepin has not been investigated in great detail thus far. Therefore, we searched cordycepin’s cytotoxicity with regard to well-know

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Nestler, Eric J. "Transcriptional mechanisms of addiction: role of ΔFosB". Philosophical Transactions of the Royal Society B: Biological Sciences 363, № 1507 (2008): 3245–55. http://dx.doi.org/10.1098/rstb.2008.0067.

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Regulation of gene expression is considered a plausible mechanism of drug addiction, given the stability of behavioural abnormalities that define an addicted state. Among many transcription factors known to influence the addiction process, one of the best characterized is ΔFosB, which is induced in the brain's reward regions by chronic exposure to virtually all drugs of abuse and mediates sensitized responses to drug exposure. Since ΔFosB is a highly stable protein, it represents a mechanism by which drugs produce lasting changes in gene expression long after the cessation of drug use. Studies

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Nelson, Erik A., Sarah R. Walker, Alicia Kepich, Shariya Terrell, Laurie Gashin, and David A. Frank. "Pimozide Inhibits STAT5 Signaling in Chronic Myelogenous Leukemia and Reduces the Viability of Both Imatinib Sensitive and Imatinib Resistant Cells." Blood 110, no. 11 (2007): 2953. http://dx.doi.org/10.1182/blood.v110.11.2953.2953.

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Abstract Chronic myelogenous leukemia (CML) is characterized by the BCR/ABL fusion tyrosine kinase which mediates its oncogenic effects in part through constitutive activation of the transcription factor STAT5. BCR/ABL can be inhibited by several kinase inhibitors, including imatinib, which leads to apoptosis of the cells. However, the development of resistance to these agents, most commonly mediated through point mutations in the kinase, is an increasing problem. Since STAT5 is a critical mediator of the effects of BCR/ABL, the development of drugs inhibiting this transcription factor holds p

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Konietzko, Uwe, Manuel T. Gersbacher, Jeremy Streuli, et al. "A fluorescent protein-readout for transcriptional activity reveals regulation of APP nuclear signaling by phosphorylation sites." Biological Chemistry 400, no. 9 (2019): 1191–203. http://dx.doi.org/10.1515/hsz-2019-0125.

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Abstract Signaling pathways that originate at the plasma membrane, including regulated intramembrane proteolysis (RIP), enable extracellular cues to control transcription. We modified the yeast Gal4 transcription system to study the nuclear translocation of transcriptionally active complexes using the fluorescent protein citrine (Cit) as a reporter. This enabled highly sensitive quantitative analysis of transcription in situ at the single cell level. The Gal4/UAS-Cit transcription assay displayed a sigmoidal response limited by the number of integrated reporter cassettes. We validated the assa

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Núñez-Acuña, Gustavo, Constanza Sáez-Vera, Valentina Valenzuela-Muñoz, Diego Valenzuela-Miranda, Gabriel Arriagada, and Cristian Gallardo-Escárate. "Tackling the Molecular Drug Sensitivity in the Sea Louse Caligus rogercresseyi Based on mRNA and lncRNA Interactions." Genes 11, no. 8 (2020): 857. http://dx.doi.org/10.3390/genes11080857.

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Caligus rogercresseyi, commonly known as sea louse, is an ectoparasite copepod that impacts the salmon aquaculture in Chile, causing losses of hundreds of million dollars per year. This pathogen is mainly controlled by immersion baths with delousing drugs, which can lead to resistant traits selection in lice populations. Bioassays are commonly used to assess louse drug sensitivity, but the current procedures may mask relevant molecular responses. This study aimed to discover novel coding genes and non-coding RNAs that could evidence drug sensitivity at the genomic level. Sea lice samples from

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Buist, Marjorie, David Fuss, and Mojgan Rastegar. "Transcriptional Regulation of MECP2E1-E2 Isoforms and BDNF by Metformin and Simvastatin through Analyzing Nascent RNA Synthesis in a Human Brain Cell Line." Biomolecules 11, no. 8 (2021): 1253. http://dx.doi.org/10.3390/biom11081253.

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Methyl CpG binding protein 2 (MeCP2) is the main DNA methyl-binding protein in the brain that binds to 5-methylcytosine and 5-hydroxymethyl cytosine. MECP2 gene mutations are the main origin of Rett Syndrome (RTT), a neurodevelopmental disorder in young females. The disease has no existing cure, however, metabolic drugs such as metformin and statins have recently emerged as potential therapeutic candidates. In addition, induced MECP2-BDNF homeostasis regulation has been suggested as a therapy avenue. Here, we analyzed nascent RNA synthesis versus steady state total cellular RNA to study the tr

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Zhao, Yanan, Padmaja Paderu, Steven Park, Aleksandra Dukhan, Meredith Senter, and David S. Perlin. "Expression Turnover Profiling To Monitor the Antifungal Activities of Amphotericin B, Voriconazole, and Micafungin against Aspergillus fumigatus." Antimicrobial Agents and Chemotherapy 56, no. 5 (2012): 2770–72. http://dx.doi.org/10.1128/aac.06163-11.

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ABSTRACTEight highly expressed candidate genes were selected for mRNA profiling to monitor the transcriptome kinetics ofAspergillus fumigatusstrains exposed to antifungal drugs as potential biomarkers of live cells to assess treatment efficacy. Mycelia were treated with fungicidal drugs amphotericin B and voriconazole, as well as the fungistatic drug micafungin. Transcription was monitored at 0, 4, 8, and 24 h posttreatment. The expression turnover profile provides a possible tool to assess antifungal therapy effects.

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Kamboj, Deepmala, and M. D. Sharma. "Effects of combined drug therapy on HIV-1 infection dynamics." International Journal of Biomathematics 09, no. 05 (2016): 1650065. http://dx.doi.org/10.1142/s1793524516500650.

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Infection of human immunodeficiency virus (HIV) is determined through the decay of healthy CD4+ T-cells in a well-mixed compartment, such as a bloodstream. A mathematical model is considered to illustrate the effects of combined drug therapy, i.e. reverse transcription plus protease inhibitor, on viral growth and T-cell population dynamics. This model is used to explain the existence and stability of infected and uninfected steady states in HIV growth. An analytical technique, called variational iteration method (VIM), is used to solve the mathematical model. This method is modified to obtain

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Lohani, Neelam, and Moganty R. Rajeswari. "Antigene and Antiproliferative Effects of Triplex-Forming Oligonucleotide (TFO) Targeted on hmgb1 Gene in Human Hepatoma Cells." Anti-Cancer Agents in Medicinal Chemistry 20, no. 16 (2020): 1943–55. http://dx.doi.org/10.2174/1871520620666200619170438.

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Background: The high mobility group box 1 (hmgb1) is one of the frequently over-expressed genes whose aberrant expression is reported in a number of human cancers. Various strategies are underway to inhibit hmgb1 expression in cancer cells having considerable therapeutic value. Objective: The present work involves selective transcriptional inhibition of the hmgb1 gene using selective DNA triplex structure-based gene technology. Here, the promoter region of the hmgb1 gene at position (-183 to -165) from the transcription start site as a target was selected using bioinformatic tools. Methods: Th

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Powell, Emily, Peter Kuhn та Wei Xu. "Nuclear Receptor Cofactors in PPARγ-Mediated Adipogenesis and Adipocyte Energy Metabolism". PPAR Research 2007 (2007): 1–11. http://dx.doi.org/10.1155/2007/53843.

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Transcriptional cofactors are integral to the proper function and regulation of nuclear receptors. Members of the peroxisome proliferator-activated receptor (PPAR) family of nuclear receptors are involved in the regulation of lipid and carbohydrate metabolism. They modulate gene transcription in response to a wide variety of ligands, a process that is mediated by transcriptional coactivators and corepressors. The mechanisms by which these cofactors mediate transcriptional regulation of nuclear receptor function are still being elucidated. The rapidly increasing array of cofactors has brought i

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Ferrarelli, Leslie K. "Repurposing an HIV drug for melanoma." Science Signaling 9, no. 423 (2016): ec85-ec85. http://dx.doi.org/10.1126/scisignal.aaf8440.

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Inhibitors of the kinases BRAF or MEK (BRAF/MEK) can reduce tumor growth in some patients with melanoma, but resistance often develops. Microphthalmia-associated transcription factor (MITF) is implicated in promoting melanoma development. Smith et al. found that long-term treatment of cell cultures and mice bearing xenografts with BRAF/MEK inhibitors increased the abundance of MITF and its transcription factor PAX3 and that silencing MITF sensitized drug-resistant melanoma cells to the inhibitors. In a screen for small molecules that could reduce the abundance of MITF or PAX3, the most effecti

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Kempf, Mirjam-Colette, Jennifer Jones, Marintha L. Heil, and Olaf Kutsch. "A High-Throughput Drug Screening System for HIV-1 Transcription Inhibitors." Journal of Biomolecular Screening 11, no. 7 (2006): 807–15. http://dx.doi.org/10.1177/1087057106290292.

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Identification of HIV-1 transcription inhibitors was previously performed using infectivity assays. As de novo HIV-1 infection is highly sensitive to even minor compound toxicities, these assays are plagued by extremely high levels of false-positive hits. Hit identification is further complicated because infectivity assays lack target specificity. The authors demonstrate that it is possible to overcome these limitations by establishing a stable, chronically actively HIV-1-infected reporter cell line that exclusively identifies HIV-1 transcription inhibitors. In the reporter cell line, 2 spectr

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Praditsuktavorn, Pannee, Benet Pera, Nicholas Kwiatkowski, et al. "Transcription Regulation Targeting in Peripheral T Cell Lymphomas Induces Apoptosis and Sensitization to BCL2 Inhibitors." Blood 124, no. 21 (2014): 810. http://dx.doi.org/10.1182/blood.v124.21.810.810.

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Abstract Peripheral T-cell lymphomas (PTCL) are clinically aggressive diseases with poor response to available (largely B-cell lymphoma–tailored) chemotherapy regimens and dismal survival. To identify active drugs for PTCL patients, we performed a cell-based progressive screen from a library of 105 anti-neoplastic drugs in clinical use. Primary screening was done in the PTCL-NOS cell line (OCI-Ly12), using three drug concentrations. We identified 3 active drug groups within the clinical-range limit: HDAC inhibitors (HDI) (romidepsin), proteasome inhibitors (bortezomib, carfilzomib) and transcr

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Arora, Pranay, Reetobrata Basu, and John Joseph Kopchick. "Effects of Growth Hormone in Human Melanoma Drug Resistance." Journal of the Endocrine Society 5, Supplement_1 (2021): A1016. http://dx.doi.org/10.1210/jendso/bvab048.2078.

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Abstract Melanoma, an extremely drug resistant form of cancer, displays elevated levels of growth hormone (GH) and growth hormone receptor (GHR) expression. We have described a GH dependent mechanism of chemoresistance in melanoma through a series of earlier studies. In GHR overexpressing human melanoma, GH action drives active drug efflux and phenotype switching by upregulating ATP-binding cassette transporters (ABC-transporters) and epithelial-to-mesenchymal transition (EMT) markers. Inhibition of GHR activation reverses these effects, increases drug retention, and sensitizes the melanoma ce

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Hallstrom, Timothy C., David J. Katzmann, Rodrigo J. Torres, W. John Sharp, and W. Scott Moye-Rowley. "Regulation of Transcription Factor Pdr1p Function by an Hsp70 Protein in Saccharomyces cerevisiae." Molecular and Cellular Biology 18, no. 3 (1998): 1147–55. http://dx.doi.org/10.1128/mcb.18.3.1147.

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ABSTRACT Multiple or pleiotropic drug resistance in the yeastSaccharomyces cerevisiae requires the expression of several ATP binding cassette transporter-encoding genes under the control of the zinc finger-containing transcription factor Pdr1p. The ATP binding cassette transporter-encoding genes regulated by Pdr1p include PDR5 and YOR1, which are required for normal cycloheximide and oligomycin tolerances, respectively. We have isolated a new member of the PDR gene family that encodes a member of the Hsp70 family of proteins found in this organism. This gene has been designated PDR13 and is re

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Tabe, Yoko, Marina Konopleva, Michael Andreeff та Akimichi Ohsaka. "Effects of PPARγLigands on Leukemia". PPAR Research 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/483656.

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Peroxisome proliferator-activated receptors (PPARs) and retinoic acid receptors (RARs), members of the nuclear receptor superfamily, are transcription factors that regulate a variety of important cellular functions. PPARs form heterodimers retinoid X receptor (RXR), an obligate heterodimeric partner for other nuclear receptors. Several novel links between retinoid metabolism and PPAR responses have been identified, and activation of PPAR/RXR expression has been shown to increase response to retinoids. PPARγhas emerged as a key regulator of cell growth and survival, whose activity is modulated

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Czyz, M., and M. Gniazdowski. "Actinomycin D specifically inhibits the interaction between transcription factor Sp1 and its binding site." Acta Biochimica Polonica 45, no. 1 (1998): 67–73. http://dx.doi.org/10.18388/abp.1998_4319.

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The mode of action of many anticancer drugs involves DNA interactions. We here examine the ability of actinomycin D to alter the specific binding of transcription factors Spl and NFkappaB to their DNA sequences. Employing an electrophoretic mobility shift assay, it is shown that actinomycin D inhibits complex formation between nuclear proteins present in the extracts from stimulated human umbilical vein endothelial cells and the Sp1-binding site. Actinomycin D is also able to induce disruption of preformed DNA-protein complexes, pointing to the importance of an equilibrium of three components:

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Wilson, Hannah E., David A. Stanton, Stephanie Rellick, Werner Geldenhuys, and Emidio E. Pistilli. "Breast cancer-associated skeletal muscle mitochondrial dysfunction and lipid accumulation is reversed by PPARG." American Journal of Physiology-Cell Physiology 320, no. 4 (2021): C577—C590. http://dx.doi.org/10.1152/ajpcell.00264.2020.

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The peroxisome proliferator-activated receptors (PPARs) have been previously implicated in the pathophysiology of skeletal muscle dysfunction in women with breast cancer (BC) and animal models of BC. This study investigated alterations induced in skeletal muscle by BC-derived factors in an in vitro conditioned media (CM) system and tested the hypothesis that BC cells secrete a factor that represses PPAR-γ (PPARG) expression and its transcriptional activity, leading to downregulation of PPARG target genes involved in mitochondrial function and other metabolic pathways. We found that BC-derived

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Braadland, Peder Rustøen, and Alfonso Urbanucci. "Chromatin reprogramming as an adaptation mechanism in advanced prostate cancer." Endocrine-Related Cancer 26, no. 4 (2019): R211—R235. http://dx.doi.org/10.1530/erc-18-0579.

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Tumor evolution is based on the ability to constantly mutate and activate different pathways under the selective pressure of targeted therapies. Epigenetic alterations including those of the chromatin structure are associated with tumor initiation, progression and drug resistance. Many cancers, including prostate cancer, present enlarged nuclei, and chromatin appears altered and irregular. These phenotypic changes are likely to result from epigenetic dysregulation. High-throughput sequencing applied to bulk samples and now to single cells has made it possible to study these processes in unprec

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Tee, Meng Kian, Ningwu Huang, Izabella Damm, and Walter L. Miller. "Transcriptional Regulation of the Human P450 Oxidoreductase Gene: Hormonal Regulation and Influence of Promoter Polymorphisms." Molecular Endocrinology 25, no. 5 (2011): 715–31. http://dx.doi.org/10.1210/me.2010-0236.

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Abstract P450 oxidoreductase (POR) is the flavoprotein that acts as the obligatory electron donor to all microsomal P450 enzymes, including those involved in hepatic drug metabolism as well as three steroidogenic P450 enzymes. The untranslated first exon of human POR was located recently, permitting analysis of human POR transcription. Expression of deletional mutants containing up to 3193 bp of the human POR promoter in human adrenal NCI-H295A and liver Hep-G2 cells located the proximal promoter at −325/−1 bp from the untranslated exon. Common human POR polymorphisms at −208 and −173 had litt

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Lloyd, Katie, Stamatia Papoutsopoulou, Emily Smith, et al. "Using systems medicine to identify a therapeutic agent with potential for repurposing in inflammatory bowel disease." Disease Models & Mechanisms 13, no. 11 (2020): dmm044040. http://dx.doi.org/10.1242/dmm.044040.

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ABSTRACTInflammatory bowel diseases (IBDs) cause significant morbidity and mortality. Aberrant NF-κB signalling is strongly associated with these conditions, and several established drugs influence the NF-κB signalling network to exert their effect. This study aimed to identify drugs that alter NF-κB signalling and could be repositioned for use in IBD. The SysmedIBD Consortium established a novel drug-repurposing pipeline based on a combination of in silico drug discovery and biological assays targeted at demonstrating an impact on NF-κB signalling, and a murine model of IBD. The drug discover

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Gabbard, Ryan D., Robert R. Hoopes, and Michael G. Kemp. "Spironolactone and XPB: An Old Drug with a New Molecular Target." Biomolecules 10, no. 5 (2020): 756. http://dx.doi.org/10.3390/biom10050756.

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Spironolactone (SP) is commonly used for the treatment of heart failure, hypertension, and complications of cirrhosis by antagonizing the mineralocorticoid receptor. However, SP also antagonizes the androgen receptor, and thus SP has also been shown to be effective in the treatment of acne, hair loss, and hirsutism in women. Interestingly, recent drug repurposing screens have identified new and diverse functions for SP as a simulator of tumor immunosurveillance and as an inhibitor of DNA repair and viral infection. These novel pharmacological effects of SP have all been linked to the ability o

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Harris, Emily, Jonathan Strope, Shaunna Beedie, et al. "Preclinical Evaluation of Discorhabdins in Antiangiogenic and Antitumor Models." Marine Drugs 16, no. 7 (2018): 241. http://dx.doi.org/10.3390/md16070241.

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Elements of the hypoxia inducible factor (HIF) transcriptional system, a key regulator of the cellular hypoxic response, are up-regulated in a range of cancer cells. HIF is fundamentally involved in tumor angiogenesis, invasion, and energy metabolism. Inhibition of the transcriptional activity of HIF may be of therapeutic benefit to cancer patients. We recently described the identification of two marine pyrroloiminoquinone alkaloids with potent activity in inhibiting the interaction between the oncogenic transcription factor HIF-1α and the coactivator protein p300. Herein, we present further c

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Yu, Lu, Wenliang Zhang, Lingling Wang, et al. "Transcriptional Profiles of the Response to Ketoconazole and Amphotericin B in Trichophyton rubrum." Antimicrobial Agents and Chemotherapy 51, no. 1 (2006): 144–53. http://dx.doi.org/10.1128/aac.00755-06.

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ABSTRACT Trichophyton rubrum is a pathogenic filamentous fungus of increasing medical concern. Two antifungal agents, ketoconazole (KTC) and amphotericin B (AMB), have specific activity against dermatophytes. To identify the mechanisms of action of KTC and AMB against T. rubrum, a cDNA microarray was constructed from the expressed sequence tags of the cDNA library from different developmental stages, and transcriptional profiles of the responses to KTC and AMB were determined. T. rubrum was exposed to subinhibitory concentrations of KTC and AMB for 12 h, and microarray analysis was used to exa

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Srivastava, Rakesh K., Carl Y. Sasaki, J. Marie Hardwick, and Dan L. Longo. "Bcl-2–Mediated Drug Resistance." Journal of Experimental Medicine 190, no. 2 (1999): 253–66. http://dx.doi.org/10.1084/jem.190.2.253.

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Bcl-2 inhibits apoptosis induced by a variety of stimuli, including chemotherapy drugs and glucocorticoids. It is generally accepted that Bcl-2 exerts its antiapoptotic effects mainly by dimerizing with proapoptotic members of the Bcl-2 family such as Bax and Bad. However, the mechanism of the antiapoptotic effects is unclear. Paclitaxel and other drugs that disturb microtubule dynamics kill cells in a Fas/Fas ligand (FasL)-dependent manner; antibody to FasL inhibits paclitaxel-induced apoptosis. We have found that Bcl-2 overexpression leads to the prevention of chemotherapy (paclitaxel)-induc

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Lohberger, Andrea, Alix T. Coste, and Dominique Sanglard. "Distinct Roles of Candida albicans Drug Resistance Transcription FactorsTAC1,MRR1, andUPC2in Virulence." Eukaryotic Cell 13, no. 1 (2013): 127–42. http://dx.doi.org/10.1128/ec.00245-13.

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ABSTRACTAzoles are widely used in antifungal therapy in medicine. Resistance to azoles can occur inCandida albicansprincipally by overexpression of multidrug transporter geneCDR1,CDR2, orMDR1or by overexpression ofERG11, which encodes the azole target. The expression of these genes is controlled by the transcription factors (TFs)TAC1(involved in the control ofCDR1andCDR2),MRR1(involved in the control ofMDR1), andUPC2(involved in the control ofERG11). Several gain-of-function (GOF) mutations are present in hyperactive alleles of these TFs, resulting in the overexpression of target genes. While

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Keller, Maria, Claudia Gebhardt, Sandra Huth, et al. "Genetically programmed changes in transcription of the novel progranulin regulator." Journal of Molecular Medicine 98, no. 8 (2020): 1139–48. http://dx.doi.org/10.1007/s00109-020-01942-7.

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Abstract Progranulin is a glycoprotein marking chronic inflammation in obesity and type 2 diabetes. Previous studies suggested PSRC1 (proline and serine rich coiled-coil 1) to be a target of genetic variants associated with serum progranulin levels. We aimed to identify potentially functional variants and characterize their role in regulation of PSRC1. Phylogenetic module complexity analysis (PMCA) prioritized four polymorphisms (rs12740374, rs629301, rs660240, rs7528419) altering transcription factor binding sites with an overall score for potential regulatory function of Sall > 7.0. The e

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Pan, Ruihuan, Mingchao Zhou, Yiping Zhong, et al. "The combination of Astragalus membranaceus extract and ligustrazine to improve the inflammation in rats with thrombolytic cerebral ischemia." International Journal of Immunopathology and Pharmacology 33 (January 2019): 205873841986905. http://dx.doi.org/10.1177/2058738419869055.

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The purpose of the study was to evaluate the effect of Astragalus membranaceus extract and ligustrazine combination on ameliorating inflammation in cerebral ischemic rats that have undergone thrombolysis. Astragalus membranaceus and ligustrazine per se, or a combination of A. membranaceus and ligustrazine was administered by intraperitoneal injection immediately after surgery and sham surgery. After the induction of thrombolysis, the neurological function was measured and cerebral lesion volume was determined. The regulatory T cells in the spleen were measured by flow cytometry. To explore the

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Chateauvieux, Sébastien, Franck Morceau, Mario Dicato, and Marc Diederich. "Molecular and Therapeutic Potential and Toxicity of Valproic Acid." Journal of Biomedicine and Biotechnology 2010 (2010): 1–18. http://dx.doi.org/10.1155/2010/479364.

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Valproic acid (VPA), a branched short-chain fatty acid, is widely used as an antiepileptic drug and a mood stabilizer. Antiepileptic properties have been attributed to inhibition of Gamma Amino Butyrate (GABA) transaminobutyrate and of ion channels. VPA was recently classified among the Histone Deacetylase Inhibitors, acting directly at the level of gene transcription by inhibiting histone deacetylation and making transcription sites more accessible. VPA is a widely used drug, particularly for children suffering from epilepsy. Due to the increasing number of clinical trials involving VPA, and

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Wang, Jun, Haishi Zheng, and Rui Ma. "Natural Occurring Compounds Inhibit Osteoclastogenesis via Targeting NFATc1-related Signaling Pathways." Current Drug Targets 21, no. 4 (2020): 358–64. http://dx.doi.org/10.2174/1389450120666191017121610.

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Osteoclasts are originated from monocytic precursors of the hematopoietic lineage. Regulation of gene expression by transcription factors is one of the major mechanisms for controlling cellular functions. This is particularly important in the process of osteoclast production. As a main regulatory transcriptional factor, nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) plays a significant role in osteoclast differentiation. Although current studies focus on the regulatory effects of treatment in the process of osteoclastogenesis, many of these drugs possess cytotoxicity which is harmf

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Carlberg, Carsten. "Vitamin D: A Micronutrient Regulating Genes." Current Pharmaceutical Design 25, no. 15 (2019): 1740–46. http://dx.doi.org/10.2174/1381612825666190705193227.

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Background:At sufficient sun exposure, humans can synthesize vitamin D3 endogenously in their skin, but today’s lifestyle makes the secosteroid a true vitamin that needs to be taken up by diet or supplementation with pills. The vitamin D3 metabolite 1α,25-dihydroxyvitamin D3 acts as a nuclear hormone activating the transcription factor vitamin D receptor (VDR).Methods:This review discusses the biological effects of micronutrient vitamin D ranging from calcium homeostasis and bone formation to the modulation of innate and adaptive immunity.Results:Since normal human diet is sufficient in vitami

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Rando, Gianpaolo, David Horner, Andrea Biserni, et al. "An Innovative Method to Classify SERMs Based on the Dynamics of Estrogen Receptor Transcriptional Activity in Living Animals." Molecular Endocrinology 24, no. 4 (2010): 735–44. http://dx.doi.org/10.1210/me.2009-0514.

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Abstract Using a mouse model engineered to measure estrogen receptor (ER) transcriptional activity in living organisms, we investigated the effect of long-term (21 d) hormone replacement on ER signaling by whole-body in vivo imaging. Estrogens and selective ER modulators were administered daily at doses equivalent to those used in humans as calculated by the allometric approach. As controls, ER activity was measured also in cycling and ovariectomized mice. The study demonstrated that ER-dependent transcriptional activity oscillated in time, and the frequency and amplitude of the transcription

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More, Vijay R., Christopher R. Campos, Rebecca A. Evans та ін. "PPAR-α, a lipid-sensing transcription factor, regulates blood–brain barrier efflux transporter expression". Journal of Cerebral Blood Flow & Metabolism 37, № 4 (2016): 1199–212. http://dx.doi.org/10.1177/0271678x16650216.

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Lipid sensor peroxisome proliferator-activated receptor alpha (PPAR- α) is the master regulator of lipid metabolism. Dietary release of endogenous free fatty acids, fibrates, and certain persistent environmental pollutants, e.g. perfluoroalkyl fire-fighting foam components, are peroxisome proliferator-activated receptor alpha ligands. Here, we define a role for peroxisome proliferator-activated receptor alpha in regulating the expression of three ATP-driven drug efflux transporters at the rat and mouse blood–brain barriers: P-glycoprotein (Abcb1), breast cancer resistance protein (Bcrp/Abcg2),

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Daujat-Chavanieu, Martine, and Sabine Gerbal-Chaloin. "Regulation of CAR and PXR Expression in Health and Disease." Cells 9, no. 11 (2020): 2395. http://dx.doi.org/10.3390/cells9112395.

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Pregnane X receptor (PXR, NR1I2) and constitutive androstane receptor (CAR, NR1I3) are members of the nuclear receptor superfamily that mainly act as ligand-activated transcription factors. Their functions have long been associated with the regulation of drug metabolism and disposition, and it is now well established that they are implicated in physiological and pathological conditions. Considerable efforts have been made to understand the regulation of their activity by their cognate ligand; however, additional regulatory mechanisms, among which the regulation of their expression, modulate th

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Rusinova, Radda, Karl F. Herold, R. Lea Sanford, Denise V. Greathouse, Hugh C. Hemmings, and Olaf S. Andersen. "Thiazolidinedione insulin sensitizers alter lipid bilayer properties and voltage-dependent sodium channel function: implications for drug discovery." Journal of General Physiology 138, no. 2 (2011): 249–70. http://dx.doi.org/10.1085/jgp.201010529.

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The thiazolidinediones (TZDs) are used in the treatment of diabetes mellitus type 2. Their canonical effects are mediated by activation of the peroxisome proliferator–activated receptor γ (PPARγ) transcription factor. In addition to effects mediated by gene activation, the TZDs cause acute, transcription-independent changes in various membrane transport processes, including glucose transport, and they alter the function of a diverse group of membrane proteins, including ion channels. The basis for these off-target effects is unknown, but the TZDs are hydrophobic/amphiphilic and adsorb to the b

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Pillman, Katherine A., Kaitlin G. Scheer, Emily Hackett-Jones, et al. "Extensive transcriptional responses are co-ordinated by microRNAs as revealed by Exon–Intron Split Analysis (EISA)." Nucleic Acids Research 47, no. 16 (2019): 8606–19. http://dx.doi.org/10.1093/nar/gkz664.

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Abstract Epithelial–mesenchymal transition (EMT) has been a subject of intense scrutiny as it facilitates metastasis and alters drug sensitivity. Although EMT-regulatory roles for numerous miRNAs and transcription factors are known, their functions can be difficult to disentangle, in part due to the difficulty in identifying direct miRNA targets from complex datasets and in deciding how to incorporate ‘indirect’ miRNA effects that may, or may not, represent biologically relevant information. To better understand how miRNAs exert effects throughout the transcriptome during EMT, we employed Exon

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