Academic literature on the topic 'Antiretroviral agents. Genetic regulation'

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Journal articles on the topic "Antiretroviral agents. Genetic regulation"

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Guimarães, Nilza Nascimento, Heloísa Helena Rodrigues de Andrade, Maurício Lehmann, Rafael Rodrigues Dihl, and Kênya Silva Cunha. "The genetic toxicity effects of lamivudine and stavudine antiretroviral agents." Expert Opinion on Drug Safety 9, no. 5 (2010): 771–81. http://dx.doi.org/10.1517/14740331003702384.

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Rotger, Margalida, Chantal Csajka, and Amalio Telenti. "Genetic, ethnic, and gender differences in the pharmacokinetics of antiretroviral agents." Current HIV/AIDS Reports 3, no. 3 (2006): 118–25. http://dx.doi.org/10.1007/bf02696655.

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Huang, Huachao, Weili Kong, Maxime Jean, et al. "A CRISPR/Cas9 screen identifies the histone demethylase MINA53 as a novel HIV-1 latency-promoting gene (LPG)." Nucleic Acids Research 47, no. 14 (2019): 7333–47. http://dx.doi.org/10.1093/nar/gkz493.

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AbstractAlthough combination antiretroviral therapy is potent to block active replication of HIV-1 in AIDS patients, HIV-1 persists as transcriptionally inactive proviruses in infected cells. These HIV-1 latent reservoirs remain a major obstacle for clearance of HIV-1. Investigation of host factors regulating HIV-1 latency is critical for developing novel antiretroviral reagents to eliminate HIV-1 latent reservoirs. From our recently accomplished CRISPR/Cas9 sgRNA screens, we identified that the histone demethylase, MINA53, is potentially a novel HIV-1 latency-promoting gene (LPG). We next val
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Tachedjian, Gilda, and Anne Mijch. "Virological significance, prevalence and genetic basis of hypersusceptibility to nonnucleoside reverse transcriptase inhibitors." Sexual Health 1, no. 2 (2004): 81. http://dx.doi.org/10.1071/sh03012.

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Nonnucleoside reverse transcriptase inhibitors (NNRTI) are used to treat HIV-infected individuals in combination with nucleoside analogues (NRTI) and protease inhibitors. Long-term treatment with antiretroviral agents results in the emergence of strains with decreased susceptibility (resistance) to the drugs and is one of the major factors in loss of drug efficacy. Conversely, there have been recent reports of HIV strains with increased susceptibility (hypersusceptibility) to NNRTIs. These isolates emerge in patients on long-term antiretroviral therapy particularly in individuals receiving NRT
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Shen, Weiping, Baoqun Li, Michele A. Wetzel, et al. "Down-regulation of the chemokine receptor CCR5 by activation of chemotactic formyl peptide receptor in human monocytes." Blood 96, no. 8 (2000): 2887–94. http://dx.doi.org/10.1182/blood.v96.8.2887.

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Abstract Interactions between cell surface receptors are important regulatory elements in the complex host responses to infections. In this study, it is shown that a classic chemotactic factor, the bacterial chemotactic peptide N-formyl-methionyl-leucylphenyl-alanine (fMLF), rapidly induced a protein-kinase-C–mediated serine phosphorylation and down-regulation of the chemokine receptor CCR5, which serves as a major human immunodeficiency virus (HIV)-1 coreceptor. The fMLF binding to its receptor, formyl peptide receptor (FPR), resulted in significant attenuation of cell responses to CCR5 ligan
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Shen, Weiping, Baoqun Li, Michele A. Wetzel, et al. "Down-regulation of the chemokine receptor CCR5 by activation of chemotactic formyl peptide receptor in human monocytes." Blood 96, no. 8 (2000): 2887–94. http://dx.doi.org/10.1182/blood.v96.8.2887.h8002887_2887_2894.

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Interactions between cell surface receptors are important regulatory elements in the complex host responses to infections. In this study, it is shown that a classic chemotactic factor, the bacterial chemotactic peptide N-formyl-methionyl-leucylphenyl-alanine (fMLF), rapidly induced a protein-kinase-C–mediated serine phosphorylation and down-regulation of the chemokine receptor CCR5, which serves as a major human immunodeficiency virus (HIV)-1 coreceptor. The fMLF binding to its receptor, formyl peptide receptor (FPR), resulted in significant attenuation of cell responses to CCR5 ligands and in
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Lizarbe, María Antonia, Jorge Calle-Espinosa, Eva Fernández-Lizarbe, et al. "Colorectal Cancer: From the Genetic Model to Posttranscriptional Regulation by Noncoding RNAs." BioMed Research International 2017 (2017): 1–38. http://dx.doi.org/10.1155/2017/7354260.

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Colorectal cancer is the third most common form of cancer in developed countries and, despite the improvements achieved in its treatment options, remains as one of the main causes of cancer-related death. In this review, we first focus on colorectal carcinogenesis and on the genetic and epigenetic alterations involved. In addition, noncoding RNAs have been shown to be important regulators of gene expression. We present a general overview of what is known about these molecules and their role and dysregulation in cancer, with a special focus on the biogenesis, characteristics, and function of mi
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Vergne, Laurence, Martine Peeters, Eitel Mpoudi-Ngole, et al. "Genetic Diversity of Protease and Reverse Transcriptase Sequences in Non-Subtype-B Human Immunodeficiency Virus Type 1 Strains: Evidence of Many Minor Drug Resistance Mutations in Treatment-Naive Patients." Journal of Clinical Microbiology 38, no. 11 (2000): 3919–25. http://dx.doi.org/10.1128/jcm.38.11.3919-3925.2000.

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Most human immunodeficiency virus (HIV) drug susceptibility studies have involved subtype B strains. Little information on the impact of viral diversity on natural susceptibility to antiretroviral drugs has been reported. However, the prevalence of non-subtype-B (non-B) HIV type 1 (HIV-1) strains continues to increase in industrialized countries, and antiretroviral treatments have recently become available in certain developing countries where non-B subtypes predominate. We sequenced the protease and reverse transcriptase (RT) genes of 142 HIV-1 isolates from antiretroviral-naive patients: 4 b
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Garg, Abhimanyu. "Lipodystrophies: Genetic and Acquired Body Fat Disorders." Journal of Clinical Endocrinology & Metabolism 96, no. 11 (2011): 3313–25. http://dx.doi.org/10.1210/jc.2011-1159.

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Abstract Context: Lipodystrophies are heterogeneous, genetic or acquired disorders characterized by selective loss of body fat and predisposition to insulin resistance. The extent of fat loss determines the severity of associated metabolic complications such as diabetes mellitus, hypertriglyceridemia, and hepatic steatosis. Evidence Acquisition and Synthesis: Both original and review articles were found via PubMed search reporting on clinical features and management of various types of lipodystrophies and were integrated with the author's knowledge of the field. Conclusion: The autosomal reces
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Moure, Ricardo, Pere Domingo, Joan Villarroya та ін. "Reciprocal Effects of Antiretroviral Drugs Used To Treat HIV Infection on the Fibroblast Growth Factor 21/β-Klotho System". Antimicrobial Agents and Chemotherapy 62, № 6 (2018): e00029-18. http://dx.doi.org/10.1128/aac.00029-18.

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ABSTRACT Following antiretroviral therapy, HIV-infected patients show increased circulating levels of the antidiabetic hormone fibroblast growth factor 21 (FGF21). In contrast, the expression of the FGF21-obligatory coreceptor β-Klotho (KLB) is reduced in target tissues. This situation is comparable to the FGF21 resistance status observed in obesity and type 2 diabetes. Here, we performed the first systematic study of the effects of distinct members of different antiretroviral drug classes on the FGF21/KLB system in human hepatic, adipose, and skeletal muscle cells. Most protease inhibitors an
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Dissertations / Theses on the topic "Antiretroviral agents. Genetic regulation"

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Casey, Ryan Edward. "Mouse strain-specific splicing of Apobec3." Digital WPI, 2006. https://digitalcommons.wpi.edu/etd-theses/950.

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"Host resolution of viral infection is dependent upon components of the innate and acquired immune system. The mammalian protein Apobec3 plays an important role as part of the immune system’s innate defenses through its modification of reverse transcribed viral DNA. Recently, Apobec3 was found to directly inhibit HIV-1 and HBV replication through deaminating newly transcribed deoxycytidine residues to deoxyuridine. The ability of mouse and simian Apobec3 variants to inhibit human retroviruses and vice versa highlights the utility of analyzing cross-species homologues. To better understan
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McFarland, Matthew R. "Transfer RNAs as regulatory agents in the translational control of gene expression." Thesis, University of Aberdeen, 2016. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=231855.

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Translational efficiency is dictated in part by the availability of charged transfer RNA. Depletion of aminoacylated tRNAs (e.g. during recombinant protein expression) can increase translational errors and associated stress responses. Here, the role of tRNAs as regulators of gene expression was explored through development of synthetic, tRNA-regulated gene circuits, and through an investigation of the impact of tRNA aminoacylation on endogenous gene expression. Synthetic gene circuits initially explored the use of dominant negative alleles of the release factor eRF1 to modulate stop codon read
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Parathyras, John Burns. "Molecular genetic analysis of human immunodeficiency virus antiretroviral therapy response in South Africa : a pharmacogenetics study." Thesis, Link to the online version, 2007. http://hdl.handle.net/10019/453.

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Thomas, Holly Reed. "Genetic and epigenetic regulation of dihydropyrimidinase and beta-ureidopropionase in individuals with altered uracil catabolism and normal dihydropyrimidine dehydrogenase enzyme activity." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2008r/thomas.pdf.

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Iu, Yan Yu. "Enhancement of gene silencing effects of small interfering RNAs to N-methyld-D-asparate receptors by gold nonoparticiples." HKBU Institutional Repository, 2013. http://repository.hkbu.edu.hk/etd_ra/1552.

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Brittain, Joel Matthew. "Dual regulation of voltage- and ligand-gated calcium channels by collapsin response mediator protein 2." Thesis, 2013. http://hdl.handle.net/1805/3613.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>Synaptic transmission is coordinated by a litany of protein-protein interactions that rely on the proper localization and function of pre- and post-synaptic Ca2+ channels. The axonal guidance/specification collapsin response mediator protein-2 (CRMP-2) was identified as a potential partner of the pre-synaptic N-type voltage-gated Ca2+ channel (CaV2.2). CRMP-2 bound directly to CaV2.2 in two regions; the channel domain I-II intracellular loop and the distal C-terminus. Both proteins co-localized within presynaptic sites in hippocam
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Huang, Wei. "Small molecule compounds targeting DNA binding domain of STAT3 for inhibition of tumor growth and metastasis." Thesis, 2014. http://hdl.handle.net/1805/5221.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>Signal transducer and activator of transcription 3 (STAT3) is constitutively activated in malignant tumors, and its activation is associated with high histological grade and advanced cancer stage. STAT3 has been shown to play important roles in multiple aspects of cancer aggressiveness including proliferation, survival, self-renewal, migration, invasion, angiogenesis and immune response by regulating the expression of diverse downstream target genes. Thus, inhibiting STAT3 promises to be an attractive strategy for treatment of advanc
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Books on the topic "Antiretroviral agents. Genetic regulation"

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Minter, Brian. Commercialization of oligonucleotides as therapeutic agents. Decision Resources, 1995.

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Nicholson, Allen W. Ribonucleases. Springer-Verlag Berlin Heidelberg, 2011.

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International Conference on Gene Regulation, Oncogenesis, and AIDS (1st 1989 Loutráki, Greece). Oncogenesis: Oncogenes in signal transduction and cell proliferation : papers delivered at the First International Conference on Gene Regulation, Oncogenesis, and AIDS, Loutraki, Greece, September 15-21, 1989. Edited by Papas Takis S. Portfolio Pub. Co., 1990.

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Aldrich-Wright, Janice. Metallointercalators: Synthesis and Techniques to Probe Their Interactions with Biomolecules. Springer-Verlag/Wien, 2011.

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Costa, E. Neurotransmitter Regulation of Gene Transcription (Fidia Research Foundations symposium series). Thieme Medical Pub, 1991.

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Jones, Peter A. Dna Methylation And Cancer (Current Topics in Microbiology & Immunology). Edited by Peter A. Jones. SPRINGER-VERLAG, 2000.

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Mortal Combat: AIDS Denialism and the Struggle for Antiretrovirals in South Africa. University of Kwazulu Natal Press, 2007.

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Aldrich-Wright, Janice. Metallointercalators: Synthesis and Techniques to Probe Their Interactions with Biomolecules. Springer, 2011.

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Aldrich-Wright, Janice. Metallointercalators: Synthesis and Techniques to Probe Their Interactions with Biomolecules. Springer, 2014.

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Grant, Warren, and Martin Scott-Brown. Principles of oncogenesis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0322.

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It is obvious that the process of developing cancer—oncogenesis—is a multistep process. We know that smoking, obesity, and a family history are strong independent predictors of developing malignancy; yet, in clinics, we often see that some heavy smokers live into their nineties and that some people with close relatives affected by cancer spend many years worrying about a disease that, in the end, they never contract. For many centuries scientists have struggled to understand the process that make cancer cells different from normal cells. There were those in ancient times who believed that tumo
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Book chapters on the topic "Antiretroviral agents. Genetic regulation"

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Lachmann, Helen J., and Philip N. Hawkins. "Autoinflammatory diseases." In Oxford Textbook of Rheumatology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0164.

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The autoinflammatory diseases are disorders of innate immunity which result in chronic or recurrent multisystem inflammatory disease. This chapter concentrates on the currently known inherited periodic fever syndromes. These rare genetic diseases have resulted in major advances in the understanding of innate immunity in general and the regulation of interleukin (IL)-1 in particular. It now seems clear that autoinflammatory conditions are disorders of the regulation of IL-1 and NFκ‎‎B. The treatment and prognosis of these diseases have been radically improved by the availability of cytokine-blocking agents.
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Eryılmaz Pehlivan, Fadime. "Diet-Epigenome Interactions: Epi-Drugs Modulating the Epigenetic Machinery During Cancer Prevention." In Epigenetics - “A Parallel Universe” in the Study of Cancer Biology [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95374.

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The roles of diet and environment on health have been known since ancient times. Cancer is both a genetic and an epigenetic disease and a complex interplay mechanism of genetic and environmental factors composed of multiple stages in which gene expression, protein and metabolite function operate synchronically. Disruption of epigenetic processes results in life-threatening diseases, in particular, cancer. Epigenetics involves altered gene expression without any change of nucleotide sequences, such as DNA methylation, histone modifications and non-coding RNAs in the regulation of genome. According to current studies, cancer is preventable with appropriate or balanced food and nutrition, in some cases. Nutrient intake is an environmental factor, and dietary components play an importent role in both cancer development and prevention. Due to epigenetic events induce changes in DNA and thus influencing over all gene expression in response to the food components, bioactive compounds and phytochemicals as potent antioxidants and cancer preventive agents have important roles in human diet. Several dietray components can alter cancer cell behavior and cancer risk by influencing key pathways and steps in carcinogenesis, including signaling, apoptosis, differentiation, or inflammation. To date, multiple biologically active food components are strongly suggested to have protective potential against cancer formation, such as methyl-group donors, fatty acids, phytochemicals, flavonoids, isothiocyanates, etc. Diet considered as a source of either carcinogens that are present in certain foods or acting in a protective manner such as vitamins, antioxidants, detoxifying substances, chelating agents etc. Thus, dietary phytochemicals as epigenetic modifiers in cancer and effects of dietary phytochemicals on gene expression and signaling pathways have been widely studied in cancer. In this chapter, current knowledge on interactions between cancer metabolism, epigenetic gene regulation, and how both processes are affected by dietary components are summerized. A comprehensive overview of natural compounds with epigenetic activity on tumorogenesis mechanisms by which natural compounds alter the cancer epigenome is provided. Studies made in epigenetics and cancer research demonstrated that genetic and epigenetic mechanisms are not separate events in cancer; they influence each other during carcinogenesis, highlighting plant-derived anticancer compounds with epigenetic mechanisms of action, and potential use in epigenetic therapy. Recent investigations involving epigenetic modulations suggest that diet rich in phytochemicals not only reduce the risk of developing cancer, but also affect the treatment outcome.
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Bonabeau, Eric, Marco Dorigo, and Guy Theraulaz. "Nest Building and Self-Assembling." In Swarm Intelligence. Oxford University Press, 1999. http://dx.doi.org/10.1093/oso/9780195131581.003.0010.

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Social insect nest architectures can be complex, intricate structures. Stigmergy (see section 1.2.3), that is, the coordination of activities through the environment, is an important mechanism underlying nest construction in social insects. Two types of stigmergy are distinguished: quantitative, or continuous stigmergy, in which the different stimuli that trigger behavior are quantitatively different; and qualitative, or discrete stigmergy, in which stimuli can be classified into different classes that differ qualitatively. If quantitative stigmergy can explain the emergence of pillars in termites, the building behavior of the paper wasps Polistes dominulus seems to be better described by qualitative stigmergy. In this chapter, a simple agent-based model inspired by discrete stigmergy is introduced. In the model, agents move in a three-dimensional grid and drop elementary building blocks depending on the configuration of blocks in their neighborhood. From the viewpoint of bricks, this model is a model of self-assembly. The model generates a large proportion of random or space-filling forms, but some patterns appear to be structured. Some of the patterns even look like wasp nests. The properties of the structured shapes obtained with the model, and of the algorithms that generate them, are reviewed. Based on these properties, a fitness function is constructed so that structured architectures have a large fitness and unstructured patterns a small fitness. A genetic algorithm based on the fitness function is used to explore the space of architectures. Several examples of self-assembling systems in robotics, engineering, and architecture are described. Self-assembling or self-reconfigurable robotic systems, although they are not directly inspired by nest construction in social insects, could benefit from the discrete-stigmergy model of nest building. The method of evolutionary design, that is, the creation of new designs by computers using evolutionary algorithms, is a promising way of exploring the patterns that self-assembling models can produce. Many animals can produce very complex architectures that fulfill numerous functional and adaptive requirements (protection from predators, substrate of social life and reproductive activities, thermal regulation, etc.).
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