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

Author: Grafiati

Published: 4 June 2021

Last updated: 9 February 2022

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1

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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2

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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3

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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4

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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7

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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8

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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10

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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11

Glazkova, D. V., E. V. Bogoslovskaya, M. L. Markelov, G. A. Shipulin, and V. V. Pokrovskii. "TREATMENT OF HIV-INFECTION BY MEANS OF GENE THERAPY." Annals of the Russian academy of medical sciences 67, no. 5 (2012): 16–23. http://dx.doi.org/10.15690/vramn.v67i5.268.

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Current methods of HIV treatment can contain a progression of the disease; however they do not lead to a cure. Lifelong antiretroviral therapy is therefore necessary, leading to problems of cost and toxicity of chemical drugs. The recent advances in science have allowed a new approach to the HIV-treatment — gene therapy. In the present publication we focus on one strategy of the gene therapy called «intracellular immunization». The strategy is based on the introducing of antiviral genes into the HIV-sensitive cells. We highlight the mechanisms of action of various antiviral genetic agents and

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12

Kuehn, Philipp, Thea Riebe, Lynn Apelt, Max Jansen, and Christian Reuter. "Sharing of Cyber Threat Intelligence between States." Sicherheit & Frieden 38, no. 1 (2020): 22–28. http://dx.doi.org/10.5771/0175-274x-2020-1-22.

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Novel environmental invasive biotechnologies, such as gene drives and Horizontal Environmental Genetic Alteration Agents exceed the classical applications of genetically modified organisms. The reason for this is that they are designed to transform wild organisms into genetically modified organisms which express desired traits. Instead of in a laboratory, this transformation takes place in the environment. The far-ranging effects that may be triggered by gene drive and Horizontal Environmental Genetic Alteration Agents require an extension of risk assessment to include socio-political conseque

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13

Shen, Jian, and Jose M. Ordovas. "Impact of Genetic and Environmental Factors on hsCRP Concentrations and Response to Therapeutic Agents." Clinical Chemistry 55, no. 2 (2009): 256–64. http://dx.doi.org/10.1373/clinchem.2008.117754.

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Abstract Background: Inflammation plays an instrumental role in all stages of atherosclerosis. High-sensitivity C-reactive protein (hsCRP), a systemic inflammatory marker, has been gaining recognition as an independent risk factor for cardiovascular disease (CVD). Both baseline hsCRP concentrations and drug-induced hsCRP changes are highly variable and potentially subject to genetic regulation. Content: This review summarizes the current studies examining the effect of genetic and environmental factors on baseline plasma hsCRP concentrations, with a main focus on C-reactive protein, pentraxin-

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14

Ghanim, George E., Donald C. Rio, and Felipe Karam Teixeira. "Mechanism and regulation of P element transposition." Open Biology 10, no. 12 (2020): 200244. http://dx.doi.org/10.1098/rsob.200244.

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P elements were first discovered in the fruit fly Drosophila melanogaster as the causative agents of a syndrome of aberrant genetic traits called hybrid dysgenesis. This occurs when P element-carrying males mate with females that lack P elements and results in progeny displaying sterility, mutations and chromosomal rearrangements. Since then numerous genetic, developmental, biochemical and structural studies have culminated in a deep understanding of P element transposition: from the cellular regulation and repression of transposition to the mechanistic details of the transposase nucleoprotein

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15

Alison, Malcolm R., and Catherine E. Sarraf. "Review : Apoptosis: regulation and relevance to toxicology." Human & Experimental Toxicology 14, no. 3 (1995): 234–47. http://dx.doi.org/10.1177/096032719501400302.

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1 Apopotosis is a remarkably stereotyped morphological event across all tissues in response to a vast array of dam aging agents. 2 Our very existence depends upon a willing exchange of old life for new: apoptotic cell death is our guardian and saviour from genetic damage. 3 There is a close link between cell proliferation and apoptosis: When a cell picks up the machinery to prolifer ate it also acquires an abort pathway - 'better dead than wrong'. 4 A wide variety of highly conserved genes have been implicated in triggering apoptosis. 5 The release of DNA loops from the nuclear scaffold is a m

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16

Larsen, A. K., C. Gobert, C. Gilbert, J. Markovits, K. Bojanowski, and A. Skladanowski. "DNA topoisomerases as repair enzymes: mechanism(s) of action and regulation by p53." Acta Biochimica Polonica 45, no. 2 (1998): 535–44. http://dx.doi.org/10.18388/abp.1998_4246.

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DNA topoisomerases regulate the organization of DNA and are important targets for many clinically used antineoplastic agents. In addition, DNA topoisomerases modulate the cellular sensitivity toward a number of DNA damaging agents. Increased topoisomerase II activities were shown to contribute to the resistance of both nitrogen mustard- and cisplatin-resistant cells. Similarly, cells with decreased topoisomerase II levels show increased sensitivity to cisplatin, carmustine, mitomycin C and nitrogen mustard. Recent studies propose that topoisomerases may be involved in damage recognition and DN

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17

Guo, Qi, Hsu-Tso Ho, Ira Dicker, et al. "Biochemical and Genetic Characterizations of a Novel Human Immunodeficiency Virus Type 1 Inhibitor That Blocks gp120-CD4 Interactions." Journal of Virology 77, no. 19 (2003): 10528–36. http://dx.doi.org/10.1128/jvi.77.19.10528-10536.2003.

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ABSTRACT BMS-378806 is a recently discovered small-molecule human immunodeficiency virus type 1 (HIV-1) attachment inhibitor with good antiviral activity and pharmacokinetic properties. Here, we demonstrate that the compound targets viral entry by inhibiting the binding of the HIV-1 envelope gp120 protein to cellular CD4 receptors via a specific and competitive mechanism. BMS-378806 binds directly to gp120 at a stoichiometry of approximately 1:1, with a binding affinity similar to that of soluble CD4. The potential BMS-378806 target site was localized to a specific region within the CD4 bindin

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18

Reeds, P. J. "Options at the fundamental level for growth regulation in farm livestock." Proceedings of the British Society of Animal Production (1972) 1987 (March 1997): 22. http://dx.doi.org/10.1017/s0308229600034632.

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New developments in immunological techniques and increasing expertise in genetic manipulation, especially by gene transfer, have opened up a wide variety of approaches to the manipulation of the growth and metabolism of farm livestock. However, the most effective use of these techniques and the design of new pharmacological agents for growth promotion and nutrient “repartitioning” might well rest on a greater understanding of the factors and cellular mechanisms that coordinate growth and protein anabolism. It is this coordidnation that must be disturbed if persistent gains are to bke made. Thi

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19

Assis, Dnieber Chagas, Deisy Vivian Resende, Marlene Cabrine-Santos, Dalmo Correia, and Márcia Benedita Oliveira-Silva. "Prevalence and genetic characterization of Cryptosporidium spp. and Cystoisospora belli in HIV-infected patients." Revista do Instituto de Medicina Tropical de São Paulo 55, no. 3 (2013): 149–54. http://dx.doi.org/10.1590/s0036-46652013000300002.

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Cryptosporidium spp. and Cystoisospora belli are monoxenic protozoa that have been recognized as the causative agents of chronic diarrhea in immunocompromised individuals, especially HIV-infected subjects. The objective of this study was to evaluate the frequency of these intestinal protozoa in HIV-positive patients in the Triângulo Mineiro region of Brazil and to correlate the presence of these infections with clinical, epidemiological and laboratory data of the patients. Oocysts were detected in stool samples of 10 (16.9%) of the 59 patients studied, while Cryptosporidium spp. were present i

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20

Wu, Chen-Ning, and Kai-Jen Tien. "The Impact of Antidiabetic Agents on Sarcopenia in Type 2 Diabetes: A Literature Review." Journal of Diabetes Research 2020 (July 9, 2020): 1–6. http://dx.doi.org/10.1155/2020/9368583.

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Sarcopenia is a geriatric syndrome characterized by decline of skeletal muscle mass and function. Contributing factors include nutritional, genetic, inflammatory, and endocrinal factors. The reported prevalence of sarcopenia in type 2 diabetes mellitus is high, especially in patients with poor glycemic control. Additionally, antidiabetic agents may alter the balance between protein synthesis and degradation through various mechanisms of skeletal muscle mass regulation. This study reviewed the literature on the pathogenesis of sarcopenia in diabetes mellitus and the current understanding of whe

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21

Jilling, T., S. Cunningham, P. E. Barker, M. W. Green, R. A. Frizzell, and K. L. Kirk. "Genetic complementation in cystic fibrosis pancreatic cells by somatic cell fusion." American Journal of Physiology-Cell Physiology 259, no. 6 (1990): C1010—C1015. http://dx.doi.org/10.1152/ajpcell.1990.259.6.c1010.

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The biochemical defect that underlies the genetic disorder cystic fibrosis (CF) has been proposed to involve an altered regulation of epithelial Cl- permeability by agents such as adenosine 3',5'-cyclic monophosphate (cAMP). We report here the successful complementation of this functional defect achieved by using the technique of somatic cell fusion to introduce the normal CF allele into mutant cells. CF epithelial cells were fused with transfectant mouse fibroblasts that contain the normal human gene. The resulting heterokaryons were examined for restoration of cAMP-activated Cl- transport us

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22

Spasskaya, Daria S., Nonna I. Nadolinskaia, Vera V. Tutyaeva, Yuriy P. Lysov, Vadim L. Karpov, and Dmitry S. Karpov. "Yeast Rpn4 Links the Proteasome and DNA Repair via RAD52 Regulation." International Journal of Molecular Sciences 21, no. 21 (2020): 8097. http://dx.doi.org/10.3390/ijms21218097.

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Environmental and intracellular factors often damage DNA, but multiple DNA repair pathways maintain genome integrity. In yeast, the 26S proteasome and its transcriptional regulator and substrate Rpn4 are involved in DNA damage resistance. Paradoxically, while proteasome dysfunction may induce hyper-resistance to DNA-damaging agents, Rpn4 malfunction sensitizes yeasts to these agents. Previously, we proposed that proteasome inhibition causes Rpn4 stabilization followed by the upregulation of Rpn4-dependent DNA repair genes and pathways. Here, we aimed to elucidate the key Rpn4 targets responsib

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23

Poroikov, V. V. "Computer-aided drug design: from discovery of novel pharmaceutical agents to systems pharmacology." Biomeditsinskaya Khimiya 66, no. 1 (2020): 30–41. http://dx.doi.org/10.18097/pbmc20206601030.

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New drug discovery is based on the analysis of public information about the mechanisms of the disease, molecular targets, and ligands, which interaction with the target could lead to the normalization of the pathological process. The available data on diseases, drugs, pharmacological effects, molecular targets, and drug-like substances, taking into account the combinatorics of the associative relations between them, correspond to the Big Data. To analyze such data, the application of computer-aided drug design methods is necessary. An overview of the studies in this area performed by the Labor

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Mickelson, J. R., and C. F. Louis. "Malignant hyperthermia: excitation-contraction coupling, Ca2+ release channel, and cell Ca2+ regulation defects." Physiological Reviews 76, no. 2 (1996): 537–92. http://dx.doi.org/10.1152/physrev.1996.76.2.537.

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Malignant hyperthermia (MH) is a disorder of skeletal muscle in which certain anesthetic agents trigger a sustained elevation in myoplasmic Ca2+ concentration that activates metabolic and contractile activity. This review focuses on the biochemical and physiological alterations in the skeletal muscle of MH-susceptible (MHS) pigs and humans that appear responsible for this inherited disorder. In porcine MH, these studies identified the skeletal muscle sarcoplasmic reticulum Ca2+ release channel gene (RYR1) as the site of the defect. A mutation in this protein results in altered excitation-contr

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Lee, Phoebe S., Jun Fang, Lea Jessop, et al. "RAD51B Activity and Cell Cycle Regulation in Response to DNA Damage in Breast Cancer Cell Lines." Breast Cancer: Basic and Clinical Research 8 (January 2014): BCBCR.S17766. http://dx.doi.org/10.4137/bcbcr.s17766.

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Common genetic variants mapping to two distinct regions of RADS1B, a paralog of RADS1, have been associated with breast cancer risk in genome-wide association studies (GWAS). RADS1B is a plausible candidate gene because of its established role in the homologous recombination (HR) process. How germline genetic variation in RADS1B confers susceptibility to breast cancer is not well understood. Here, we investigate the molecular function of RADS1B in breast cancer cell lines by knocking down RADS1B expression by small interfering RNA and treating cells with DNA-damaging agents, namely cisplatin,

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26

Foster, Caroline, Sara Ayers, and Sarah Fidler. "Antiretroviral adherence for adolescents growing up with HIV: understanding real life, drug delivery and forgiveness." Therapeutic Advances in Infectious Disease 7 (January 2020): 204993612092017. http://dx.doi.org/10.1177/2049936120920177.

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Poorer adherence to medication is normal in adolescence and is one of a range of risk-taking behaviours common during a developmental stage that encompasses enormous cognitive, physical, sexual, social and emotional change. For adolescents living with human immunodeficiency virus (HIV) infection, poor adherence to antiretroviral therapy (ART) confers two significant challenges: poor health, but also the specific additional burden of onward transmission to partners. Late adolescence (15–19 years) is the only age group where HIV-associated mortality is rising, driven by poor adherence to ART and

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Zuzic, Marta, Jesus Eduardo Rojo Arias, Stefanie Gabriele Wohl, and Volker Busskamp. "Retinal miRNA Functions in Health and Disease." Genes 10, no. 5 (2019): 377. http://dx.doi.org/10.3390/genes10050377.

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The health and function of our visual system relies on accurate gene expression. While many genetic mutations are associated with visual impairment and blindness, we are just beginning to understand the complex interplay between gene regulation and retinal pathologies. MicroRNAs (miRNAs), a class of non-coding RNAs, are important regulators of gene expression that exert their function through post-transcriptional silencing of complementary mRNA targets. According to recent transcriptomic analyses, certain miRNA species are expressed in all retinal cell types, while others are cell type-specifi

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Rolland, Steven, Luce Mengue, Cyril Noël, et al. "Encystment Induces Down-Regulation of an Acetyltransferase-Like Gene in Acanthamoeba castellanii." Pathogens 9, no. 5 (2020): 321. http://dx.doi.org/10.3390/pathogens9050321.

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Acanthamoeba castellanii is a ubiquitous free-living amoeba. Pathogenic strains are causative agents of Acanthamoeba keratitis and granulomatous amoebic encephalitis. In response to adverse conditions, A. castellanii differentiate into cysts, which are metabolically inactive and resistant cells. This process, also named encystment, involves biochemical and genetic modifications that remain largely unknown. This study characterizes the role of the ACA1_384820 Acanthamoeba gene during encystment. This gene encodes a putative N-acetyltransferase, belonging to the Gcn5-related N-acetyltransferase

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29

Das, Siba R., Maciej Maselko, Ambuj Upadhyay, and Michael J. Smanski. "Genetic engineering of sex chromosomes for batch cultivation of non-transgenic, sex-sorted males." PLOS Genetics 16, no. 11 (2020): e1009180. http://dx.doi.org/10.1371/journal.pgen.1009180.

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The field performance of Sterile Insect Technique (SIT) is improved by sex-sorting and releasing only sterile males. This can be accomplished by resource-intensive separation of males from females by morphology. Alternatively, sex-ratio biasing genetic constructs can be used to selectively remove one sex without the need for manual or automated sorting, but the resulting genetically engineered (GE) control agents would be subject to additional governmental regulation. Here we describe and demonstrate a genetic method for the batch production of non-GE males. This method could be applied to gen

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30

Deng, Min, Jing Lin, Somaira Nowsheen, et al. "Extracellular matrix stiffness determines DNA repair efficiency and cellular sensitivity to genotoxic agents." Science Advances 6, no. 37 (2020): eabb2630. http://dx.doi.org/10.1126/sciadv.abb2630.

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DNA double-strand breaks (DSBs) are highly toxic lesions that can drive genetic instability. These lesions also contribute to the efficacy of radiotherapy and many cancer chemotherapeutics. DNA repair efficiency is regulated by both intracellular and extracellular chemical signals. However, it is largely unknown whether this process is regulated by physical stimuli such as extracellular mechanical signals. Here, we report that DSB repair is regulated by extracellular mechanical signals. Low extracellular matrix (ECM) stiffness impairs DSB repair and renders cells sensitive to genotoxic agents.

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Peters, Solange, Miguel Muñoz, Sabine Yerly, et al. "Resistance to Nucleoside Analog Reverse Transcriptase Inhibitors Mediated by Human Immunodeficiency Virus Type 1 p6 Protein." Journal of Virology 75, no. 20 (2001): 9644–53. http://dx.doi.org/10.1128/jvi.75.20.9644-9653.2001.

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ABSTRACT Resistance of human immunodeficiency virus type 1 (HIV-1) to antiretroviral agents results from target gene mutation within thepol gene, which encodes the viral protease, reverse transcriptase (RT), and integrase. We speculated that mutations in genes other that the drug target could lead to drug resistance. For this purpose, the p1-p6 gag -p6 pol region of HIV-1, placed immediately upstream ofpol, was analyzed. This region has the potential to alter Pol through frameshift regulation (p1), through improved packaging of viral enzymes (p6Gag), or by changes in activation of the viral pr

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Lakhotia, S. C. "The 93D heat shock locus of Drosophila melanogaster: modulation by genetic and developmental factors." Genome 31, no. 2 (1989): 677–83. http://dx.doi.org/10.1139/g89-124.

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The 93D locus in Drosophila melanogaster and the 93D-like loci in other species of Drosophila, collectively termed hsr ω (heat shock RNA omega) locus, display several unique and intriguing features: (i) developmental regulation and selective induction by several agents like benzamide, colchicine, thiamphenicol, vit-B6; (ii) functional conservation in the genus but a very rapid DNA base sequence divergence; (iii) in spite of the rapid DNA sequence divergence, a strong conservation of organization (a 5′ unique region and a 3′ long tandem repeat region) and the pattern of multiple ω transcripts i

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Gao, Jian Feng, Stanford B. Call, Parley D. Fillmore, Takeshi Watanabe, Nathan D. Meeker, and Cory Teuscher. "Analysis of the Role of Bphs/Hrh1 in the Genetic Control of Responsiveness to Pertussis Toxin." Infection and Immunity 71, no. 3 (2003): 1281–87. http://dx.doi.org/10.1128/iai.71.3.1281-1287.2003.

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ABSTRACT In vivo intoxication with Bordetella pertussis toxin (PTX) elicits a variety of physiological responses including a marked leukocytosis, disruption of glucose regulation, adjuvant activity, alterations in vascular function, hypersensitivity to vasoactive agents, and death. We recently identified Bphs, the locus controlling PTX-induced hypersensitivity to the vasoactive amine histamine, as the histamine H1 receptor (Hrh1). In this study Bphs congenic mice and mice with a disrupted Hrh1 gene were used to examine the role of Bphs/Hrh1 in the genetic control of susceptibility to a number

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Cooper, Desmond W., and Catherine A. Herbert. "Genetics, biotechnology and population management of over-abundant mammalian wildlife in Australasia." Reproduction, Fertility and Development 13, no. 8 (2001): 451. http://dx.doi.org/10.1071/rd01072.

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Wildlife management involves regulation of population numbers of wild vertebrate species. In some cases there are too many animals and in others there are too few. Genetic issues arise in both instances. The historical and genetic evidence for the number of mammals that were in the founder populations of successful colonizing species in Australia and New Zealand is reviewed here. Small numbers have often given rise to large populations, despite the concomitant loss of genetic variability. Restriction of the number of over-abundant and pest species by either physical or chemical methods frequen

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Hustedt, Nicole, Alejandro Álvarez-Quilón, Andrea McEwan, et al. "A consensus set of genetic vulnerabilities to ATR inhibition." Open Biology 9, no. 9 (2019): 190156. http://dx.doi.org/10.1098/rsob.190156.

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The response to DNA replication stress in eukaryotes is under the control of the ataxia–telangiectasia and Rad3-related (ATR) kinase. ATR responds to single-stranded (ss) DNA to stabilize distressed DNA replication forks, modulate DNA replication firing and prevent cells with damaged DNA or incomplete DNA replication from entering into mitosis. Furthermore, inhibitors of ATR are currently in clinical development either as monotherapies or in combination with agents that perturb DNA replication. To gain a genetic view of the cellular pathways requiring ATR kinase function, we mapped genes whose

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36

Huang, Chien-feng, Jasleen Kaur, Ana Maguitman, and Luis M. Rocha. "Agent-Based Model of Genotype Editing." Evolutionary Computation 15, no. 3 (2007): 253–89. http://dx.doi.org/10.1162/evco.2007.15.3.253.

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Evolutionary algorithms rarely deal with ontogenetic, non-inherited alteration of genetic information because they are based on a direct genotype-phenotype mapping. In contrast, several processes have been discovered in nature which alter genetic information encoded in DNA before it is translated into amino-acid chains. Ontogenetically altered genetic information is not inherited but extensively used in regulation and development of phenotypes, giving organisms the ability to, in a sense, re-program their genotypes according to environmental cues. An example of post-transcriptional alteration

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Bender, Carol L., Francisco Alarcón-Chaidez, and Dennis C. Gross. "Pseudomonas syringae Phytotoxins: Mode of Action, Regulation, and Biosynthesis by Peptide and Polyketide Synthetases." Microbiology and Molecular Biology Reviews 63, no. 2 (1999): 266–92. http://dx.doi.org/10.1128/mmbr.63.2.266-292.1999.

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SUMMARY Coronatine, syringomycin, syringopeptin, tabtoxin, and phaseolotoxin are the most intensively studied phytotoxins of Pseudomonas syringae, and each contributes significantly to bacterial virulence in plants. Coronatine functions partly as a mimic of methyl jasmonate, a hormone synthesized by plants undergoing biological stress. Syringomycin and syringopeptin form pores in plasma membranes, a process that leads to electrolyte leakage. Tabtoxin and phaseolotoxin are strongly antimicrobial and function by inhibiting glutamine synthetase and ornithine carbamoyltransferase, respectively. Ge

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Sasca, Daniel, Jakub Szybinski, Andrea Schüler, et al. "NCAM1 (CD56) promotes leukemogenesis and confers drug resistance in AML." Blood 133, no. 21 (2019): 2305–19. http://dx.doi.org/10.1182/blood-2018-12-889725.

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Abstract Neural cell adhesion molecule 1 (NCAM1; CD56) is expressed in up to 20% of acute myeloid leukemia (AML) patients. NCAM1 is widely used as a marker of minimal residual disease; however, the biological function of NCAM1 in AML remains elusive. In this study, we investigated the impact of NCAM1 expression on leukemogenesis, drug resistance, and its role as a biomarker to guide therapy. Beside t(8;21) leukemia, NCAM1 expression was found in most molecular AML subgroups at highly heterogeneous expression levels. Using complementary genetic strategies, we demonstrated an essential role of N

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Balla, Tamas. "Phosphoinositides: Tiny Lipids With Giant Impact on Cell Regulation." Physiological Reviews 93, no. 3 (2013): 1019–137. http://dx.doi.org/10.1152/physrev.00028.2012.

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Phosphoinositides (PIs) make up only a small fraction of cellular phospholipids, yet they control almost all aspects of a cell's life and death. These lipids gained tremendous research interest as plasma membrane signaling molecules when discovered in the 1970s and 1980s. Research in the last 15 years has added a wide range of biological processes regulated by PIs, turning these lipids into one of the most universal signaling entities in eukaryotic cells. PIs control organelle biology by regulating vesicular trafficking, but they also modulate lipid distribution and metabolism via their close

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George, Bhawana, Sayan Mullick Chowdhury, Amber Hart, et al. "Ibrutinib Resistance Mechanisms and Treatment Strategies for B-Cell Lymphomas." Cancers 12, no. 5 (2020): 1328. http://dx.doi.org/10.3390/cancers12051328.

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Chronic activation of B-cell receptor (BCR) signaling via Bruton tyrosine kinase (BTK) is largely considered to be one of the primary mechanisms driving disease progression in B–Cell lymphomas. Although the BTK-targeting agent ibrutinib has shown promising clinical responses, the presence of primary or acquired resistance is common and often leads to dismal clinical outcomes. Resistance to ibrutinib therapy can be mediated through genetic mutations, up-regulation of alternative survival pathways, or other unknown factors that are not targeted by ibrutinib therapy. Understanding the key determi

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Jones, Emma V., Mark J. Dickman, and Alan J. Whitmarsh. "Regulation of p73-mediated apoptosis by c-Jun N-terminal kinase." Biochemical Journal 405, no. 3 (2007): 617–23. http://dx.doi.org/10.1042/bj20061778.

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The JNK (c-Jun N-terminal kinase)/mitogen-activated protein kinase signalling pathway is a major mediator of stress responses in cells, including the response to DNA damage. DNA damage also causes the stabilization and activation of p73, a member of the p53 family of transcription factors. p73, like p53, can mediate apoptosis by up-regulating the expression of pro-apoptotic genes, including Bax (Bcl2-associated X protein) and PUMA (p53 up-regulated modulator of apoptosis). Changes in p73 expression have been linked to tumour progression, particularly in neuroblastomas, whereas in tumours that

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Villarreal, Luis P., and Guenther Witzany. "Genomics Insights: The DNA Habitat and its RNA Inhabitants: At the Dawn of RNA Sociology." Genomics Insights 6 (January 2013): GEI.S11490. http://dx.doi.org/10.4137/gei.s11490.

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Most molecular biological concepts derive from physical chemical assumptions about the genetic code that are basically more than 40 years old. Additionally, systems biology, another quantitative approach, investigates the sum of interrelations to obtain a more holistic picture of nucleotide sequence order. Recent empirical data on genetic code compositions and rearrangements by mobile genetic elements and noncoding RNAs, together with results of virus research and their role in evolution, does not really fit into these concepts and compel a reexamination. In this review, we try to find an alte

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Sufiawati, Irna, Risti Saptarini, and Eriska Riyanti. "HUBUNGAN POLIMORFISME GEN RESEPTOR ESTROGEN ALFA DENGAN JUMLAH SEL T CD4+ PADA ANAK TERINFEKSI HIV." ODONTO : Dental Journal 4, no. 2 (2017): 94. http://dx.doi.org/10.30659/odj.4.2.94-100.

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Background: Estrogen plays a key role in human physiological processes. Polymorphisms of estrogen receptors have been implicated in the development of numerous diseases. The aim of this study was to evaluate the frequency of ERα gene Pvull and Xbal polymorphisms and assessing their association with CD4+ T-cell counts in HIV-infected children on highly active antiretroviral therapy.Methods: CD4+ T cell counts were determined using the FACS count system. ERα PvuII and XbaI polymorphisms were analyzed by PCR-RFLP.Results: This study enrolled 34 HIV-infected children on HAART. The frequencies of t

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Dueñas, Angel, Almudena Expósito, Amelia Aranega, and Diego Franco. "The Role of Non-Coding RNA in Congenital Heart Diseases." Journal of Cardiovascular Development and Disease 6, no. 2 (2019): 15. http://dx.doi.org/10.3390/jcdd6020015.

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Cardiovascular development is a complex developmental process starting with the formation of an early straight heart tube, followed by a rightward looping and the configuration of atrial and ventricular chambers. The subsequent step allows the separation of these cardiac chambers leading to the formation of a four-chambered organ. Impairment in any of these developmental processes invariably leads to cardiac defects. Importantly, our understanding of the developmental defects causing cardiac congenital heart diseases has largely increased over the last decades. The advent of the molecular era

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Clément, Y., E. Lepicard, and G. Chapouthier. "An animal model for the study of the genetic bases of behaviour in men: the multiple marker strains (MMS)." European Psychiatry 16, no. 4 (2001): 246–54. http://dx.doi.org/10.1016/s0924-9338(01)00572-7.

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SummaryAnimal models are often used for preclinical research on the neurobiology of psychiatric disorders. Whereas many are employed to screen new therapeutic agents, few of them are used to study the genetic bases of psychiatric diseases, probably because of the complex genetic determinism underlying quantitative behavioral traits such as mood, personality or intelligence. The present article presents a short review introducing an analysis model using mi the marker strains model. Using this model it is possible both to display genetic determinism data and to locate some of the chromosomal fra

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Martinez-Useros, Javier, and Jesus Garcia-Foncillas. "The Role of BRCA2 Mutation Status as Diagnostic, Predictive, and Prognosis Biomarker for Pancreatic Cancer." BioMed Research International 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/1869304.

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Pancreatic cancer is one of the deadliest cancers worldwide, and life expectancy after diagnosis is often short. Most pancreatic tumours appear sporadically and have been highly related to habits such as cigarette smoking, high alcohol intake, high carbohydrate, and sugar consumption. Other observational studies have suggested the association between pancreatic cancer and exposure to arsenic, lead, or cadmium. Aside from these factors, chronic pancreatitis and diabetes have also come to be considered as risk factors for these kinds of tumours. Studies have found that 10% of pancreatic cancer c

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Silvestri, Laura, Alessia Pagani, Antonella Nai, and Clara Camaschella. "Novel Insights Into Systemic Iron Regulation." Blood 132, Supplement 1 (2018): SCI—1—SCI—1. http://dx.doi.org/10.1182/blood-2018-99-109518.

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Abstract Iron, an essential element in mammals, is absorbed by duodenal enterocytes, enters the circulation through the iron exporter ferroportin, (FPN), circulates bound to transferrin and is uptaken through Transferrin Receptor 1. If in excess, iron is stored in macrophages and hepatocytes and released when needed. To maintain systemic iron homeostasis and to avoid the formation of "non transferrin bound iron" (NTBI), a highly reactive form which causes organ damage, the liver synthetizes hepcidin that, binding FPN, blocks iron export to the circulation. Hepcidin integrates signals from body

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Heinrich, Michael C., Maureen E. Hoatlin, Amy J. Zigler, et al. "DNA Cross-Linker–Induced G2/M Arrest in Group C Fanconi Anemia Lymphoblasts Reflects Normal Checkpoint Function." Blood 91, no. 1 (1998): 275–87. http://dx.doi.org/10.1182/blood.v91.1.275.275_275_287.

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Cells from individuals with Fanconi anemia (FA) arrest excessively in the G2/M cell cycle compartment after exposure to low doses of DNA cross-linking agents. The relationship of this abnormality to the fundamental genetic defect in such cells is unknown, but many investigators have speculated that the various FA genes directly regulate cell cycle checkpoints. We tested the hypothesis that the protein encoded by the FA group C complementing gene (FAC) functions to control a cell cycle checkpoint and that cells from group C patients (FA[C]) have abnormalities of cell cycle regulation directly r

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Mullighan, Charles G. "Genome sequencing of lymphoid malignancies." Blood 122, no. 24 (2013): 3899–907. http://dx.doi.org/10.1182/blood-2013-08-460311.

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Abstract Our understanding of the pathogenesis of lymphoid malignancies has been transformed by next-generation sequencing. The studies in this review have used whole-genome, exome, and transcriptome sequencing to identify recurring structural genetic alterations and sequence mutations that target key cellular pathways in acute lymphoblastic leukemia (ALL) and the lymphomas. Although each tumor type is characterized by a unique genomic landscape, several cellular pathways are mutated in multiple tumor types—transcriptional regulation of differentiation, antigen receptor signaling, tyrosine kin

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Dias, Francisca, Cristina Almeida, Ana Luísa Teixeira, Mariana Morais, and Rui Medeiros. "LAT1 and ASCT2 Related microRNAs as Potential New Therapeutic Agents against Colorectal Cancer Progression." Biomedicines 9, no. 2 (2021): 195. http://dx.doi.org/10.3390/biomedicines9020195.

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The development and progression of colorectal cancer (CRC) have been associated with genetic and epigenetic alterations and more recently with changes in cell metabolism. Amino acid transporters are key players in tumor development, and it is described that tumor cells upregulate some AA transporters in order to support the increased amino acid (AA) intake to sustain the tumor additional needs for tumor growth and proliferation through the activation of several signaling pathways. LAT1 and ASCT2 are two AA transporters involved in the regulation of the mTOR pathway that has been reported as up

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