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Choi, Jennifer Kristel. ""Open" chromatin : histone acetylation, linker histones & histone variants." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/45271.
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Man, Pui-sum Ellen. "Histone acetylation in gynaecological malignancies." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B31972068.
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Cervoni, Nadia. "DNA demethylation and histone acetylation." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=38166.
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Unlike in somatic cells, cancer cells adopt an aberrant pattern of methylation as well as histone acetylation, and therefore distort the chromatin structure. Chapters 2--4 of this thesis look at mechanisms carried out by the recently cloned DNA demethylase, how its demethylation activity is closely linked with the semblance of acetylation of chromatin, and how this relationship can be skewed in cancer. The three intriguing mechanisms described provide attractive models by which to explain general genome wide demethylation, site specific demethylation of genes upon their activation, and the relationship between aberrant methylation and histone acetylation in cancer. The thesis begins by characterizing the mechanism of demethylation carried out by the bona fida DNA demethylase---an enzyme identified and cloned in our laboratory found to demethylate both hemi and double-stranded DNA in vitro. This enzyme manifests the removal of methyl groups from DNA without damaging the DNA and is therefore a candidate protein responsible for hypomethylation seen during development as well as in transformed cells. One essential property of an enzyme that removes methylation from wide regions of the genome could be processivity. Southern blot analysis and sodium bisulfite mapping experiments determine that purified demethylase demethylates DNA in a processive manner in vitro. Experiments in Chapter 3 demonstrate how an active demethylase enzyme is involved in shaping patterns of methylation relative to the state of histone acetylation. We present evidence suggesting demethylase activity is directed by the state of histone acetylation, therefore contrasting the accepted dogma, and suggesting that the local histone acetylation state determines the resulting methylation pattern. Aberrant DNA methylation and histone deacetylation are frequently associated with silencing of tumor suppressor genes in cancer and yet cannot simply be explained by the level of methyltransferase(s) enzyme(s)
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Man, Pui-sum Ellen, and 萬佩心. "Histone acetylation in gynaecological malignancies." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B31972068.
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Venkataraman, Shanmugasundaram. "Histone acetylation and nucleosome dynamics." Thesis, University of Edinburgh, 2001. http://hdl.handle.net/1842/23234.
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In this report, I will describe purification of core histone octamers from chicken blood, HeLa nuclei and yeast cells, along with preparation of DNA fragments containing the 208 bp 5S rDNA gene and the adult beta (bA)-globin gene promoter. In vitro experiments studying the effect of histone acetylation on the positioning and mobility of nucleosomes on the sea urchin 5S rDNA gene and the chicken bA-globin gene promoter will be described. The former provides a well studied nucleosome positioning and mobility model system, while the latter is a developmentally regulated gene, with globin gene switching through the early stages of the lifetime of the chicken, and a proposed involvement of positioned nucleosomes in its regulation. The aim was to determine the difference between hypoacetylated and hyperacetylated core histones in terms of their influence upon nucleosome positioning and mobility. In earlier studies, it was noted that there was a difference in relative positioning intensities between the two forms (ie. hypoacetylated core histones preferentially positioned at certain sites, while hyperacetylated core histones positioned at the same sites but with different relative affinities). Therefore, acetylation affects where a nucleosomes is able to position. I have carried on this work to further characterize nucleosome positioning and to study the implications of histone acetylation on nucleosome mobility. I have found subtle differences in the thermodynamics and kinetics of hyperacetylated nucleosomes compared to hypeoacetylated nucleosomes: hyperacetylated nucleosomes appear to have a lower threshold in both these parameters when studied using the 208 pb rDNA fragment. Experiments involving two other types of core histones, trypsinized chicken core histone octamers and chicken core histone tetramers will also be described, which will be placed into the context of the results found with the other types of core histones. Finally, I will describe the effect of reconstituting hyperacetylated core histones with methylated DNA, long known to be a mediator of transcriptional repression, in the form of the chicken bA-globin gene promoter.
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Hebbes, T. R. "Histone acetylation and transcriptionally active chromatin." Thesis, University of Portsmouth, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382541.
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Clayton, Alison Louise. "Core histone acetylation of active genes." Thesis, University of Portsmouth, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240358.
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Choudhury, Mahua Shukla Shivendra D. "Alcohol induced histone acetylation mediated by histone acetyl transferase GCN5 in liver." Diss., Columbia, Mo. : University of Missouri-Columbia, 2008. http://hdl.handle.net/10355/6866.
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The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from PDF of title page (University of Missouri--Columbia, viewed on April 6, 2010). Vita. Thesis advisor: Shivendra D. Shukla. "August 2008" Includes bibliographical references
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Ou, Jing Ni. "Epigenetic crosstalk between DNA demethylation and histone acetylation." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32413.
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Abnormal methylation patterns such as regional hypermethylation and genomic hypomethylation often result in transcriptional changes of critical genes that are central to the progression of human cancers. It is therefore important to identify the mechanisms that are responsible for the alterations in order to identify proper pharmacological targets. This thesis examines whether specific cellular factors are involved in establishing the state of DNA hypomethylation in cancer cells and whether changes in chromatin structure could affect DNA methylation. MBD2 is a protein that has been previously characterized to possess distinct transcription activities; it can either function as a methylation-dependent transcription repressor, a methylation-independent transcription activator, as well as an inducer of DNA demethylation. Chapters 3 and 4 demonstrate that MBD2 induces gene-specific DNA demethylation in pancreatic and bladder cancer cells by recruiting transcriptional activator AP-2, Sp1 and the histone acetyltransferase CBP to the associated promoters. These results substantiate the idea that demethylation induced by MBD2 might facilitate the recruitment of transcription factors to the gene to activate its expression. Histone deacetylase (HDAC) inhibitors are drugs designed to target chromatin modification. In chapter 5, we showed that increasing histone acetylation by HDAC inhibitor TSA was associated with a significant decrease in global methylation. TSA also induces histone acetylation, DNA demethylation and expression of specific methylated tumor suppressor genes, such as E-CADHERIN and RARβ2 in different human cancer cell lines. Our findings provide evidence for aUn patron de méthylation anormal, tel que l'hyperméthylation régionale ou l'hypométhylation génomique, modifie la transcription de gènes critiques jouant ainsi un rôle central dans la progression de nombreux cancers chez l'humain. Il est donc devenu essentiel d'identifier les mécanismes responsables de ces altérations afin de développer des traitements pharmacologiques ciblés. Le but principal de cette thèse est d'examiner si certains facteurs cellulaires sont impliqués dans l'établissement de l'ADN hypométhylé des cellules cancéreuses, ainsi que l'effet des changements dans la structure de la chromatine sur la méthylation de l'ADN. Il a été préalablement démontré que la protéine MBD2 possède plusieurs rôles distincts lors de la transcription, elle peut agir à la fois comme un répresseur de la transcription dépendant de la méthylation, comme un inducteur de la déméthylation ainsi qu'un activateur de la transcription indépendant de la méthylation. Les chapitres 3 et 4 présentés dans cet ouvrage démontrent que MBD2 induit la déméthylation de gènes spécifiques dans les cellules cancéreuses pancréatiques et urinaires grâce au recrutement des activateurs transcriptionnels AP-2, Sp1 ainsi que de l'histone acétyltransférase CBP au promoteur impliqué. Ces résultats supportent l'hypothèse selon laquelle la déméthylation induite par MBD2 faciliterait le recrutement de facteurs de transcription au sein du gène afin d'activer son expression. Les inhibiteurs de l'Histone déacétylase (HDAC) sont des drogues pharmaceutiques développées afin de cibler les modifications de la chromatine. Nous sommes parvenus à démontrer, dans le
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Smith, Anna Elizabeth. "The role of histone acetylation in recognition memory." Thesis, University of Bristol, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.715770.
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Jin, Yi. "Genetic and genomic studies of histone H3 methylation and acetylation." Pullman, Wash. : Washington State University, 2008. http://www.dissertations.wsu.edu/Dissertations/Fall2008/Y_Jin_120108.pdf.
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Pourhanifeh-Lemeri, Roghayeh. "Identification of Non-histone Acetylation Targets in Saccharomyces cerevisiae." Thesis, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/22885.
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Lysine acetylation is a conserved post-translational modification (PTM) which was traditionally believed to be limited to histones and the regulation of gene expression. However, recent proteomic studies have identified lysine acetylation on proteins implicated in virtually all cellular processes indicating that this PTM plays a global regulatory role. Indeed, in humans, aberrance of lysine acetyltransferase (KAT) activity is associated with various pathogenesis. To date, over 2500 human proteins are known to be acetylated in vivo, but very few acetylations have been linked to specific KATs. Hence, to understand the biological relevance of KATs and acetylation in human pathology, it is important to learn about the mechanism regulating KAT activity and the identity of their in vivo targets. This is a complex task and will require the use of model organisms and system biology approaches. The work presented here explores the significance of self-acetylation in regulating KAT function by focusing on the highly NuA4 lysine acetyltransferase in the model organism Saccharomyces cerevisiae or budding yeast. Using genetics and biochemical assays I have identified NuA4 subunit Epl1 as a novel in vivo NuA4 substrate. I have also shown that Epl1 acetylation regulates NuA4 function at elevated temperatures. In an attempt to identify new biological processes regulated by yeast KATs and putative novel substrates, I have also performed a genome-wide synthetic dosage lethality screen with six non-essential yeast KATs; Hat1, Rtt109, Hpa2, Sas3, Sas2, and Elp3. My screen identified largely distinct sets of genetic interactions for each KAT suggesting that each KAT has specific cellular functions. Together, this study demonstrates the importance of auto-acetylation in regulating KAT function and the diversity of cellular processes impacted by KAT activity in vivo.
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Crosato, Milena. "Characterization of histone acetylation in butyrate-resistant HeLa cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0033/MQ64337.pdf.
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Crosato, Milena. "Characterization of histone acetylation in butyrate-resistant HeLa cells." Thesis, McGill University, 1999. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=30361.
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Butyrate is a short chained fatty acid that induces histone hyperacetylation by inhibiting histone deacetylases. This hyperacetylation of histones then leads to a change in chromatin conformation and transcription of genes. Histone deacetylases have recently been found to directly affect gene expression by associating with transcriptional repressor complexes. The present thesis describes the initial characterization of histone deacetylase activity in variants of HeLa cells that are capable of growth in cytotoxic concentrations of butyrate. Analysis of acetylation levels of total histones by triton-acid-urea gels indicated that the histone deacetylases in the variants are less sensitive to the effects of histone deacetylase inhibitors than the parental HeLa cells. Control experiments showed that this resistance was not due to the transport of butyrate into the cell nor from the overexpression of HDAC1 or HDAC2, further suggesting that the resistance to butyrate is due to an alteration in a gene encoding HDAC.
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Tsaprouni, Loukia G. "Histone acetylation and inflammatory mediators in inflammatory bowel disease." Thesis, University of Bedfordshire, 2003. http://hdl.handle.net/10547/620761.
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During cell activation the tightly compacted DNA is made available to DNA-binding proteins allowing the induction of gene transcription. In the resting cell, DNA is packaged into chromatin whose fundamental subunit is the nucleosome, composed of an octamer of four core histones (H) 3, 4, 2A and 2B. During the induction of gene transcription, modification of histones, by acetylation, methylation etc., results in unwinding of the DNA, permitting access of large DNAbinding proteins, such as RNA polymerase II, and subsequent induction of gene transcription. This investigation initially examined the effects of pro-inflammatory stimuli LPS and TNF-a on the production of IL-8 in a macrophage cell line (U937 cells) and in two T-cell lines (Jurkat and HUT-78 cells) as a marker of NF-KB-directed inflammatory gene expression. The ability of dexamethasone (Dex) and triamcinolone acetonide (TA) (synthetic glucocorticoid agonists) to suppress expression of the inflammatory cytokine IL-8 and to regulate histone acetylation was also investigated in these cells. LPS and TNF-a caused an increase in IL-8 expression, which was further enhanced by the histone deacetylases inhibitor trichostatin A (TSA), suggesting a role for histone acetylation in IL-8 production in these cells. Dex and TA, repressed LPS- and TNF-a -induced IL-8 expression in all three cell lines. This effect of both Dex and TA was attenuated by TSA in all cell lines studied, where the effect of TSA was greater in TA stimulated cells. Stimulation of all cell lines with LPS and TNF-a induced acetylation of H4 lysine residues (K5, 8, 12 and 16), the highest elevation of which was for K8 and K12. Also demonstrate is a K5 and K16 specificity of acetylation by glucocorticoids, apparent in all cell lines studied. Dex and, to a greater extent, TA suppressed LPS- and TNFa-induced K8 and K12 acetylation. TSA attenuated the inhibitory effect of the glucocorticoids for all three cell lines. An inCrease in HDAC activity with GCs was observed and ChiP assay showed these events occur on the native IL-8 promoter via histone acetylation. Further studies investigated whether there were any links between histone acetylation and the regulation of apoptosis. It was showed that TSA induced apoptosis in cells previously stimulated with the inducer of oxidative stress hydrogen peroxide (H20 2). Studies into the activation of caspase 3 in LPS- and TNF-a stimulated cells revealed that the combinatory effect of Dex or TA with TSA Significantly enhanced expression of the marker in all three cell lines. In resting cells, Dex, and TA, in the presence of TSA downregulated caspase 3 expression. These findings support the notion that glucocorticoid actions on apoptosis is mediated, at least in part, through an action on histone acetylation. Finally, histone acetylation was investigated in vivo in two rat models of inflammation and in human subjects with inflammatory bowel disease (IBD). The results showed an increase in histone H4 acetylation lysine specificity of acetylation on K8 and K12 in inflamed tissue and Peyer's patches in animal models and in IBD patients. Whereas H3 acetylation was not elevated to the same extent in tissue and was restricted to the mantle zone of Peyer's patches. In general, the present studies on histone acetylation and inflammation (in animal models and IBD patients) underlined the possibility of a general mechanism linking activation of the transcription factor NFKB with histone acetylation. The ultimate objective of this work is to aid in the understanding of the mechanisms of how deregulation of chromosome structure leads to progression of the disease state. This knowledge may aid in the development of new therapeutic approaches or improved glucocorticoids.
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Carey, Krystle Lea. "The search for small molecule inhibitors of histone acetylation." Thesis, University of Southampton, 2010. https://eprints.soton.ac.uk/173969/.
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Histone acetylation is a key mechanism of transcriptional regulation, which is mediated by two sets of enzymes; HATs and HDACs. Under normal physiological circumstances there is an orchestrated balance between the actions of HATs and HDACs. Disruption of this balance can lead to a number of cellular events which can cause the onset of various diseases for example cancer and HIV. The search for small molecule inhibitors of histone acetylation focuses on anacardic acid and the azumamides. Anacardic acid is a natural compound found in cashew nut shell liquid. Its structure consists of salicylic acid and a long hydrophobic alkyl tail, which suggests that the compound would be rather insoluble and unable to permeate cells. However, it has been discovered that anacardic acid has micro molar HAT inhibitory activity towards the HATs PCAF and p300 and is able to suppress cancer cell growth. In contrast, the azumamides are a series of cyclic tetrapeptides that were discovered in Mycale izuensis, a Japanese marine invertebrate. Azumamides A-E exhibit nano molar HDAC inhibitory activity and cytotoxic effects. This report details the synthesis of anacardic acid by Suzuki coupling and the application of the Mitsunobu synthesis to generate a series of anacardic acid analogues. In vitro biological assays were used to assess the potency of anacardic acid and forty four analogues towards cancer cell growth inhibition, HAT, xanthine oxidase, luciferase and p21 reporter activity. Analogue KC_19 was identified to inhibit HAT and xanthine oxidase activity with equivalent potency to anacardic acid. KC_39 (IC50 = 18.2 ± 2.6 μM) was the most potent analogue in the MCF7 cell growth inhibition but it showed no evidence of HAT inhibition. Analogue KC_14 was determined in terms of ease of synthesis, MCF7 growth inhibition (IC50 = 52.4 ± 4.5) and PCAF inhibition (IC50 = 31.7 ± 5.0 μM) to be the best anacardic acid analogue overall. The report ends with a small investigation in the inhibition of HDACs by the azumamides A, E and three novel azumamides. The azumamide hydroxamic acid was discovered to be potent inhibitor of HeLa HDAC activity (IC50 = 7.0 ± 2.5 nM).
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Hammond, Colin. "The structural analysis of histone H3 lysine 56 acetylation and related histone chaperone complexes." Thesis, University of Dundee, 2013. https://discovery.dundee.ac.uk/en/studentTheses/2e55b2c4-4821-4961-b4bb-eae1b24a446e.
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Sherman, Robyn. "Regulation of Histone H3 Proteolysis by Acetylation in Tetrahymena thermophila." Scholarship @ Claremont, 2015. http://scholarship.claremont.edu/scripps_theses/598.
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Chromatin is the combination of DNA and proteins in the nucleus that is used to aid in the compaction of DNA. Histones are a group of proteins used to condense DNA by forming a complex (nucleosome) around which DNA wraps around; there are two of each type of histone in a nucleosome: H2A, H2B, H3 and H4. Once the DNA is wrapped around the histones, the genome is further compacted. A shortened, "clipped" version of histone H3 has been found in some organisms including yeasts, flies, mammalian stem cells, and the ciliated protozoan, Tetrahymena thermophila. In each organism, clipping occurs at a different site on the N-terminus, usually before an alanine residue. Clipping is important as it may affect other epigenetic modifications and gene regulation in cell differentiation, but the regulation of this histone proteolysis has remained largely unstudied. In Tetrahymena thermophila, approximately half of the histone H3 molecules are clipped between residues 6 and 7 on histone H3, solely in the transcriptionally silent micronucleus. The histones in the micronuclei are deacetylated, while histones in the macronuclei can be acetylated or deacetylated. It is hypothesized that the post-translational acetylation modification to the histone tails may inhibit histone H3 clipping. Immunoblot analyses were carried out with acetylated and deacetylated micronuclei, demonstrating an increase of clipping when acetylated. Additionally, mutations were created at lysine 9 upstream of the clip site on the histone H3 tails to mimic acetylation and deacetylation to study whether the modification of that site has a regulatory effect.
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Siriaco, Giorgia. "Relationship between histone acetylation and the transcriptional activity of genes." Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/12953.
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Naiyachit, Yanin. "Global analysis of histone variant H2A.Z acetylation in Saccharomyces cerevisiae." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/global-analysis-of-histone-variant-h2az-acetylation-in-saccharomyces-cerevisiae(47129712-8f67-427f-bb7a-50e4e91260db).html.
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The histone variant H2A.Z is an evolutionarily conserved variant which is an essential chromatin component for many organisms. H2A.Z plays a pivotal role in a diverse array of chromatin-based processes such as gene transcription and chromosome segregation. In yeast, H2A.Z is acetylated at four N-terminal lysine residues (K3, K8, K10 and K14). Previous studies have shown that these acetylation sites are critical for H2A.Z function. My research aim was to examine how these four acetylatable lysines act to regulate the function of H2A.Z. Genome mapping of the acetylated K8, K10, K14 isoforms revealed that these acetyl marks are co-localised across the budding yeast genome, indicating that acetylation is a common feature of H2A.Z. Examinations of individual acetylation sites using mutational and phenotypical analyses did not reveal any distinct phenotypes between individual lysine residues. These findings indicated that individual acetylation sites are functionally redundant. Intriguingly, H2A.Z is mis-regulated when all four lysine were mutated to arginine (H2A.Z K3, 8, 10, 14 R) by showing sensitivity to a variety of agents. The global distribution profiles of H2A.Z, however, were unaffected by N-terminal lysine mutations. In fact, unacetylatable H2A.Z alleles perturbed H2A.Z chromatin abundance. Biochemical evidence showed that the altered chromatin level was severely defective when combined unacetylatable allele with mutations of SWR-C components. Together, the data presented here suggested that the N-terminal acetylation of H2A.Z regulates its genome abundance independent of its deposition pathway by SWR-C complex.
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Taylor, Gillian Catherine Agnes. "H4K16 acetylation during embryonic stem cell differentiation." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8069.
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Eukaryote DNA is organised into the more compact nucleosome by wrapping 147bp of DNA around a histone octamer core. The N-terminal tails of the histones protrude through the DNA and can be modified by a variety of enzymes. Acetylation of Histone 4 Lysine 16 (H4K16ac) is an important modification associated with an increase in transcription, and in flies is an important component of the doseage compensation system. It is also unique amongst histone modifications in that it has been directly associated with chromatin decompaction. H4K16ac has been linked to development through its Histone Acetyltransferase, MOF. Deletion of MOF in mice leads to mass chromatin defects, and embryonic lethality prior to the blastocyst stage. I set out to understand the role of H4K16ac in differentiating Embryonic Stem cells (ES cells) and chromatin compaction in vivo. I generated a ChIP-seq profile for H4K16ac in undifferentiated ES cells, and after 3 days of retinoic acid (RA) differentiation. This revealed an association of H4K16ac with the promoters of transcribed genes in pluripotent ES cells, followed by loss H4K16ac on ES cell specific genes and gain of the modification on differentiation specific genes. There were some silent genes in ES cells, however, which were acetylated on their promoters. Through this study I also found that H4K16ac and MOF mark active enhancers in ES cells, along with H3K4me1 and H3K27Ac and p300. H4K16ac did not mark a known regulatory region in limb cells, and it is possible that it marks active enhancers only of ES cells. Furthermore, I looked at the compaction state large regions (>100kb) which lost H4K16ac upon differentiation by FISH, to determine if loss of H4K16ac could predict compaction. The regions selected showed no change in compaction state between UD and D3 cells, meaning that loss of H4K16ac does not directly lead to chromatin compaction in vivo. However loss of H4K16ac may be necessary for any subsequent compaction, or the change in compaction may take place at nucleosomal level. Finally, I attempted both to overexpress and reduce the level of MOF in ES cells. I was unable to manipulate the level of MOF in this cell type in either direction; expression of endogenous MOF was silenced after very little time, and stable MOF shRNA cell lines showed no reduction in levels of MOF. Therefore, potentially, dosage of MOF/H4K16ac in this cell type is critical. This study may help to understand the significance of H4K16ac in ES cell differentiation and chromatin compaction.
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Ladipo, Paul B. "The effects of histone acetylation on the maize allele PL1-blotched." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/5038.
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Thesis (M.A.)--University of Missouri-Columbia, 2007.The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on September 29, 2008) Includes bibliographical references.
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Orr, Jenny Alexandra. "Chromatin phenotype and the role of histone acetylation in prostate cancer." Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426718.
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Yau, Peter Mo-Ping. "Structural analysis of the nucleosome and the effects of histone acetylation." Thesis, Liverpool John Moores University, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261657.
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Manohar, Mridula. "Chemically Modified Histone H3 to Study Acetylation at the Nucleosome Dyad." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1243525554.
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Agudelo, Garcia Paula A. "Identification of New Roles for Histone Acetyltransferase 1." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1492599746298382.
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Qin, Song. "Acetylation of histone n-terminal tails contributes to DNA double strand break repair." The Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=osu1134575402.
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Randall, Tamzin Ellen. "The role of histone acetylation in the imprinted expression of IGF2-H19." Thesis, University of Birmingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270059.
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Rose, Sally Louisa. "Phosphorylation and acetylation of histone H3 concomitant with immediate early gene induction." Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251624.
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Greenberger, Benjamin A. "Combined Effect of Histone Acetylation and Acetyl Mark Readers on Radiation Sensitivity." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:27007761.
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We are interested in studying potential drugs that have the ability to make tumors more sensitive to radiation. There has been much interest in examining the effect of modulation to chromatin structure on the DNA damage response (DDR). We therefore examined histone deacetylase (HDAC) inhibitors, small molecules that modify the structural features of chromatin involved in the packaging of DNA. HDAC inhibitors are considered to be potential drug candidates to complement radiation therapy, yet the mechanisms underlying their effects have been elusive.
To study the DDR signaling effects of HDAC inhibitors, we developed a high-throughput automated microscopy assay to assess effects on elements of DNA damage-mediated signaling through quantification of H2AX phosphorylation, cell cycle profiling, and cell survival following irradiation. We then applied this assay to a library of diverse HDAC inhibitors as well as a collection of shRNAs targeting the individual HDACs. We next assessed DSB induction and repair kinetics on a selection of active HDAC inhibitors with CometChip, a novel high-throughput adaptation of the single-cell DSB comet assay. Finally, with the recent discovery of the role of the bromodomain chromatin reader protein Brd4 in the insulation of chromatin from the DDR, we explored combinatorial use of HDACi and JQ1 to achieve altered DDR through simultaneous alteration of chromatin structure and acetyl-lysine reading.
Our data suggest that class I HDAC inhibitors potently elevate H2AX phosphorylation, but without strong effects on DSB induction or repair kinetics. We find that many HDAC inhibitors also enhance G2/M cell cycle arrest and decrease proliferation, even in the absence of irradiation. These data suggest that HDAC inhibitors influence radiation effects primarily through altering DNA damage-induced signaling events. We have also found that overexpression of specific Brd4 isoforms can abrogate the elevated H2AX phosphorylation induced by HDAC inhibition and lead to preferential cell death. This may have important implications for the clinical use of these agents.
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Yildirim, Ferah [Verfasser]. "Involvement of histone acetylation in neuroprotection against brain ischemic injury / Ferah Yildirim." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2010. http://d-nb.info/1024502422/34.
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Hamed, Munerah. "Effect of p300 HAT Activity on Myogenic Differentiation." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23707.
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Skeletal muscle specification and differentiation programs are regulated by the myogenic regulatory factors which include Myf5, MyoD, myogenin and Mrf4. Upstream of the MRFs, the transcription co-activators and other intracellular and extracellular signals play crucial roles in regulating skeletal myogenesis. Histone acetyltransferase activity of p300 is required for Myf5 and MyoD expression. Furthermore, the MyoD core enhancer region is indispensable for MyoD expression. However, the mechanism by which p300 activates MyoD gene expression is to be determined. The histone acetyltransferase activity of p300 can be inhibited by small molecule inhibitors such as curcumin. Thus, using the inhibitor approach on stem cells is useful to investigate the role of p300 in activating MyoD expression during myogenesis. We here show that curcumin was able to inhibit stem cell determination and differentiation into skeletal myocytes. We also show that p300 is present, and histone acetylation is high at the core enhancer region. Therefore, we provide evidence that p300 is directly involved in MyoD gene expression during skeletal myogenesis.
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Danilenko, Nataliya [Verfasser]. "Structural basis for histone H3 acetylation by Rtt109 in complex with histone chaperones Asf1 and Vps75 / Nataliya Danilenko." Hannover : Gottfried Wilhelm Leibniz Universität Hannover, 2020. http://d-nb.info/1209268515/34.
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Tuttle, Camilla Susannah Laura. "The expression of HAT and HDAC enzymes in asthma airways." Thesis, Queensland University of Technology, 2013. https://eprints.qut.edu.au/62873/1/Camilla_Tuttle_Thesis.pdf.
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Asthma is chronic inflammatory disease of the lower airways that is both, genetically inherited and environmentally influenced. This project investigated how molecular mechanisms known to be influenced both genetically and environmentally, contribute to the onset of asthma.
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Wu, Jheng-Yu. "Regulation of Extracellular Signal-Regulated Kinase by Histone Deacetylase 6." Scholar Commons, 2017. http://scholarcommons.usf.edu/etd/6985.
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Extracellular signal-regulated kinases 1/2 (ERK1/2) are important kinases regulating cell proliferation and cell migration, and have been established as therapeutic targets for cancer treatment. Previously, we found that ERK1 phosphorylates histone deacetylase 6 (HDAC6) to regulate its enzymatic activity. However, whether HDAC6 reciprocally modulates ERK1 activity is unknown. Here, we have discovered that ERK1/2 are acetylated proteins and shown that HDAC6 manipulates ERK1’s kinase activity via deacetylation. We demonstrated that both ERK1 and ERK2 interact with HDAC6 physically. We showed that the acetylation level of GST-ERK1/2 increased in a dose- and time-dependent manner upon treatment with a pan-HDAC inhibitor, Trichostatin A. Furthermore, the treatment by HDAC6-specific inhibitor, ACY-1215, also increased the level of acetylated GST-ERK1/2. We also noted that ERK1/2 acetylation levels increased in HDAC6-knockout mouse embryonic fibroblasts and in HDAC6-knockdown A549 cell lines compared with controls. In addition, we determined that acetyltransferases CBP and p300 acetylate ERK1/2. We have identified novel acetylation sites located in ERK1 and ERK2 by mass-spectrometry analysis. Among these acetylation sites, ERK1 lysine 72 acetylation status is related to ERK1 phosphorylation. The acetylation-mimicking mutant exhibits a decreased kinase activity toward ELK1, while the deacetylation-mimicking mutant exhibits a similar level of kinase activity as the wild-type ERK1, suggesting that acetylation/deacetylation alters ERK1 enzymatic activities. Taken together, our results suggest that HDAC6 may regulate ERK1’s kinase activity via deacetylation of its lysine 72 residue.
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Tong, Kevin. "Characterization of the Schizosaccharomyces Pombe Hat1 Complex: the Role of Histone H4 Acetylation in Telomeric Silencing." Thesis, Boston College, 2009. http://hdl.handle.net/2345/2222.
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Thesis advisor: Anthony T. AnnunziatoThesis advisor: Charles Hoffman
The Hat1 complex was characterized in S. pombe. Through tandem affinity purification and mass spectrometry, it was determined that Hat1 is associated with Mis16 (an orthologue of HAT2). Unlike HAT2 in S. cerevisiae, we confirm mis16 to be an essential gene in S. pombe. As expected, the S. pombe Hat1 complex was found to acetylate lysines 5 and 12 of histone H4. In contrast to budding yeast, deletion of hat1 alone resulted in the loss of telomeric silencing without concomitant mutations of the H3 N-terminal domain. Deletion of hat1 caused an increase of H4 acetylation at telomeres. Additionally, the hyperacetylation of histones also results in the loss of telomeric silencing. Loss of Hat1 did not affect silencing at the inner most repeat (imr) or outer repeat (otr) regions of the centromere, but did appear to increase silencing at the central core region (cnt) of the centromere. The experiments described herein demonstrate Hat1 to be essential for the establishment of proper telomeric silencing in fission yeast, and suggest that the timely acetylation of H4 during chromatin assembly is a unique factor in generating the correct epigenetic state at telomeres in S. pombe. Additionally, Hat1 and its acetylation of new H4 may have entirely different roles during telomeric silencing than during silencing at the centromeric central core. Our studies in HeLa cells demonstrated that transcription is involved in the exchange of H2A/H2B in acetylated chromatin regions. The finding that cytosolic H2A can be acetylated at lysine 5 is the first demonstration that cytosolic H2A can be specifically modified in vivo. Our results support a model in which H2A/H2B exchange during transcription is mediated by the NAP1 chaperone
Thesis (PhD) — Boston College, 2009
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Biology
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Alzoubi, Samer. "Histone acetylation and chemoresistance in colorectal cancer : an opportunity for effective personalized treatment." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/11581.
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Colorectal cancer (CRC) is the most common cause of deaths in the West. Despite many therapeutic opportunities, drug resistance or recurrence has significant rates among patients. Nearly 50% of CRC patients develop metastases. Therefore, sensitive biomarker and effective treatments with minimal toxicity are needed. Genetic and epigenetic alterations play major roles in initiation, development, and chemoresistance of CRC. Histone deacetylase2 (HDAC2) over-expression is well-known in CRC. Many studies have associated HDAC2 over-expression and TP53 mutations with late stages of metastatic CRC (mCRC). However, the relationship between HDAC2 expression level and TP53 status and mCRC drug resistance is unclear. Here, I have investigated HDAC2 role in drug resistance and assessed the synergistic effects of DNA chemotherapeutics agents and HDAC inhibitors (HDACIs) on TP53 status in mCRC cell lines. I have shown for the first time that in mutated p53 mCRC cells (Sw480 and HT-29) the steady-state level of HDAC2 is low compared to wild-type p53 cells (HCT116 p53+/+). I have also found that increase in HDAC2 expression level in the highly resistant cell line HT-29 enhances drug resistance and its depletion by shRNA sensitises HT-29 to 5Fluorouracil (5FU) or Oxaliplatin (Oxa). The combined treatment of suberoylanilide hydroxamic acid (SAHA)/5FU and SAHA/Oxa was able to reduced HDAC2 expression level and induced mitotic cell death. However, SAHA/Doxorubicin combined treatment induced cell death in wild-type p53 (HCT116 p53+/+), null p53 (HCT116 p53-/-), and SW480 cell lines. This cell death associated with decrease in HDAC2 level. I have shown the association between sensitivity to treatment and reduction of HDAC2 level via bioluminescence imaging in combination with liposomal-encapsulated SAHA/Doxorubicin delivery to monitor tumour growth. I have observed a significant decrease in tumour growth and HADC2 level. Therefore, I suggest that unlike mutated p53, HDAC2 could be an epigenetic prognostic biomarker to predict therapeutic response in mCRC.
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Dobosy, Joseph R. "Involvement of histone deacetylases in DNA methylation in Neurospora crassa, and characterization of four other histone acetylation associated genes /." view abstract or download file of text, 2003. http://wwwlib.umi.com/cr/uoregon/fullcit?p3102161.
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Thesis (Ph. D.)--University of Oregon, 2003.Typescript. Includes vita and abstract. Includes bibliographical references (leaves 91-96). Also available for download via the World Wide Web; free to University of Oregon users.
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Chen, Chang-Shi. "Beyond induction of histone acetylation the multi-facets of the antineoplastic effect of HDAC inhibitors /." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1164649581.
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Lim, Sean. "The Relationship Between Metabolic Circumstance and Epigenetic Acetylation in Myoblast Fate and Function." Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/42659.
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Muscle tissue is grown and maintained by muscle stem cells termed satellite cells. Activated satellite cells become myoblasts, which must proliferate then differentiate into functional muscle. This process, known as myogenesis, is controlled by a cascade of epigenetic regulatory events. One facet of this regulation is histone acetylation, which can be influenced by the availability of metabolites within a cell. In this study, the ability of glucose, pyruvate, or glutamine to change histone acetylation levels in cultured myoblasts was investigated. Changing concentrations of glucose or pyruvate had no effect but decreasing the availability of glutamine in cell culture from 2mM to 0.2mM resulted in proliferating myoblasts accruing a hyperacetylated histone phenotype. However, when the same concentration of glutamine was used on differentiating myoblasts the hyperacetylated phenotype was lost and no change to differentiation was observed. This study demonstrates the potentials and limitations of altering epigenetic acetylation with metabolic circumstance. -- Le développement du tissu musculaire est soutenu par les cellules souches musculaires, communément appelées cellules satellites. Les cellules satellites activées se transforment en myoblastes qui doivent ensuite proliférer et se différencier en muscle fonctionnel. Ce processus, connu comme myogenèse, est contrôlé par une cascade de régulation épigénétique. Un aspect de ce processus est l’acétylation d’histones, qui peut être influencée par la disponibilité de métabolites dans la cellule. Dans cette étude de cas, la capacité du glucose, pyruvate, ou glutamine à changer les niveaux d’acétylation d’histones a été examinée. Le changement des concentrations de glucose ou de pyruvate n’a généré aucun effet, mais la diminution de la disponibilité de la glutamine dans la culture cellulaire de 2mM à 0.2mM a eu pour résultat une prolifération de myoblastes présentant un phénotype d’histones hyper-acétylées. Pourtant, quand la même concentration de glutamine a été utilisée pour différencier les myoblastes, le phénotype hyper-acétylé n’a pas été observé et aucun changement de différenciation n’a pu être détecté. Cette étude démontre le potentiel et les limites des modifications de l’acétylation épigénétique selon les circonstances métaboliques.
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Politis, Panagiotis K. "The role of chromatin in the regulation of PHO5 and PHO3 genes in Saccharomyces cerevisiae." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343632.
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Basford, Joshua E. "Colinear Expression of the Mouse HoxB Cluster: Potential Regulatory Role of Histone H4 Acetylation." University of Cincinnati / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ucin997988435.
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Juliano, Camila Nóbrega. "Avaliação do padrão de acetilação das histonas por técnica imunohistoquímica em adenocarcinoma de pâncreas : influência epigenética na carcinogenese." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2012. http://hdl.handle.net/10183/40121.
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Introdução: O Adenocarcinoma ductal pancreático é um tumor bastante agressivo que apresenta uma alta de letalidade e, para o qual, poucas opções terapêuticas estão disponíveis. Isto pode ser parcialmente explicado pela complexidade derivada de múltiplas aberrações genéticas e da população celular mista presente em um tumor pancreático, o que também pode explicar o curso clínico heterogêneo observado na prática diária. Ultimamente, pesquisas científicas têm contribuído para ampliar o conhecimento sobre o impacto das alterações epigenéticas no desenvolvimento de múltiplos tipos de câncer, porém no pâncreas essas alterações ainda são incertas e, por isso, foco de investigação. A desregulação epigenética parece estar envolvida no ciclo celular da célula tumoral, incluindo o crescimento celular, diferenciação, progressão tumoral e morte celular, e a acetilação das histonas é um importante mecanismo que regula a transcrição de genes envolvidos nesses processos. Padrões globais de modificações das histonas foram recentemente apontados como preditores de desfecho em pacientes com câncer, mas poucos estudos têm sido realizados nesta área, inclusive em Adenocarcinoma ductal pancreático (ADP). Objetivos: O presente estudo foi desenvolvido a fim de investigar o padrão de modificação de acetilação das histonas em adenocarcinoma pancreático, através da análise imunohistoquímica. Materiais e métodos: Uma análise clinicopatológica retrospectiva foi realizada em 119 pacientes diagnosticados com câncer de pâncreas entre os anos de 2005 e 2011, e realizado estudo imunohistoquímico com os anticorpos contra H4K12ac, H3K9ac e H3K18ac. Marcação nuclear positiva para cada histona foi medida quanto à intensidade e expressão, sendo classificadas em grupos de baixa ou de alta intensidade/expressão. Os resultados foram analisados em relação aos parâmetros clinicopatológicos de cada paciente. Resultados: Houve uma relação positiva entre diferenciação tumoral e alta expressão de H4K12ac (P <0,05), bem como a intensidade forte dos três marcadores correlacionou-se positivamente com o estágio do tumor (P <0,01). Análise univariada mostrou pior sobrevida em pacientes com níveis elevados de expressão de H4K12ac (p = 0,038) e H3K18Ac (P = 0,033). Modelo de risco proporcional de Cox revelou o efeito prognóstico independente de níveis elevados de H4K12ac H3K18ac (taxas de risco de 1,6 e 1,7, respectivamente, p <0,05), especialmente para pacientes em estágios iniciais. Sugerimos como hipótese que as modificações na acetilação das histonas H4K12 e H3K18 podem ser consideradas fatores prognósticos importantes para o câncer de pâncreas, embora o mecanismo envolvido necessite de mais investigação. Aumentando a compreensão e o conhecimento sobre o padrão de acetilação das histonas, poder-se-ão finalmente gerar novas idéias para um diagnóstico molecular racional e novas abordagens terapêuticas.Introduction: Ductal pancreatic adenocarcinoma (DPAs) is a highly aggressive tumor, with a high letality rate, for which few therapeutic options are available. This may be partially explained by the notorious complexity derived from the multiple genetic aberrations and mixed cellular population present in a pancreatic tumor, which can also explain the heterogeneous clinical course observed in daily practice. Lately, there is an increase in the literature about the impact of epigenetic changes on the development of several cancer, however in the pancreas these changes are still uncertain. Epigenetic deregulation may be involved in tumor cell biology, including cell growth, differentiation, tumor progression and cell death, and histone acetylation is a major mechanism that regulates gene transcription. Patterns of global histone modifications have been recently suggested as outcome predictors in cancer patients, but few studies have been conducted on pancreatic ductal adenocarcinomas. Objectives: This study was designed to investigate the predictive value of histone acetylation modifications on pancreatic cancer. Material and methods: A retrospective clinicopathologic analysis was undertaken in 119 patients diagnosed with PDAC between 2005 and 2011, and immunohistochemistry performed with antibodies against H4K12ac, H3K9ac and H3K18ac. Positive nuclear staining for each histone was measured as the intensity and expression, being classified into low or high-staining groups. Results were analyzed in relation to patients’ clinicopathologic parameters. Results: There was a positive relationship between tumor differentiation and H4K12ac high scores (P<0.05) and staining of the three markers correlated positively with tumor stage (P<0.01). Univariate analysis showed worse survival in patients with high detection levels of H4K12ac (p=0.038) and H3K18Ac (P=0.033). A backwards Cox proportional hazards model revealed the independent prognostic effect of high H4K12ac and H3K18ac levels (hazard ratios of 1.6 and 1.7 respectively, p<0.05), especially for patients at early stages. We hypothesize that acetylation of H4K12 and H3K18 may be considered valuable prognostic factors for pancreatic cancer, although the mechanism involved needs further investigation. Increasing insights into histone acetylation modifications can ultimately generate new ideas for rationally and molecularly based diagnostic and therapeutic approaches.
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Eisenstatt, Jessica R. "Histone H4 Acetylation in the DNA Damage Response and Telomere Formation of Schizosaccharomyces pombe." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1440417554.
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Wettermark, Anna. "Histone modifications and their role in splicing." Thesis, Linköpings universitet, Biologi, 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-166639.
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Splicing is the process when introns gets removed and exons are spliced together. This is an important step to form a clean mRNA with no unnecessary sequences that could interrupt protein synthesis. There are different types of splicing and some of them need a complex called spliceosome. The spliceosome requires ATP, small nuclear RNAs and splicing factors. The spliceosome and the process splicing can be regulated by epigenetics, and one epigenetic mechanism is histone modification. There are four types of histone modifications; methylation, phosphorylation, ubiquitination and acetylation. They regulate splicing to different extents by altering the chromatin structure, affect the assembly of the spliceosome and regulate the attraction of splicing factors. This review will investigate if histone modifications affect splicing and to what extent. Suggestions for further research regarding the relationship between splicing and histone modifications will also be provided. The review is based on 30 articles and two books and the search was conducted between 30th of March 2020 and 13th of April 2020. Ubiquitination and phosphorylation have a minor effect on splicing meanwhile methylation and acetylation affect splicing in great extent.
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Ge, Zhongqi. "Role of Nuclear Hat1p Complex and Acetylation of Newly Synthesized Histone H4 in Chromatin Assembly." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1356622980.
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Rahman, Sunniyat. "Molecular mechanisms and outcomes of arsenic-induced histone acetylation and microRNA regulation in cellular transformation." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/30712.
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Chronic exposure to arsenic causes negative health outcomes, particularly malignant neoplasms of the skin, lung and bladder. Although epidemiological data has associated arsenic exposure to cancer, a clear molecular mechanism has remained elusive. This thesis studied the impact of arsenic trioxide (ATO) exposure on histone acetylation and microRNA expression at both tolerated and toxic levels in vitro to determine an epigenetic-based mechanism of carcinogenesis. This thesis outlines a framework for identifying tolerated and toxic ATO exposures, as a prerequisite to epigenetic characterisation. Tolerated ATO exposure increased cellular survival, anchorage-independent colony formation, cell-cycle progression and proliferation in HEK293T cells. HEK293T and UROtsa cells treated with tolerated ATO exhibited global H3K9 hyperacetylation at 3 hours and global H3K9 hypoacetylation at 72 hours. This was mediated by an imbalance in the intracellular HDAC2 to PCAF mRNA expression ratio. Global H3K9 hypoacetylation occurred for both tolerated and toxic exposures, giving poor mechanistic differentiation between these separated cellular outcomes. Chromatin immunoprecipitation identified PCAF recruitment, E2F1 binding and H3K9 acetylation at the FOS proto-oncogenic promoter leading to an elevation in FOS mRNA levels at the tolerated concentration only. This thesis also reports ATO-induced chromatin relaxation in HEK293T cells followed by a return to nominal levels for the tolerated concentration. This is in contrast to the toxic exposure, which leads to clear chromatin condensation and apoptosis. This thesis postulates that arsenic-induced global H3K9 hypoacetylation is caused by a miR-372 -mediated attenuation mechanism targeting PCAF mRNA, as predicted through bioinformatic analysis. In summary, tolerated ATO exposure resulted in measurable perturbations in both global and promoter-specific histone acetylation in addition to the aberrant expression of microRNAs, which led to cellular transformation over toxicity.
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Crump, Nicholas T. "The role of p300/CBP in dynamic acetylation of histone H3K4me3 and immediate-early gene regulation." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534164.
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Kruhlak, Michael John. "Sub-nuclear distribution and mobility of nuclear proteins involved in histone acetylation and pre-mRNA splicing." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ64821.pdf.
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Shukla, Abhijit. "HISTONE POSTTRANSLATIONAL MODIFICATIONS AND GENE EXPRESSION IN SACCHAROMYCES CEREVISIAE." Available to subscribers only, 2009. http://proquest.umi.com/pqdweb?did=1967969411&sid=3&Fmt=2&clientId=1509&RQT=309&VName=PQD.
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Thesis (Ph. D.)--Southern Illinois University Carbondale, 2009."Department of Molecular Biology, Microbiology and Biochemistry." Includes bibliographical references (p. 131-155). Also available online.