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Assay strategies for identification of therapeutic leads that target protein trafficking. Trends Pharmacol Sci. Screening in a spirit haunted world. Apparent activity in high-throughput screening: origins of compound-dependent assay interference. Redox cycling compounds generate H 2 O 2 in HTS buffers containing strong reducing reagents-real hits or promiscuous artifacts? The essential roles of chemistry in high-throughput screening triage.

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Use of Epigenetic Drugs in Disease: An Overview

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The use of differential scanning fluorimetry to detect ligand inter-actions that promote protein stability. Nat Protoc. Recent developments in the use of differential scanning fluorometry in protein and small molecule discovery and characterization. Expert Opin Drug Discov. Evaluation of fluorescence-based thermal shift assays for hit identification in drug discovery. Anal Biochem. Biophysical screening for the discovery of small-molecule ligands.

Br J Hosp Med Lond. Breast Cancer Res. Flow cytometry for high-throughput, high-content screening. Novel fluorescence sensing methods for high throughput screening. Fluorescence anisotropy polarization : from drug screening to precision medicine. Screening technologies for small molecule discovery: the state of the art. Probes for biomolecules detection based on RET-enhanced fluorescence polarization.

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The development of high-content screening HCS technology and its importance to drug discovery. Bioluminescent assays for high-throughput screening. Photoproteins: important new tools in drug discovery. Seeing the light: luminescent reporter gene assays. Comb Chem High Throughput Screen. A cell-based high-throughput screen for novel chemical inducers of fetal hemoglobin for treatment of hemoglobinopathies. Development of an aequorin luminescence calcium assay for high-throughput screening using a plate reader, the LumiLux.

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Drug Discovery World (DDW), the Quarterly Business Review of Drug Discovery & Development

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Review ARTICLE

Targeting histone methyltransferases and demethylases in clinical trials for cancer therapy. Clin Epigen. Adverse epigenetic signatures by histone methyltransferase Set7 contribute to vascular dysfunction in patients with type 2 diabetes mellitus. Circ Cardiovasc Genet. Readers, writers, and erasers: chromatin as the whiteboard of heart disease. Circ Res. Histone demethylation catalysed by LSD1 is a flavin-dependent oxidative process. FEBS Lett. Human histone demethylase LSD1 reads the histone code.

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Expert Rev Hematol. Acetyl-lysine erasers and readers in the control of pulmonary hypertension and right ventricular hypertrophy. Biochem Cell Biol. Development of novel cellular histone-binding and chromatin-displacement assays for bromodomain drug discovery. Bromodomain Histone Readers and Cancer. J Mol Biol. Mol Oncol. Both conditions occur due to defects in the repair and replications of genomic DNA. CIN refers to a persistent high rate of chromosome missegregation, which leads to alterations in the increase or loss of chromosome numbers in colon cells.

CIN may originate from an event in mitosis leading to a chromosome error like a kinetochore defect, alterations in the spindle apparatus, chromosomal adhesion defect or mitotic spindle checkpoint defect. CIN can also occur due to an error in premitotic phases, such as cellular replication stress that may lead to an aberration in the chromosome structure and dysregulation of the centrosome leading to multipolar mitosis [ 26 ].

All these events, plus chromosome pulverization resulting from errors in mitosis, ultimately lead to a damage to the genomic stability of cells and the incorporation of errors in cellular genome replications [ 27 ]. Erroneous cytokinesis and subsequent pdependent confiscation of the cell result in the development of polyploidy in a cell, which leads to aneuploid daughter cells via multipolar mitosis [ 28 ]. Conversely, the loss of p53 may result in a polyploidy-multipolar mitosis-aneuploid cycle, which is highly detrimental to the genomic stability of the cells.

In addition, a MIN-type chromosomal modification or its underlying causes can also lead to mitotic errors and CIN [ 29 ]. According to a study by Dunican et al. Epigenetic alterations in colon cancer affect the expression of hundreds of genes. Probiotics, prebiotics and dietary phytometabolites such as polyphenols, phytoestogens, nonprotein amino acids and saponins, etc. Among the beneficial effects of probiotics observed in humans are the stimulation of gut immunity through various mechanisms, prevention of diarrhea and enhanced tolerance to lactose [ 35 ].

In addition, lactobacilli have other prohealth attributes, such as the synthesis of vitamin B, the improvement of mineral and nutrient absorption, and the degradation or removal of certain antinutritional phytometabolites [ 36 , 37 ]. However, the criteria for the selection of probiotics of human gut origin and traditionally fermented foods are somewhat empirical.

The selection is based on parameters like enhancing the host endogenous defense mechanisms by ameliorating the humoral immunity, and it is thus promoting the gut immunological barriers [ 38 ]. In addition, probiotics have been found to stimulate nonspecific resistance to invading pathogens [ 39 ], thereby aiding in modulating host immunity to harmful antigens with a potential to downregulate hypersensitivity reactions [ 40 ].

The expression and regulation of genes is highly dependent on and coordinated by nutrients, micronutrients and microbial metabolites [ 18 , 41 ]. Fiber and some fermentable oligosaccharides are subjected to gut microbial breakdown, resulting primarily in the production of short-chain fatty acids SCFAs , i. In addition, formate, valerate, caproate and branched-chain fatty acids, such as isobutyrate, 2-methylvalerate, and isovalerate, are also produced in low quantities from the catabolism of some branched-chain amino acids [ 42 ].

SCFAs are bioactive molecules and possess anti-inflammatory activities that play a vital role in the regulation of immune functions at the intestinal mucosal surface and are postulated to be important effector molecules with multiple roles. There is evidence for the ability of SCFAs to activate the apoptosis cascade and reduce the risk of cancer [ 43 ].

Studies have revealed that polyunsaturated fatty acids and volatile fatty acids usually interact and bestow protection against colon cancer [ 44 , 45 ]. SCFAs have been found to induce apoptosis, presumably related to epigenetic modification, cell cycle arrest and activation of proapoptotic cellular genes. Although the incorporation of fatty acids into CRC chemotherapy regimens is still in its infancy, evidence is accumulating to allow the identification of the length of fatty acid chains capable of exerting most effectively antineoplastic activity. The data on the effect of butyrate on colon cancer is extensive, but it cannot be considered conclusive.

Based on studies on the absorption and metabolism of SCFAs, the daily production of butyrate in the human large bowel is estimated to be more than mmol, which is readily absorbed across mucosa [ 46 ]. Based on observations in other species studied, it was inferred that human beings have a larger capacity for absorption and metabolism of SCFAs in the GI tract [ 46 ].

Three major pathways are involved in the uptake of butyrate in the GI tract: 1 diffusion of the undissociated form through lipid membranes of the distal colon, 2 countertransportation mediated by bicarbonate ions and 3 paracellular diffusion of the anionic form in the proximal colon [ 47 ]. It is believed that butyrate can minimize the incidence of CRC.

Clustering of SCFAs within the colonic lumen aids in maintaining a favorable low pH, which is vital for the effectiveness of numerous enzymes and for inhibiting the metabolism of carcinogenic agents in the gut [ 48 ]. SCFAs exert several other important health-promoting actions, such as lowering intestinal pH, acting as energy sources for colonocytes, the stimulation of colonic blood flow, contraction of smooth muscle cells, transepithelial chloride secretion and proliferation of colonic epithelial cells through various proliferative stimuli [ 49 ]. Evidence shows that dietary fibers and SCFAs lower the incidence of inflammatory bowel disease by decreasing the expression of proinflammatory cytokines induced by nuclear factor kappa B and by stimulating the absorption of sodium and water [ 50 , 51 ].

In addition, n-butyrate is also known to influence cell-specific gene expression in intestinal cells, thereby influencing immune responses and oxidative and metabolic stress [ 54 , 55 ]. Several lines of evidence indicate that SCFAs may serve as epigenetic drugs or HDAC inhibitors that play an important role as anticancer biomolecules with antiproliferative effects against tumor cells [ 56 , 57 ]. Fermented fecal supernatants were found to be rich in butyrate and propionate and to exhibit strong anti-HDAC activity in colon cancer cell lines [ 59 ].

The anti-HDAC activity was attributed to the disruption of processes involved in the generation of dendritic cells from bone marrow stem cells, primarily through associated sodium-coupled monocarboxylate transporter S1c5a8 -dependent inhibition of HDACs [ 60 ]. S1c5a8 is responsible for the transportation of butyrate and propionate into cells, and it is likely that these acids block the development of dendritic cell precursor cells [ 60 ]. Cohort studies have been unable to detect significant effects, but most case-control investigations advocate a protective role of probiotics in fermented dairy foods against colon cancer [ 61 ].

The majority of the anticarcinogenic effects of butyrate have been observed in vitro using cancer cell lines. In these models, the addition of butyrate has been found to inhibit cellular proliferation and to induce apoptosis, necrosis and differentiation of carcinoma cell lines [ 62 , 63 , 64 , 65 ].

Butyrate has also been shown to stimulate a physiological pattern of cellular proliferation in the basal crypts in the colon as well as a reduction in the number and size of aberrant cryptic foci, which serve as earliest detectable neoplastic lesions in colon carcinoma [ 66 ]. Butyrate reduces the expression of the genes cyclin D1 and c-myc, which are vital for the development of CRC [ 67 ].

An optimal anticancer drug would be one that destroys tumoral cells, but not healthy somatic cells. Another important mechanism by which butyrate interferes with colon carcinoma cells is the inhibition of HDAC, which leads to the hyperacetylation of histone residues. The aberrant histone acetylation leads to impaired transcription and silencing of genes involved in the control of cell cycle, differentiation and apoptosis [ 69 ].

As an HDAC inhibitor, butyrate increases the expression of p21 WAFI by selectively regulating the acetylation of gene-associated histones and by inducing cell cycle arrest at the GI stage [ 70 ]. Manipulation of the gut ecosystem through dietary probiotics and prebiotics to reduce the risk of colon cancers heralds niche areas of investigation in controlling gut disease [ 71 , 72 ]. Epigenetic modification, which refers to the methylation of DNA through the covalent addition of a methyl moiety to the nucleotide cytosine, has an important role in the regulation of gene expression.

Virtually every step of carcinogenesis or tumorigenesis is dependent on epigenetic modifications in the cellular genome. A few genes, called imprinted genes, are regulated by the methylation of CpG islands in their promoter. Volume 46 Issue 2. Volume 46 Issue 1. Volume 45 Issue Volume 45 Issue 9. Volume 45 Issue 8. Volume 45 Issue 7. Volume 45 Issue 6. Volume 45 Issue 5. Volume 45 Issue 4.

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The quest for an effective and safe personalized cell therapy using epigenetic tools

Volume 43 Issue 3. Volume 43 Issue 2. Volume 43 Issue 1. Volume 42A Issue 4. Volume 42A Issue 3. Volume 42A Issue 2. Volume 42A Issue 1. Volume 42 Issue 3. Volume 42 Issue 2. Volume 42 Issue 1. Volume 41 Issue 3. Volume 41 Issue 2. Volume 41 Issue 1. Volume 40 Issue 3. Volume 40 Issue 2. Submit Subscribe. This Journal. Quick Search in Journals Search this journal. Journal Menu. Review Translational Physiology. Galina Y.

Jagodic, Dept. This is the final version - click for previous version. Export citation Add to favorites Get permissions Track citations. Abstract Multiple sclerosis MS is a chronic inflammatory and demyelinating disease of the central nervous system. Calabrese et al. Kumagai et al. Graves et al. Decreased global 5hmC level and slightly increased 5mC level in MS. Maltby et al. Bos et al. DNA methylation difference between MS patients with different disease duration. Kulakova et al.

PPMS vs. Neven et al. No association between repetitive element methylation and MS course. Ayuso et al. No relationship of alternative promoter methylation level with MS clinical parameters. Ruhrmann et al. Mastronardi et al. Huynh et al. Correlation with expression of a portion of corresponding genes. Field et al. Download figure Download PowerPoint. The emerging role of 5-hydroxymethylcytosine in neurodegenerative diseases. Front Neurosci 8 : , Vitamin D receptor gene is epigenetically altered and transcriptionally up-regulated in multiple sclerosis. PLoS One 12 : e, Lower brain-derived neurotrophic factor in serum of relapsing remitting MS: reversal by glatiramer acetate.

J Neuroimmunol : —, Genome, epigenome and RNA sequences of monozygotic twins discordant for multiple sclerosis. Nature : —, PLoS One 10 : e, Smoking and risk of multiple sclerosis: evidence of modification by NAT1 variants. Epidemiology 25 : —, Butcher LM, Beck S. Probe Lasso: a novel method to rope in differentially methylated regions with K DNA methylation data. Methods 72 : 21—28, TET2 gene expression and 5-hydroxymethylcytosine level in multiple sclerosis peripheral blood cells.

Biochim Biophys Acta : —, Methylation-dependent PAD2 upregulation in multiple sclerosis peripheral blood. Mult Scler 18 : —, Transcriptional therapy with the histone deacetylase inhibitor trichostatin A ameliorates experimental autoimmune encephalomyelitis. J Neuroimmunol : 10—21, Acute treatment with valproic acid and l-thyroxine ameliorates clinical signs of experimental autoimmune encephalomyelitis and prevents brain pathology in DA rats.

Neurobiol Dis 71 : —, Epigenetics in multiple sclerosis susceptibility: difference in transgenerational risk localizes to the major histocompatibility complex. Hum Mol Genet 18 : —, Molecular and therapeutic potential and toxicity of valproic acid.

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J Biomed Biotech : , Crossref PubMed Google Scholar Genetic drivers of epigenetic and transcriptional variation in human immune cells. Cell : —, Evolving concepts in the treatment of relapsing multiple sclerosis. Lancet : —, Compston A, Coles A. Multiple sclerosis.

Functional annotation of the human brain methylome identifies tissue-specific epigenetic variation across brain and blood. Genome Biol 13 : R43, Immunopathology of multiple sclerosis. Nat Rev Immunol 15 : —, DNA methylation pathways and their crosstalk with histone methylation. Nat Rev Mol Cell Biol 16 : —, Comparison of Beta-value and M-value methods for quantifying methylation levels by microarray analysis. BMC Bioinformatics 11 : , Parent-of-origin effect in multiple sclerosis: observations in half-siblings. Expression of DNA methylation genes in secondary progressive multiple sclerosis.

J Neuroimmunol : 66—69, Genes Immun 18 : 59—66, Increased plasma levels of brain derived neurotrophic factor BDNF after multiple sclerosis relapse. Neurosci Lett : —, Gagliano SA. Biol Psychiatry 81 : —, DNA methylation changes of whole blood cells in response to active smoking exposure in adults: a systematic review of DNA methylation studies.

Clin Epigenetics 7 : , Neuronal cell injury precedes brain atrophy in multiple sclerosis. Neurology 62 : —, Vorinostat, a histone deacetylase inhibitor, suppresses dendritic cell function and ameliorates experimental autoimmune encephalomyelitis. Exp Neurol : 56—66, Analysis of DNA methylation in a three-generation family reveals widespread genetic influence on epigenetic regulation. PLoS Genet 7 : e, Application of nanomedicine for crossing the blood-brain barrier: Theranostic opportunities in multiple sclerosis.

J Immunotoxicol 13 : —, Abundant quantitative trait loci exist for DNA methylation and gene expression in human brain. PLoS Genet 6 : e, Total brain N-acetylaspartate: a new measure of disease load in MS. Neurology 54 : 15—19, Mult Scler 20 : —, A cell epigenotype specific model for the correction of brain cellular heterogeneity bias and its application to age, brain region and major depression. Epigenetics 8 : —, Active, phosphorylated fingolimod inhibits histone deacetylases and facilitates fear extinction memory.

Nat Neurosci 17 : —, Genome-wide methylation profiles reveal quantitative views of human aging rates. Mol Cell 49 : —, Smoking and two human leukocyte antigen genes interact to increase the risk for multiple sclerosis. Brain : —, SIRT1 as a potential biomarker of response to treatment with glatiramer acetate in multiple sclerosis. Exp Mol Pathol : —, DNA methylation contributes to natural human variation. Genome Res 23 : —, Nat Biotechnol 33 : —, Genome-wide association study identifies peanut allergy-specific loci and evidence of epigenetic mediation in US children. Nat Commun 6 : , DNA methylation arrays as surrogate measures of cell mixture distribution.

BMC Bioinformatics 13 : 86, Reference-free cell mixture adjustments in analysis of DNA methylation data. Bioinformatics 30 : —, Epigenome-wide differences in pathology-free regions of multiple sclerosis-affected brains. Analysis of immune-related loci identifies 48 new susceptibility variants for multiple sclerosis.

Nat Genet 45 : —, Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis. Neurons show distinctive DNA methylation profile and higher interindividual variations compared with non-neurons.


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    BMC Bioinformatics 18 : , Nat Genet 40 : —, Axonal metabolic recovery and potential neuroprotective effect of glatiramer acetate in relapsing-remitting multiple sclerosis. Mult Scler 11 : —, Mol Neurobiol 53 : —, Multiple sclerosis animal models: a clinical and histopathological perspective. Brain Pathol 27 : —, Differences in DNA methylation between human neuronal and glial cells are concentrated in enhancers and non-CpG sites.

    Nucleic Acids Res 42 : —, Substantial DNA methylation differences between two major neuronal subtypes in human brain. Nucleic Acids Res 44 : —, Kriaucionis S, Tahiliani M. Expanding the epigenetic landscape: novel modifications of cytosine in genomic DNA. Cold Spring Harb Perspect Biol 6 : a, Whole-genome DNA methylation analysis of peripheral blood mononuclear cells in multiple sclerosis patients with different disease courses.

    Acta Naturae 8 : —, Amsterdam: Elsevier, , p. Google Scholar Increased promoter methylation of the immune regulatory gene SHP-1 in leukocytes of multiple sclerosis subjects. J Neuroimmunol : 51—57, DNA methylation signatures within the human brain. Am J Hum Genet 81 : —,