Academic literature on the topic 'H3K9ac'
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Journal articles on the topic "H3K9ac":
Cui, Long, Jun Miao, Tetsuya Furuya, Xinyi Li, Xin-zhuan Su, and Liwang Cui. "PfGCN5-Mediated Histone H3 Acetylation Plays a Key Role in Gene Expression in Plasmodium falciparum." Eukaryotic Cell 6, no. 7 (April 20, 2007): 1219–27. http://dx.doi.org/10.1128/ec.00062-07.
Sahai, Vaibhav, Surabhi Dangi-Garimella, Kazumi Ebine, Krishan Kumar, and Hidayatullah G. Munshi. "Promotion of gemcitabine resistance in pancreatic cancer cells by three-dimensional collagen I through HMGA2-dependent histone acetyltransferase expression." Journal of Clinical Oncology 31, no. 4_suppl (February 1, 2013): 172. http://dx.doi.org/10.1200/jco.2013.31.4_suppl.172.
Ebrahimi, Azadeh, Jens Schittenhelm, Juergen Honegger, and Hermann Schluesener. "Prognostic relevance of global histone 3 lysine 9 acetylation in ependymal tumors." Journal of Neurosurgery 119, no. 6 (December 2013): 1424–31. http://dx.doi.org/10.3171/2013.9.jns13511.
Radovani, Ernest, Matthew Cadorin, Tahireh Shams, Suzan El-Rass, Abdel R. Karsou, Hyun-Soo Kim, Christoph F. Kurat, Michael-Christopher Keogh, Jack F. Greenblatt, and Jeffrey S. Fillingham. "The Carboxyl Terminus of Rtt109 Functions in Chaperone Control of Histone Acetylation." Eukaryotic Cell 12, no. 5 (March 1, 2013): 654–64. http://dx.doi.org/10.1128/ec.00291-12.
Tsurubuchi, Takao, Shunsuke Ichi, Kyu-won Shim, William Norkett, Elise Allender, Barbara Mania-Farnell, Tadanori Tomita, David G. McLone, Norman Ginsberg, and C. Shekhar Mayanil. "Amniotic fluid and serum biomarkers from women with neural tube defect–affected pregnancies: a case study for myelomeningocele and anencephaly." Journal of Neurosurgery: Pediatrics 12, no. 4 (October 2013): 380–89. http://dx.doi.org/10.3171/2013.7.peds12636.
Wei, Wenbin, Yuemin Liu, Yating Qiu, Minjie Chen, Yiwen Wang, Zixiang Han, and Ying Chai. "Characterization of Acetylation of Histone H3 at Lysine 9 in the Trigeminal Ganglion of a Rat Trigeminal Neuralgia Model." Oxidative Medicine and Cellular Longevity 2022 (May 4, 2022): 1–13. http://dx.doi.org/10.1155/2022/1300387.
Ispada, Jessica, Aldcejam Martins da Fonseca Junior, Otávio Luiz Ramos Santos, Camila Bruna de Lima, Erika Cristina dos Santos, Vinicius Lourenço da Silva, Fernanda Nascimento Almeida, Saul de Castro Leite, Pablo Juan Ross, and Marcella Pecora Milazzotto. "Metabolism-driven post-translational modifications of H3K9 in early bovine embryos." Reproduction 162, no. 3 (September 1, 2021): 181–91. http://dx.doi.org/10.1530/rep-21-0134.
Chacón, Liliana, Martha C. Gómez, Jill A. Jenkins, Staley P. Leibo, Gemechu Wirtu, Betsy L. Dresser, and C. Earle Pope. "Effect of cryopreservation and in vitro culture of bovine fibroblasts on histone acetylation levels and in vitro development of hand-made cloned embryos." Zygote 19, no. 3 (July 7, 2010): 255–64. http://dx.doi.org/10.1017/s0967199410000316.
Hezroni, Hadas, Badi Sri Sailaja, and Eran Meshorer. "Pluripotency-related, Valproic Acid (VPA)-induced Genome-wide Histone H3 Lysine 9 (H3K9) Acetylation Patterns in Embryonic Stem Cells." Journal of Biological Chemistry 286, no. 41 (August 17, 2011): 35977–88. http://dx.doi.org/10.1074/jbc.m111.266254.
Steilmann, C., A. Paradowska, M. Bartkuhn, M. Vieweg, H. C. Schuppe, M. Bergmann, S. Kliesch, W. Weidner, and K. Steger. "Presence of histone H3 acetylated at lysine 9 in male germ cells and its distribution pattern in the genome of human spermatozoa." Reproduction, Fertility and Development 23, no. 8 (2011): 997. http://dx.doi.org/10.1071/rd10197.
Dissertations / Theses on the topic "H3K9ac":
Hache, Antoine. "Molecular basis of transcriptional dysregulations in the spinocerebellar ataxia type 7, a neurodegenerative polyglutamine disorder." Thesis, Strasbourg, 2020. http://www.theses.fr/2020STRAJ083.
SCA7 is a genetic disorder whose one of its main symptoms is a progressive loss of visual acuity which can ultimately lead to blindness. The mutation responsible for this disease is an unstable CAG expansion within ATXN7, a gene encoding a subunit of the SAGA complex, a co-activator of the RNA polymerase II. Previous studies performed on transgenic mouse models highlighted a neuronal identity loss of the photoreceptors at the morphological, functional and molecular levels. During my PhD a characterization of a new SCA7 knock-in mouse model was performed. This model, which expresses the mutated genes at endogenous level recapitulates the retinal impairments observed in transgenic models and in patients. A transcriptomic (RNA-seq) and epigenomic (ChIP-seq) analyses were performed on this model and highlight global acetylation defects on lysine 9 and 27 of histone H3 (H3K9ac and H3K27ac). Moreover, investigations on non-coding RNAs identified the presence of enhancer RNAs (eRNAs) on photoreceptor specific genes such as Rho. These eRNAs, which were never described before, undergo a downregulation in symptomatic SCA7 mice
Beyer, Susanne [Verfasser], and Udo [Akademischer Betreuer] Jeschke. "Immunhistochemische Untersuchung der Expression von H3K9ac, H3K4me3 und GR an Zervix-Karzinom-Präparaten sowie deren prognostische Analyse / Susanne Beyer ; Betreuer: Udo Jeschke." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2020. http://d-nb.info/1209472627/34.
Rifai, Khaldoun. "Etude des modifications épigénétiques en fonction de l'agressivité du cancer sporadique du sein : l'implication de l'histone désacétylase SIRT1 dans la progression tumorale." Thesis, Université Clermont Auvergne (2017-2020), 2018. http://www.theses.fr/2018CLFAS011/document.
With 59,000 new cases in 2017, breast cancer is the most frequently diagnosed cancer among French women, and poses a real public health problem in France, but also worldwide. It is well established that the complexity of carcinogenesis involves profound epigenetic deregulations that contribute to the tumorigenesis process. Deregulated H3 and H4 acetylated histone marks are amongst those alterations. Acetylation and deacetylation are major post-translational protein modifications that regulate gene expression and the activity of a myriad of oncoproteins. Aberrant deacetylase activity can promote or suppress tumorigenesis in different types of human cancers, including breast cancer. The deacetylase SIRT1 and the acetyltransferase TIP60 are 2 antagonistic epigenetic enzymes that are well implicated in apoptosis, gene regulation, genomic stability, DNA repair, and cancer development. In this manuscript, we identified the dysregulation of the histones H3 and H4 acetylation profiles in different molecular subtypes of sporadic breast cancer, and investigated the involvement of SIRT1 and TIP60 in breast tumorigenesis. First, we highlighted the roles of SIRT1 and TIP60 as potential prognostic biomarkers by revealing their differential expression patterns depending on breast cancer aggressiveness. Then, we demonstrated their differential epigenetic regulation of histone targets according to molecular subtype, and revealed their modulation of the H3K4ac epigenetic marker. Moreover, Epi-drugs mediated inhibition of these 2 enzymes has proven to be an effective strategy in the treatment of cancer. Thus, this work highlights the potential use of SIRT1 and TIP60 as epigenetic therapeutic targets for sporadic breast cancer
Audergon, Pauline Nicole Clotilde Beatrice. "Restricted epigenetic inheritance of H3K9 methylation." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/16212.
Ferguson, Fleur Marcia. "Molecular recognition in the BAZ2B bromodomain: histone H3K14ac complex : biophysical studies and fragment-based targeting." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708479.
Audonnet, Laure. "Caractérisation fonctionnelle de JMJ24, une déméthylase d’histone de la famille JUMONJI, chez Arabidopsis thaliana." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA112033/document.
Numerous studies over the last decade have reported the characterization of the JUMONJI (JMJ) proteins, showing their critical importance in regulating genes and organism’s development. These proteins are able to demethylate a subset of histone tail residues and were clustered into distinct groups using a phylogenetic analysis based on their catalytic domain conservation. Furthermore, modification of one to three specific residues has been attributed to each JMJ group. Within the KDM3 subfamily, of which target is the H3K9 residue, only one member, IBM1, was first characterized in Arabidopsis. In this report, we showed that the mutation of JMJ24, another member of this subfamily, resulted in an increase of the root length, cotyledon and floral organ size, suggesting that JMJ24 functions is needed at different developmental stage. In addition, the analysis of the tissue-specific expression of JMJ24 indicated that the gene is expressed within the phloem of all organs, correlating with the pleiotropic effect of the gene mutation. Last, our data also suggested that JMJ24 interacts with other JMJ protein like JMJ14 and IBM1, but also with the DCL proteins knowing to be involved in genes and transposable elements regulation
Sklias, Athéna. "Epigenetic regulation by estrogen receptor in breast cancer cells." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1149/document.
Previous epidemiological and experimental studies have strongly implicated estrogens in breast cancer risk and Estrogen Receptor (ER), the transcription factor to which estrogen binds, is considered as the major molecular driver of around 70% breast cancers. The importance of the deregulated estrogen signalling is further highlighted by increasing evidence that current chemopreventive and therapeutic strategies that target hormonally responsive breast cancers frequently result in the development of resistance to anti-estrogens and metastatic progression, highlighting the need for understanding the molecular underlying mechanisms. While until recently, ER was believed to act as a stand-alone transcription factor, which can directly bind its motifs in DNA, it is now accepted that ER activity is a complex and dynamic process that requires highly concerted actions of a dozen transcriptional cofactors and various chromatin regulators at DNA. Recent studies focused on characterising ER-associated cofactors and their role in opening the chromatin provided a remarkable insight into transcriptional regulation mediated by ER. However DNA methylation and histone acetylation are poorly understood in the context of ER’s dynamic binding. In this thesis, I combined a cell culture protocol adapted for studying estradiol (E2) deprivation and re-stimulation in stricto sensu in ER-positive breast cancer cells with the latest methylation array, that allowed a genome-wide interrogation of DNA methylation (including a comprehensive panel of enhancers). I further investigated histone acetylation (ChIP-seq) and transcriptome (RNA-seq) after E2 deprivation and re-stimulation to better characterise the ability of ER to coordinate gene regulation. I found that E2 deprivation and re-stimulation result in time-dependent DNA methylation changes and in histone acetylation across diverse genomic regions, many of which overlap with enhancers. Further enrichment analysis of transcription factor (TF) binding and motif occurrence highlights the importance of ER tethering mainly through two partner TF families, AP-1 and FOX, in the proximity of enhancers that are differentially methylated and acetylated. This is the first study that comprehensively characterized DNA methylation at enhancers in response to inhibition and activation of ER signalling. The transcriptome and genome occupancy data further reinforced the notion that ER activity may orchestrate a broad transcriptional programme through regulating a limited panel of critical enhancers. Finally, the E2 re-stimulation experiments revealed that although the majority of the observed epigenetic changes induced by E2 deprivation could be largely reversed when the cells were re-stimulated we show that DNA hypermethylation and H3K27 acetylation at enhancers as well as several gene expression changes are selectively retained. The partial reversibility can be interpreted as a sign of treatment efficiency but also as a mechanism by which ER activity may contribute to endocrine resistance. This study provides entirely new information that constitutes a major advance in our understanding of the events by which ER and its cofactors mediate changes in DNA methylation and chromatin states at enhancers. These findings should open new avenues for studying role of the deregulated estrogen signalling in the mechanism underlying the “roots” of endocrine resistance that commonly develops in response to anti-estrogen therapy
Battisti, Valentine. "Rôle d'histones methyltransférases spécifiques de H3K9 dans l'équilibre prolifération et différenciation cellulaire." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T092/document.
In eukaryotes, gene expression partly relies on chromatin compaction degree. Chromatin status is controlled by epigenetic marks, such as histones (chromatin structural proteins) posttranslational modifications. As an example, histone H3 lysine 9 (H3K9) methylation on gene promoters is mainly associated with transcriptional repression. H3K9 is methylated by several enzymes called lysine methyltransferases (KMTs). The aim of my thesis project was to understand the role of the H3K9 KMTs, G9a, GLP, Suv39h1 and SETDB1 in regulating the balance between proliferation and terminal differentiation. For this purpose, I used skeletal muscle terminal differentiation as model. Upon muscle terminal differentiation, myoblasts exit, in an irreversible way, from the cell cycle and under go differentiation where cells fusion and form myotubes. During this process, cell cycle genes are permanently silenced and muscle specific genes are activated. Thesis introduction is divided into three chapters. The first chapter focuses on chromatin and post-translational modifications. The second chapter describes H3K9 methylation characteristics and the role of the four KMTs that I studied during my thesis project: G9a,GLP, Suv39h1 and SETDB1. In the third chapter, the skeletal muscle terminal differentiation model is described in details. Results section reports my two major studies outcomes and their discussion. The first concerns the antagonistic roles of G9a and GLP regarding the muscle terminal differentiation and the second focuses on the role of SETDB1 during muscle differentiation. Finally, I conclude this manuscript by a plainer discussion followed by long term perspectives and an appendix presents other research articles, in which I collaborated during my PhD
Malik, Athar Naveed. "Genome-Wide Identification and Characterization of Stimulus-Responsive Enhancers in the Nervous System." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11026.
Leung, Danny Chi Yeu. "Transcriptional silencing of endogenous retroviruses : interplay between histone H3K9 methylation and DNA methylation." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/38966.
Book chapters on the topic "H3K9ac":
Minh, N. T., N. B. Tu, N. T. T. Tram, H. T. Bui, and N. Van Thuan. "Histone Deacetylase Inhibitor Corrects Histone H3K9 Modification in Round Spermatid DNA at the 2-Cell Stage and Increases the Development of ROSI Embryos." In 6th International Conference on the Development of Biomedical Engineering in Vietnam (BME6), 877–81. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4361-1_149.
"H3K9." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 885. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_7691.
Nestorov, Peter, Mathieu Tardat, and Antoine H. F. M. Peters. "H3K9/HP1 and Polycomb." In Current Topics in Developmental Biology, 243–91. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-416027-9.00008-5.
Yang, Xu, Wei Li, Hangyuan He, Yongjian Qi, Jacques Magdalou, Hui Wang, and Liaobin Chen. "H3K9 Acetylation Level of 11β-HSD2 in Human Wharton’s Jelly-Derived Mesenchymal Stem Cells: A Potential Biomarker for Evaluating Susceptibility to Multiple Chronic Diseases in Adulthood." In Stem Cells and Regenerative Medicine. IOS Press, 2021. http://dx.doi.org/10.3233/bhr210009.
Sidhaye, Aniket R., Shunichi Matsumoto, Rong Huang, Shonoi Barnett, Philip A. Cole, and Fredric E. Wondisford. "Thyroid Hormone–Induced Changes in H3K4 Methylation and H3K9 Acetylation in the TSHB Promoter Region Suggest a Role for Epigenetic Modifications in TSHB Gene Regulation." In BASIC - Hypothalamic-Pituitary-Thyroid Axis: Thyroid Hormone Metabolism, Cellular Uptake & Action, P1–646—P1–646. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p16.p1-646.
Conference papers on the topic "H3K9ac":
Berger, L., T. Kolben, S. Meister, T. M. Kolben, E. Schmoeckel, D. Mayr, S. Mahner, U. Jeschke, N. Ditsch, and S. Beyer. "Expression von H3K4me3 und H3K9ac in Brustkrebs." In 94. Kongress der Bayerischen Gesellschaft für Geburtshilfe und Frauenheilkunde e. V. (BGGF). Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1713965.
Estevan, Mariana, Pablo Vargas, Gleyson Amaral-Silva, Vivian Wagner, Bruno Mariz, Alan Santos-Silva, Marcio Lopes, and Oslei Almeida. "Evaluation of the H3K9ac immunoexpression in lip carcinogenesis." In Congresso de Iniciação Científica UNICAMP. Universidade Estadual de Campinas, 2019. http://dx.doi.org/10.20396/revpibic2720192623.
Berger, L., T. Kolben, S. Meister, TM Kolben, E. Schmoeckel, D. Mayr, S. Mahner, U. Jeschke, N. Ditsch, and S. Beyer. "Expression of H3K4me3 and H3K9ac in breast cancer." In Kongressabstracts zur Tagung 2020 der Deutschen Gesellschaft für Gynäkologie und Geburtshilfe (DGGG). © 2020. Thieme. All rights reserved., 2020. http://dx.doi.org/10.1055/s-0040-1717839.
Meister, S., L. Hahn, S. Beyer, C. Kuhn, M. Jegen, V. von Schönfeldt, S. Corradini, et al. "Die epigenetische Modifikation durch H3K4me3 und H3K9ac ist in Präeklampsieplazenten reduziert." In Kongressabstracts zur Gemeinsamen Jahrestagung der Österreichischen Gesellschaft für Gynäkologie und Geburtshilfe (OEGGG) und der Bayerischen Gesellschaft für Geburtshilfe und Frauenheilkunde e.V. (BGGF). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1730489.
Meister, S., L. Hahn, S. Beyer, C. Paul, S. Mitter, C. Kuhn, V. von Schönfeldt, et al. "Die Expression von PPARγ in der Präeklampsie reguliert die Histonmodifikationen H3K4me3 und H3K9ac." In Kongressabstracts zur Gemeinsamen Jahrestagung der Österreichischen Gesellschaft für Gynäkologie und Geburtshilfe (OEGGG) und der Bayerischen Gesellschaft für Geburtshilfe und Frauenheilkunde e.V. (BGGF). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1730490.
Wehrmann, M., T. Kolben, S. Meister, T. M. Kolben, E. Schmoeckel, D. Mayr, A. Burges, et al. "Gal-8, Gal-9, H3K9ac, H3K4me3 und der Glukokortikoidrezeptor als prognostische Marker im Endometriumkarzinom." In 94. Kongress der Bayerischen Gesellschaft für Geburtshilfe und Frauenheilkunde e. V. (BGGF). Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1713967.
Fong, Pui Kwan, and Nung Kion Lee. "Improved H3K27ac histone mark prediction using k-mer proximity feature." In 2015 9th International Conference on IT in Asia (CITA). IEEE, 2015. http://dx.doi.org/10.1109/cita.2015.7349830.
Tang, Chunlao, Vipin Yadav, Hui-Rong Qian, Jason B. Cunningham, Hong Gao, Yushi Liu, Jason C. Ting, et al. "Abstract 1446: Super-enhancer identification via Bru/BrUV-Seq and H3K27Ac ChIP-Seq." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1446.
Kellner, I., S. Beyer, S. Corradini, N. Rogenhofer, TM Kolben, U. Hasbargen, A. Hester, et al. "Epigenetische Modifikationen durch H3K4me3 und H3K9acan der fetomaternalen Grenzzone der Plazenta im Abortgeschehen." In Kongressabstracts zur Gemeinsamen Jahrestagung der Österreichischen Gesellschaft für Gynäkologie und Geburtshilfe (OEGGG) und der Bayerischen Gesellschaft für Geburtshilfe und Frauenheilkunde e.V. (BGGF). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1730484.
Giannikou, Krinio, Clemens K. Probst, Mahsa Zarei, Xintao Qiu, Melissa Duarte, Nikolas Kesten, Zachary Hebert, et al. "Abstract PO-010: Kidney angiomyolipomas are defined by a unique transcriptomic profile and H3K27ac chromatin state." In Abstracts: AACR Special Virtual Conference on Epigenetics and Metabolism; October 15-16, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.epimetab20-po-010.