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Artykuły w czasopismach na temat "Histone acetylation in brain cells"

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Demyanenko, Svetlana, and Svetlana Sharifulina. "The Role of Post-Translational Acetylation and Deacetylation of Signaling Proteins and Transcription Factors after Cerebral Ischemia: Facts and Hypotheses." International Journal of Molecular Sciences 22, no. 15 (2021): 7947. http://dx.doi.org/10.3390/ijms22157947.

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Histone deacetylase (HDAC) and histone acetyltransferase (HAT) regulate transcription and the most important functions of cells by acetylating/deacetylating histones and non-histone proteins. These proteins are involved in cell survival and death, replication, DNA repair, the cell cycle, and cell responses to stress and aging. HDAC/HAT balance in cells affects gene expression and cell signaling. There are very few studies on the effects of stroke on non-histone protein acetylation/deacetylation in brain cells. HDAC inhibitors have been shown to be effective in protecting the brain from ischemi
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Demyanenko, Svetlana, Valentina Dzreyan, and Svetlana Sharifulina. "Histone Deacetylases and Their Isoform-Specific Inhibitors in Ischemic Stroke." Biomedicines 9, no. 10 (2021): 1445. http://dx.doi.org/10.3390/biomedicines9101445.

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Cerebral ischemia is the second leading cause of death in the world and multimodal stroke therapy is needed. The ischemic stroke generally reduces the gene expression due to suppression of acetylation of histones H3 and H4. Histone deacetylases inhibitors have been shown to be effective in protecting the brain from ischemic damage. Histone deacetylases inhibitors induce neurogenesis and angiogenesis in damaged brain areas promoting functional recovery after cerebral ischemia. However, the role of different histone deacetylases isoforms in the survival and death of brain cells after stroke is s
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Yang, Chao, Lijun Ge, Xiyong Yu, Philip Lazarovici, and Wenhua Zheng. "Artemisinin Confers Cytoprotection toward Hydrogen Peroxide-Induced Cell Apoptosis in Retinal Pigment Epithelial Cells in Correlation with the Increased Acetylation of Histone H4 at Lysine 8." Molecules 29, no. 8 (2024): 1789. http://dx.doi.org/10.3390/molecules29081789.

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Increased oxidative stress is one of the critical pathologies inducing age-related macular degeneration (AMD), characterized by retinal pigment epithelial (RPE) cell damage and death. The unbalanced acetylation and deacetylation of histones have been implicated in AMD pathogenesis or hydrogen peroxide (H2O2)-induced cell damage. Therefore, strategies aimed at controlling the balance between acetylation and deacetylation may effectively protect RPE cells from oxidative damage. Artemisinin is an antimalarial lactone drug derived from Artemisia annua, with antioxidant activity known to modulate h
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Castro, Kamilah, and Patrizia Casaccia. "Epigenetic modifications in brain and immune cells of multiple sclerosis patients." Multiple Sclerosis Journal 24, no. 1 (2018): 69–74. http://dx.doi.org/10.1177/1352458517737389.

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Multiple sclerosis (MS) is a debilitating neurological disease whose onset and progression are influenced by the interplay of genetic and environmental factors. Epigenetic modifications, which include post-translational modification of the histones and DNA, are considered mediators of gene–environment interactions and a growing body of evidence suggests that they play an important role in MS pathology and could be potential therapeutic targets. Since epigenetic events regulate transcription of different genes in a cell type–specific fashion, we caution on the distinct functional consequences t
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Iaconelli, Jonathan, Lucius Xuan, and Rakesh Karmacharya. "HDAC6 Modulates Signaling Pathways Relevant to Synaptic Biology and Neuronal Differentiation in Human Stem-Cell-Derived Neurons." International Journal of Molecular Sciences 20, no. 7 (2019): 1605. http://dx.doi.org/10.3390/ijms20071605.

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Recent studies show that histone deacetylase 6 (HDAC6) has important roles in the human brain, especially in the context of a number of nervous system disorders. Animal models of neurodevelopmental, neurodegenerative, and neuropsychiatric disorders show that HDAC6 modulates important biological processes relevant to disease biology. Pan-selective histone deacetylase (HDAC) inhibitors had been studied in animal behavioral assays and shown to induce synaptogenesis in rodent neuronal cultures. While most studies of HDACs in the nervous system have focused on class I HDACs located in the nucleus (
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Roesler, Prof Rafael, Ms Natalia Hogetop Freire, Dr Caroline Brunetto de Farias, et al. "EPIGENETIC MODULATION OF STEMNESS AND DIFFERENTIATION BY VALPROIC ACID IN MEDULLOBLASTOMA." Neuro-Oncology 26, Supplement_7 (2024): vii19. http://dx.doi.org/10.1093/neuonc/noae158.077.

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Abstract AIMS Changes in epigenetic processes, including histone acetylation, are proposed as key events affecting tumor cell function and the initiation and progression of pediatric brain cancers. Valproic acid (VPA) is an antiepileptic drug that acts partially by inhibiting histone deacetylases (HDACs) and could be repurposed as an epigenetic anticancer therapy. Here, we report VPA-induced alterations in features related to stemness and differentiation in medulloblastoma (MB) cells. METHOD Human MB cells were treated with different concentrations of VPA and cell viability was measured with a
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Lisiero, Dominique Naomi, Horacio Soto, Shanna Fang, Antoni Ribas, Linda Liau, and Robert Prins. "Histone deacetylase inhibitor, LBH589, synergizes with an immunotherapy treatment in an in vivo murine brain tumor model (41.35)." Journal of Immunology 182, no. 1_Supplement (2009): 41.35. http://dx.doi.org/10.4049/jimmunol.182.supp.41.35.

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Abstract Cancer immunotherapy treatments may show low response rates due to an anti-apoptotic tumor environment. We hypothesized a treatment of immunotherapy and histone deacetylase inhibitor, LBH589, could induce tumor cell expression of pro-apoptotic molecules and sensitize these cells to immune mediated cell death. Treatment with adoptive transfer immunotherapy and LBH589 resulted in synergistically reduced s.c. tumor burden, and prolonged survival in an intracranial tumor model. In vivo studies in non-tumor bearing mice treated with this combination therapy showed a 2-fold increase in the
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Espinos, Estelle, Agathe Le Van Thaï, Christelle Pomiès, and Michel J. Weber. "Cooperation between Phosphorylation and Acetylation Processes in Transcriptional Control." Molecular and Cellular Biology 19, no. 5 (1999): 3474–84. http://dx.doi.org/10.1128/mcb.19.5.3474.

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ABSTRACT We previously reported that the activation of the M promoter of the human choline acetyltransferase (ChAT) gene by butyrate and trapoxin in transfected CHP126 cells is blocked by PD98059, a specific mitogen-activated protein kinase kinase (MEK) inhibitor (E. Espinos and M. J. Weber, Mol. Brain Res. 56:118–124, 1998). We now report that the transcriptional effects of histone deacetylase inhibitors are mediated by an H7-sensitive serine/threonine protein kinase. Activation of the ChAT promoter by butyrate and trapoxin was blocked by 50 μM H7 in both transient- and stable-transfection as
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Bergamasco, Maria I., Waruni Abeysekera, Alexandra L. Garnham, et al. "KAT6B is required for histone 3 lysine 9 acetylation and SOX gene expression in the developing brain." Life Science Alliance 8, no. 2 (2024): e202402969. http://dx.doi.org/10.26508/lsa.202402969.

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Heterozygous mutations in the histone lysine acetyltransferase geneKAT6B(MYST4/MORF/QKF) underlie neurodevelopmental disorders, but the mechanistic roles of KAT6B remain poorly understood. Here, we show that loss of KAT6B in embryonic neural stem and progenitor cells (NSPCs) impaired cell proliferation, neuronal differentiation, and neurite outgrowth. Mechanistically, loss of KAT6B resulted in reduced acetylation at histone H3 lysine 9 and reduced expression of key nervous system development genes in NSPCs and the developing cortex, including the SOX gene family, in particularSox2, which is a
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Freire, Natália Hogetop, Alice Laschuk Herlinger, Julia Vanini, et al. "Modulation of Stemness and Differentiation Regulators by Valproic Acid in Medulloblastoma Neurospheres." Cells 14, no. 2 (2025): 72. https://doi.org/10.3390/cells14020072.

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Changes in epigenetic processes such as histone acetylation are proposed as key events influencing cancer cell function and the initiation and progression of pediatric brain tumors. Valproic acid (VPA) is an antiepileptic drug that acts partially by inhibiting histone deacetylases (HDACs) and could be repurposed as an epigenetic anticancer therapy. Here, we show that VPA reduced medulloblastoma (MB) cell viability and led to cell cycle arrest. These effects were accompanied by enhanced H3K9 histone acetylation (H3K9ac) and decreased expression of the MYC oncogene. VPA impaired the expansion of
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Rozprawy doktorskie na temat "Histone acetylation in brain cells"

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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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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 tr
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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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VIANELLO, ELEONORA. "In vivo evaluation of biomolecular mechanisms of bilirubin toxicity and pre-clinical therapies." Doctoral thesis, Università degli Studi di Trieste, 2017. http://hdl.handle.net/11368/2908155.

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Introduction. Neonatal jaundice is a common and benign condition usually resolved during the first week of life. Neonates with very high level of unconjugated bilirubin (UCB), with an increase of the free bilirubin (Bf), may develop encephalopathy, with different grade of severity. Typical symptoms include motor disorder, auditory dysfunction, memory and learning deficits, reflecting selective damage respectively for cerebellum and basal ganglia, inferior colliculus, and hippocampus. Several studies reported that bilirubin may activate signal cascades that culminate to cell survival or death,
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Pourian, Ali. "The effect of valproic acid on histone acetylation in FaDu-luc head and neck squamous cell carcinoma cells." Thesis, University of Iowa, 2011. https://ir.uiowa.edu/etd/1256.

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Ene, Chibawanye Isidore. "Relevance of histone 3 lysine 27 modifiers in neural stem cells and malignant brain tumours." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610540.

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Khilji, Saadia. "Dissecting the Epigenetic Signaling Underlying Early Myogenic Differentiation." Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/42092.

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Bressan, Raul Bardini. "Genome editing as a tool to explore transcriptional and epigenetic regulation in neural stem cells and brain cancer." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31095.

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Mammalian neural stem cell (NSC) lines provide a useful experimental model for basic and applied research across stem cell and developmental biology, regenerative medicine and neuroscience. NSCs are clonally expandable, genetically stable, and easily transfectable - experimental attributes compatible with functional genetic analyses. However, targeted genetic manipulations have not been reported for mammalian NSC lines. Here, we deploy the CRISPR/Cas9 technology and demonstrate a variety of diverse targeted genetic modifications in both mouse and human NSC lines such as: targeted transgene ins
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Guimarães, Douglas Magno. "Uso de inibidores de Histona Deacetilase como estratégia terapêutica para sensibilizar células-tronco tumorais a quimioterapia: uma nova visão terapêutica sobre carcinomas mucoepidermoide bucais." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/23/23141/tde-21092015-164942/.

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Carcinoma mucoepidermóide (CME) é o tumor maligno de glândulas salivares mais comum, representando cerca de 30% dos tumores malignos. O tratamento do CME é a ressecção cirúrgica com eventual radioterapia. Assim, o tratamento do CME pode levar a varias complicações estéticas e funcionais. A quimioterapia tem sido utilizadas apenas em casos recorrentes ou com metástases à distancia. Vários relatos na literatura tem mostrado que o tratamento com drogas isoladas ou combinadas possuem uma resposta insatisfatória e de curta duração em grande parte devido a aquisição de resistência a quimioterapia. R
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Książki na temat "Histone acetylation in brain cells"

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O'Neill, Laura Patricia. Histone acetylation and transcription in Eukaryotic cells. University of Birmingham, 1994.

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Części książek na temat "Histone acetylation in brain cells"

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Myrum, Craig, and Peter R. Rapp. "Isolation and Quantification Brain Region-Specific and Cell Subtype-Specific Histone (De)Acetylation in Cognitive Neuroepigenetics." In Methods in Molecular Biology. Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9434-2_16.

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Liu, Liqiong. "Evaluating Histone Acetylation in Mouse Hematopoietic Stem and Progenitor Cells Using Chromatin Immunoprecipitation." In Methods in Molecular Biology. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2679-5_3.

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Yamauchi, Yukako, and Henry F. Duncan. "Characterization of the Expression and Role of Histone Acetylation and Deacetylation in Dental Pulp Cells." In Methods in Molecular Biology. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2780-8_17.

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Rahman, Irfan, Peter S. Gilmour, Luis Albert Jimenez, and William MacNee. "Oxidative stress and TNF-a induce histone Acetylation and NF-кB/AP-1 activation in Alveolar epithelial cells: Potential mechanism In gene transcription in lung inflammation." In Oxygen/Nitrogen Radicals: Cell Injury and Disease. Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1087-1_28.

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Razavi, Arezousadat, and Xiang-Jiao Yang. "Lysine Acetyltransferase 6A and Its Paralog: From Biological Functions to Neurodevelopmental Disorders, Cancer and New Therapeutics." In Understanding Developmental Disorders [Working Title]. IntechOpen, 2025. https://doi.org/10.5772/intechopen.1009241.

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Post-translational modifications of histones, such as lysine acetylation and methylation, significantly influence chromatin structure in the eukaryotic nucleus. Lysine acetyltransferase 6A (KAT6A) and its paralog, KAT6B, participate in a variety of cellular processes crucial for normal development by influencing cell cycle progression, cell differentiation, signal transduction and responses to cellular stress. Studies using knockout mouse models have revealed the important effects of KAT6A and KAT6B on development, with the absence of the former resulting in embryonic lethality and the loss of
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Yang, Xu, Wei Li, Hangyuan He, et al. "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.

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Objective: A large number of studies have suggested that low birth weight fetuses were susceptible to fetal-originated diseases in adulthood. The purpose of this study was to investigate whether the histone 3 Lysine 9 (H3K9) acetylation level of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) in human Wharton’s jelly-derived mesenchymal stem cells (WJ-MSCs) was an early warning marker for the susceptibility of multiple chronic diseases in adulthood. Methods: The epigenetic and expressional abnormality of 11β-HSD2 in human WJ-MSCs induced by a variety of prenatal adverse xenobiotic factors w
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Zhai, Jiayuan, and Wanchao Yang. "The Research Progress of Molecular Hydrogen in the Treatment of Traumatic Brain Injury: A Review." In Traumatic Brain Injury - Challenges [Working Title]. IntechOpen, 2024. http://dx.doi.org/10.5772/intechopen.1004701.

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Molecular hydrogen, a medical gas with potent antioxidant and anti-inflammatory effects, exhibits significant therapeutic potential for various diseases. Traumatic brain injury (TBI) is often accompanied by extensive cognitive dysfunction, characterized by complex pathogenesis and poor prognosis. Recent studies have demonstrated that inhalation of a high concentration of molecular hydrogen can improve the prognosis of TBI; however, the specific mechanism remains unclear. This article provides a comprehensive review on the mechanisms underlying the action of a high concentration of molecular hy
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Subramanian, Subha, and James B. Potash. "Epigenetics in Psychiatry." In Psychiatric Genetics. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190221973.003.0011.

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Epigenetic modifications such as DNA methylation (DNAm), histone acetylation and methylation, and those directed by small RNAs, are widely studied in psychiatry and may play a role in the etiology and pathophysiology of psychiatric disorders. This chapter provides a brief overview of the mechanisms regulating these epigenetic marks and the challenges in obtaining biologically meaningful epigenetic data, given the inaccessibility of the living human brain. Significant results to date from studies on the epigenetics of psychiatric disorders are presented, including the impact of stress on DNAm i
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A. Klupczyńska, Ewelina. "DNA Methylation in Cancer Epigenetics." In Epigenetics - Regulation and New Perspectives. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.110506.

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DNA methylation is one of the most important epigenetic modifications next to acetylation or histone modifications, as it has a role in the homeostatic control of the cell and is strongly involved in the control of genome expression. DNA methylation, which is catalyzed by DNA methyltransferases (DNMTs), is one of the primary epigenetic mechanisms that control cell proliferation, apoptosis, differentiation, cell cycle, and transformation in eukaryotes. Hypomethylation and hypermethylation result in the activation or repression of genes and in a normal cell there is a strict balance between thes
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Carabenciov, Ivan D., and Michael W. Ruff. "Progressive Bilateral Arm Pain, Gait Disturbance, Constipation, and Urinary Retention." In Mayo Clinic Cases in Neuroimmunology, edited by Andrew McKeon, B. Mark Keegan, and W. Oliver Tobin. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197583425.003.0075.

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A 48-year-old woman sought care for progressive right arm and hand pain with radial nerve–distribution sensory loss. She had a past history of multiple prior athletics-associated, musculoskeletal, upper cervical spine injuries. Her symptoms were initially attributed to a right C6 radiculopathy. Over the next several months, the sensory loss spread to involve the entire right hand and subsequently the entire left hand. She had development of diffuse right hand weakness and a sense of imbalance that was particularly prominent while in the dark. Finally, she experienced progressive constipation a
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Streszczenia konferencji na temat "Histone acetylation in brain cells"

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Stefanowicz, Dorota, Tillie-Louise Hackett, Peter D. Paré, and Darryl A. Knight. "Alterations In Histone Acetylation In Asthmatic Airway Epithelial Cells." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1448.

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Yao, Hongwei, Sangwoon Chung, Isaac K. Sundar, and Irfan Rahman. "Cigarette Smoke Causes A Residue-Specific Histone Methylation And Its Cross-Talk With Histone Acetylation In Human Lung Epithelial Cells." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3474.

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Mithraprabhu, Sridurga, Tiffany Khong, Simon S. Jones, and Andrew Spencer. "Abstract 1007: Histone acetylation mediated by inhibition of Class I histone deacetylases is critical for induction of cell death in multiple myeloma cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1007.

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Pace, Elisabetta, Serena Di Vincenzo, Maria Ferraro, et al. "Effects of beclomethasone and carbocysteine in histone acetylation/deacetylation processes of bronchial epithelial cells exposed to cigarette smoke." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa3990.

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Uitrakul, Suriyon, Gareth James Veal, Claire Hutton, and David Jamieson. "Abstract 2583: Imaging flow cytometry assay development and validation for the detection of histone H4 acetylation in white blood cells." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2583.

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Vaapil, Marica, Karolina Helczynska, Siv Beckman, Sven Påhlman, and Annika Jögi. "Abstract 463: Hypoxia leads to impaired differentiation and sustained global histone acetylation in immortalized mammary epithelial cells cultured as acini." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-463.

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Litherland, S. A., Robert Reynolds, Louis Barr, Alvin JO Almodovar, and David A. Decker. "Abstract P4-01-15: Assay Development for detection of estrogen responsive gene histone acetylation in breast cancer circulating tumor cells." In Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.sabcs14-p4-01-15.

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John, Alison E., Rachel L. Clifford, Christopher E. Brightling, and Alan J. Knox. "Basal Hypersecretion Of CXCL8 In Asthmatic Human Airway Smooth Muscle Cells Is Associated With Increased Binding Of Histone Acetyltransferases To The CXCL8 Promoter And Acetylation Of Histone H3." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2145.

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Singh, Tripti, and Santosh K. Katiyar. "Abstract 4079: Proanthocyanidins reactivate silenced tumor suppressor genesp16INK4aandCip1/p21by reducing DNA methylation and increasing histone acetylation in human non-small cell lung cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4079.

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Meeran, Syed M., Shweta N. Patel, Tak-Hang Chan, and Trygve O. Tollefsbol. "Abstract 3206: A novel prodrug of the green tea polyphenol (−)-epigallocatechin-3-gallate inhibits the telomerase gene by modifying DNA methylation and histone acetylation in breast cancer cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3206.

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Raporty organizacyjne na temat "Histone acetylation in brain cells"

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Meiri, Noam, Michael D. Denbow, and Cynthia J. Denbow. Epigenetic Adaptation: The Regulatory Mechanisms of Hypothalamic Plasticity that Determine Stress-Response Set Point. United States Department of Agriculture, 2013. http://dx.doi.org/10.32747/2013.7593396.bard.

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Our hypothesis was that postnatal stress exposure or sensory input alters brain activity, which induces acetylation and/or methylation on lysine residues of histone 3 and alters methylation levels in the promoter regions of stress-related genes, ultimately resulting in long-lasting changes in the stress-response set point. Therefore, the objectives of the proposal were: 1. To identify the levels of total histone 3 acetylation and different levels of methylation on lysine 9 and/or 14 during both heat and feed stress and challenge. 2. To evaluate the methylation and acetylation levels of histone
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