Relevant bibliographies by topics / Epigentic control

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Academic literature on the topic 'Epigentic control'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Epigentic control"

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Davies, P. C. W. "The epigenome and top-down causation." Interface Focus 2, no. 1 (September 14, 2011): 42–48. http://dx.doi.org/10.1098/rsfs.2011.0070.

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Genes store heritable information, but actual gene expression often depends on many so-called epigenetic factors, both physical and chemical, external to DNA. Epigenetic changes can be both reversible and heritable. The genome is associated with a physical object (DNA) with a specific location, whereas the epigenome is a global, systemic, entity. Furthermore, genomic information is tied to specific coded molecular sequences stored in DNA. Although epigenomic information can be associated with certain non-DNA molecular sequences, it is mostly not. Therefore, there does not seem to be a stored ‘epigenetic programme’ in the information-theoretic sense. Instead, epigenomic control is—to a large extent—an emergent self-organizing phenomenon, and the real-time operation of the epigenetic ‘project’ lies in the realm of nonlinear bifurcations, interlocking feedback loops, distributed networks, top-down causation and other concepts familiar from the complex systems theory. Lying at the heart of vital eukaryotic processes are chromatin structure, organization and dynamics. Epigenetics provides striking examples of how bottom-up genetic and top-down epigenetic causation intermingle. The fundamental question then arises of how causal efficacy should be attributed to biological information. A proposal is made to implement explicit downward causation by coupling information directly to the dynamics of chromatin, thus permitting the coevolution of dynamical laws and states, and opening up a new sector of dynamical systems theory that promises to display rich self-organizing and self-complexifying behaviour.
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Ramos, Kristie N., Irma N. Ramos, Yi Zeng, and Kenneth S. Ramos. "Genetics and epigenetics of pediatric leukemia in the era of precision medicine." F1000Research 7 (July 18, 2018): 1104. http://dx.doi.org/10.12688/f1000research.14634.1.

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Pediatric leukemia represents a heterogeneous group of diseases characterized by germline and somatic mutations that manifest within the context of disturbances in the epigenetic machinery and genetic regulation. Advances in genomic medicine have allowed finer resolution of genetic and epigenetic strategies that can be effectively used to risk-stratify patients and identify novel targets for therapy. This review discusses the genetic and epigenetic mechanisms of leukemogenesis, particularly as it relates to acute lymphocytic leukemias, the mechanisms of epigenetic control of leukemogenesis, namely DNA methylation, histone modifications, microRNAs, and LINE-1 retroelements, and highlights opportunities for precision medicine therapeutics in further guiding disease management. Future efforts to broaden the integration of advances in genomic and epigenomic science into the practice of pediatric oncology will not only identify novel therapeutic strategies to improve clinical outcomes but also improve the quality of life for this unique patient population. Recent findings in precision therapeutics of acute lymphocytic leukemias over the past three years, along with some provocative areas of epigenetics research, are reviewed here.
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Krämer, Anne I., and Christoph Handschin. "How Epigenetic Modifications Drive the Expression and Mediate the Action of PGC-1α in the Regulation of Metabolism." International Journal of Molecular Sciences 20, no. 21 (October 31, 2019): 5449. http://dx.doi.org/10.3390/ijms20215449.

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Epigenetic changes are a hallmark of short- and long-term transcriptional regulation, and hence instrumental in the control of cellular identity and plasticity. Epigenetic mechanisms leading to changes in chromatin structure, accessibility for recruitment of transcriptional complexes, and interaction of enhancers and promoters all contribute to acute and chronic adaptations of cells, tissues and organs to internal and external perturbations. Similarly, the peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is activated by stimuli that alter the cellular energetic demand, and subsequently controls complex transcriptional networks responsible for cellular plasticity. It thus is of no surprise that PGC-1α is under the control of epigenetic mechanisms, and constitutes a mediator of epigenetic changes in various tissues and contexts. In this review, we summarize the current knowledge of the link between epigenetics and PGC-1α in health and disease.
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Deng, Xian, Xianwei Song, Liya Wei, Chunyan Liu, and Xiaofeng Cao. "Epigenetic regulation and epigenomic landscape in rice." National Science Review 3, no. 3 (September 1, 2016): 309–27. http://dx.doi.org/10.1093/nsr/nww042.

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Abstract Epigenetic regulation has been implicated in the control of complex agronomic traits in rice (Oryza sativa), a staple food crop and model monocot plant. Recent advances in high-throughput sequencing and the moderately complex genome of rice have made it possible to study epigenetic regulation in rice on a genome-wide scale. This review discusses recent advances in our understanding of epigenetic regulation in rice, with an emphasis on the roles of key epigenetic regulators, the epigenomic landscape, epigenetic variation, transposon repression, and plant development.
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McCaw, Beth A., Tyler J. Stevenson, and Lesley T. Lancaster. "Epigenetic Responses to Temperature and Climate." Integrative and Comparative Biology 60, no. 6 (May 29, 2020): 1469–80. http://dx.doi.org/10.1093/icb/icaa049.

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Synopsis Epigenetics represents a widely accepted set of mechanisms by which organisms respond to the environment by regulating phenotypic plasticity and life history transitions. Understanding the effects of environmental control on phenotypes and fitness, via epigenetic mechanisms, is essential for understanding the ability of organisms to rapidly adapt to environmental change. This review highlights the significance of environmental temperature on epigenetic control of phenotypic variation, with the aim of furthering our understanding of how epigenetics might help or hinder species’ adaptation to climate change. It outlines how epigenetic modifications, including DNA methylation and histone/chromatin modification, (1) respond to temperature and regulate thermal stress responses in different kingdoms of life, (2) regulate temperature-dependent expression of key developmental processes, sex determination, and seasonal phenotypes, (3) facilitate transgenerational epigenetic inheritance of thermal adaptation, (4) adapt populations to local and global climate gradients, and finally (5) facilitate in biological invasions across climate regions. Although the evidence points towards a conserved role of epigenetics in responding to temperature change, there appears to be an element of temperature- and species-specificity in the specific effects of temperature change on epigenetic modifications and resulting phenotypic responses. The review identifies areas of future research in epigenetic responses to environmental temperature change.
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Howlett, Kirsten F., and Sean L. McGee. "Epigenetic regulation of skeletal muscle metabolism." Clinical Science 130, no. 13 (May 23, 2016): 1051–63. http://dx.doi.org/10.1042/cs20160115.

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Normal skeletal muscle metabolism is essential for whole body metabolic homoeostasis and disruptions in muscle metabolism are associated with a number of chronic diseases. Transcriptional control of metabolic enzyme expression is a major regulatory mechanism for muscle metabolic processes. Substantial evidence is emerging that highlights the importance of epigenetic mechanisms in this process. This review will examine the importance of epigenetics in the regulation of muscle metabolism, with a particular emphasis on DNA methylation and histone acetylation as epigenetic control points. The emerging cross-talk between metabolism and epigenetics in the context of health and disease will also be examined. The concept of inheritance of skeletal muscle metabolic phenotypes will be discussed, in addition to emerging epigenetic therapies that could be used to alter muscle metabolism in chronic disease states.
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Venkatesh, Ishwariya, and Khadijah Makky. "Teaching Epigenetic Regulation of Gene Expression Is Critical in 21st-Century Science Education: Key Concepts & Teaching Strategies." American Biology Teacher 82, no. 6 (August 1, 2020): 372–80. http://dx.doi.org/10.1525/abt.2020.82.6.372.

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The field of epigenetics is progressing rapidly and becoming indispensable to the study of fundamental gene regulation. Recent advances are redefining our understanding of core components that regulate gene expression during development and in human diseases. Scientific knowledge on the importance of epigenetic regulation is now well known and accepted, and it is not surprising to see epigenetics being introduced into many biology curricula at the high school and college levels. Yet the core concepts of epigenetic regulation are differently perceived by the academic communities. Therefore, it is critical that fundamental concepts of epigenetic regulation are taught to the next generation in a simple yet precise manner to avoid any misconceptions. To that end, this article starts by distilling the extensive scientific literature on epigenetic control of gene regulation into a simple primer on the core fundamental concepts. Next and more importantly, it provides suggestions for student-friendly classroom practices and activities that are centered on these core concepts to ensure that students both recognize and retain knowledge on the importance of epigenetic control in eukaryotic gene regulation.
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Verdikt, Roxane, and Patrick Allard. "Metabolo-epigenetics: the interplay of metabolism and epigenetics during early germ cells development†." Biology of Reproduction 105, no. 3 (June 16, 2021): 616–24. http://dx.doi.org/10.1093/biolre/ioab118.

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Abstract Metabolites control epigenetic mechanisms, and conversly, cell metabolism is regulated at the epigenetic level in response to changes in the cellular environment. In recent years, this metabolo-epigenetic control of gene expression has been implicated in the regulation of multiple stages of embryonic development. The developmental potency of stem cells and their embryonic counterparts is directly determined by metabolic rewiring. Here, we review the current knowledge on the interplay between epigenetics and metabolism in the specific context of early germ cell development. We explore the implications of metabolic rewiring in primordial germ cells in light of their epigenetic remodeling during cell fate determination. Finally, we discuss the relevance of concerted metabolic and epigenetic regulation of primordial germ cells in the context of mammalian transgenerational epigenetic inheritance.
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Bellmunt, Joaquim, Guangwu Guo, Stephanie A. Mullane, Anna Orsola, Lillian Werner, Paul Van Hummelen, Aaron Thorner, et al. "Genomic landscape of high-grade T1 micropapillary bladder tumors." Journal of Clinical Oncology 33, no. 7_suppl (March 1, 2015): 299. http://dx.doi.org/10.1200/jco.2015.33.7_suppl.299.

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299 Background: The genomic landscape of high-grade T1 micropapillary bladder tumors (HGT1micropap) is unknown. Clinically, micropapillary bladder cancer is an aggressive and possibly lethal disease. Our main objective was to assess the genomic landscape of HGT1micropap through identifying mutations, insertions/deletions (indels), translocations, and copy number variations (CNVs). Methods: We prospectively identified nine HGT1micropap with 45.4 months of median follow up. Patients were treated in a uniform manner using TUR, BCG, and appropriate follow up. We performed whole exome sequencing using Ilumina Exome _v5 plus translocation. Mutations and indels were called using the Firehose pipeline. CNVs were called using ExomeCNV. We examined the mutational landscape and compared the genomic alterations to TCGA (>T2, n=131)2 and publicly available data on non-muscle invasive bladder tumors (Ta/T1, n=37)1. Results: Within the HGT1micropap, mutations on TP53, KMT2D, TSC1, and ATM were suggested to occur more frequently compared to the NMIBC control group1. FGFR3 was seen at the expected frequency for NMIBC. The mutations of interest are presented in Table 1 with the percentage seen in the other cohorts. Of interest, TSC1 was seen in higher frequency in micropapillary than in the NMIBC or the TCGA cohort2. We did not see any patterns between CNVs and mutations. We also saw two patients with severe chromothripsis. 3 patients had loss of chromosome 9 or 9q without any other severe chromosome alterations. CNV alterations will be presented and compared to MIBC. Conclusions: In this preliminary analysis, our HGT1micropap, showed a mutational landscape more similar to MIBC compared to NMIBC bladder landscape. We did not find any clear driver of the micropapillary histology at the exome level in this limited sample of patient, which may indicate that tumor heterogeneity or epigentic changes may be driving this aggressive phenotype. [Table: see text]
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Zaidi, Sayyed K., Daniel W. Young, Martin Montecino, Jane B. Lian, Janet L. Stein, Andre J. van Wijnen, and Gary S. Stein. "Architectural Epigenetics: Mitotic Retention of Mammalian Transcriptional Regulatory Information." Molecular and Cellular Biology 30, no. 20 (August 9, 2010): 4758–66. http://dx.doi.org/10.1128/mcb.00646-10.

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ABSTRACT Epigenetic regulatory information must be retained during mammalian cell division to sustain phenotype-specific and physiologically responsive gene expression in the progeny cells. Histone modifications, DNA methylation, and RNA-mediated silencing are well-defined epigenetic mechanisms that control the cellular phenotype by regulating gene expression. Recent results suggest that the mitotic retention of nuclease hypersensitivity, selective histone marks, as well as the lineage-specific transcription factor occupancy of promoter elements contribute to the epigenetic control of sustained cellular identity in progeny cells. We propose that these mitotic epigenetic signatures collectively constitute architectural epigenetics, a novel and essential mechanism that conveys regulatory information to sustain the control of phenotype and proliferation in progeny cells by bookmarking genes for activation or suppression.
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Dissertations / Theses on the topic "Epigentic control"

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Lezcano, Magda. "The Control of the Epigenome." Doctoral thesis, Uppsala universitet, Zoologisk utvecklingsbiologi, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7190.

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The genetic information required for the existence of a living cell of any kind is encoded in the sequence information scripted in the double helix DNA. A modern trend in biology struggles to come to grip with the amazing fact that there are so many different cell types in our body and that they are directed from the same genomic blueprint. It is clear, that the key to this feature is provided by epigenetic information that dictates how, where and when genes should be expressed. Epigenetic states “dress up” the genome by packaging it in chromatin conformations that differentially regulate accessibility for key nuclear factors and in coordination with differential localizations within the nucleus will dictate the ultimate task, expression. In the imprinted Igf2/H19 domain, this feature is determined by the interaction between the chromatin insulator protein CTCF and the unmethylated H19 imprinting control region. Here I show that CTCF interacts with many sites genome-wide and that these sites are generally protected from DNA methylation, suggesting that CTCF function has been recruited to manifest novel imprinted states during mammalian development. This thesis also describes the discovery of an epigenetically regulated network of intra and interchromosomal complexes, identified by the invented 4C method. Importantly, the disruption of CTCF binding sites at the H19 imprinting control region not only disconnects this network, but also leads to significant changes in expression patterns in the interacting partners. Interestingly, CTCF plays an important role in the regulation of the replication timing not only of the Igf2 gene, but also of all other sequences binding this factor potentially by a cell cycle-specific relocation of CTCF-DNA complexes to subnuclear compartments. Finally, I show that epigenetic marks signifying active or inactive states can be gained and lost, respectively, upon exposure to stress. As many genes belonging to the apoptotic pathway are upregulated we propose that stress-induced epigenetic lesions represent a surveillance system marking the affected cells for death to the benefit of the individual. This important observation opens our minds to the view of new intrinsic mechanisms that the cell has in order to maintain proper gene expression, and in the case of misleads there are several check points that direct the cell to towards important survival decisions.
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Sima, Teruel Núria. "Paper de SirT2 en el control epigenètic de la mitosi." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/386527.

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La cromatina és una estructura nucleoproteica, dinàmica i jeràrquicament organitzada dins del nucli cel•Iular. La seva estructura, organització i funció està controlada al llarg del cicle cel.lular, per processos epigenètics que produeixen canvis heretables que no afecten la seqüència de DNA. Entre aquests canvis es troben la metilació del DNA, les modificacions postraduccionals de les histones i desplegament de la cromatina orquestrat pels complexes remodeladors i proteïnes estructurals. Les modificacions postraduccionals de les histones es donen principalment de forma dinàmica i regulada a l'extrem N-terminal, canviant la seva càrrega i funció. Entre les diferents modificacions descrites, l'acetilació i la metilació de les histones H3 i H4, semblen tenir una importància especial sobre l'estructura i estat de la cromatina. En particular, l'acetilació de la lisina 16 de la histona H4 (H4K16Ac) per se impedeix la formació d'estructures compactes de cromatina. D'aquesta manera, s'associa l'estat desacetilat d'aquest residu a zones d'heterocromatina i transcripcionalment inactives, mentre que la hiperacetilació d'H4K16 està estretament vinculada a zones eucromàtiques i transcripcionalmentactives. La dinàmica d'acetilació-desacetiIació d' H 4K 16 està controlada principalment per l'equilibri de les activitats acetiltransferasa de MOF i desacetilasa de Si rT1 i Si rT2. Per tant, aquests dos grups d'enzims són essencials per el control de l'expressió gènica i de l'arquitectura de la cromatina dins del nucli, regulant la transició entre l'estat transcripcionalment actiu i inactiu de la cromatina. MOF és crucial per el desenvolupament embrionari , I a reparació del DNA i la progressió del cicle cel .lular, i la seva pèrdua està associada a l'augment de les aberracions cromosòmiques, a l'aturada del cicle cel.lular en G2/M i a l'augment de la inestabilitat genòmica. SirT1 i Si rT2 pertanyen a la classe III de desacetilases d'histones (HDACs), conegudes com sirtuïnes, i són crucials per el manteniment de la integritat genòmica, l'adaptació a l'entorn i l'envelliment, entre altres funcions. No obstant, dels set membres de sirtuïnes presents a mamífers, només Si rT2 i en menor mesura SirT1, han estat vinculades amb el control del cicle cel.lular. Concretament, Si rT2, tot i ser principalment citoplasmàtica, és transportada al nucli durant I a transició G2/M , moment en el que a través de la desacetilació d'H4K16 permet la monometilació d'H4K20 per PR-SET7 (la monometiI transferasa d'H4K20), determinant els nivells d'H4K2Ome2,3 en la resta del cicle cel.lular. Com a conseqüència, SirT2 està implicat en processos estrictament associat a aquestes modificacions, com la compactació dels cromosomes metafàsics, Ia progressió a través de mitosi, la replicació i reparació del DNA o la formació de l'heterocromatina. Fins al moment el paper de Si rT2 en el control de I a progressió a través de la mitosi ha estat atribuït a la regulació de diferents substrats. En particular, el control d'H4K2Ome1 dependent de SirT2 ha estat relacionat amb l'activació del checkpoint de G2/M en resposta a estrès, tot i que els mecanismes involucrats en l'aturada del cicle cel.lular eren del tot desconeguts. En aquest treball hem volgut indagar sobre com Si rT2 regula la transició G2/M i la seva coordinació amb la maquinària regulatória del checkpoint. Les nostres dades semblen indicar que SirT2 condueix a l'activació del checkpoint de G2/M a través de la regulació d' H4K 1 6Ac, H4K2Ome1 i el control de I a transcripció de gens relacionats amb el cicle cel.lular. Es descriu per primera vegada, com SirT2 controla H4K16Ac a través de la regulació de l'activitat i de l'estabilitat proteica de MOF durant G2/M. Concretament, SirT2 desacetila MOF durant G2/M i en promou la sortida de la cromatina, la inactivació i degradació, afavorint l'estat desacetilat d'H4K16 i la monometilació d'H4K20. En concordança, hem vist que MOF controla negativament la presència de PR-SET7 a la cromatina, mantenint així uns nivells adequats d'H4K2Omel abans d'entrar a mitosi i evitant la condensació prematura dels cromosomes. El nostre estudi suggereix que la interconnexió entre SirT2 i MOF està directament implicada en el control epigenètic del cicle cel.lular, contribuint al manteniment de l'estabilitat genòmica.
Chromatin is a dynamical structure hierarchically organized to fit inside the nucleus. The structure, organization and function of chromatin are tightly controlled throughout the cell cycle by different epigenetic mechanisms, including DNA methylation and histone modifications. The histone post-translational modifications occur mainly in their N-terminal tail, and give rise to changes in the charge and function of the protein. Among the different histone modifications, lysine acetylation (K) is one of the best characterized. Acetylation of lysine 16 of histone H4 is the most frequently acetylated residue in eukaryotes and is a key regulator of high orders of chromatin structure. Thus, the deacetylated state of this residue is associated with heterochromatic and transcriptional inactive regions, whereas the acetylated form is found in euchromatic and transcriptional active regions. The dynamics of this histone mark is mainly governed by the acetyltransferase MOF and the NAD±-dependent deacetylases SirT1 and SirT2, which makes both groups of enzymes essential for the regulation of the gene expression and the control of chromatin organization. MOF is crucial in embryogenesis, DNA repair and the cell cycle progression. In fact, loss of MOF has been shown to induce cell cycle arrest during G2/M transition, increased chromosomal aberrations and genome instability. SirT 1 and SirT2 belong to Class III of histone deacetylases (HDACs), commonly referred as sirtuins. They play a key role in stress response, and in particular in protecting genome integrity. Among the seven mammalian sirtuins (SirT1-7), only SirT2 and to a lesser extend SirT1, have been linked with cell cycle regulation. In particular, SirT2, which mainly localizes to the cytoplasm during most of the cell cycle, shuttles to the nucleus in G2/M transition, where deacetylates H4K16Ac driving, among other things, H4K2Omel deposition by the histone methyltransferase PR-SETT. The control of H4K2Omel deposition determines the levels of H4K2Ome2,3 in the next cell cycle, which links SirT2 to the regulation of DNA replication and repair, as well as heterochromatin formation. Work from our group and others have shown that SirT2 plays a role in the control of mitosis progression. In particular, SirT2 is required for the cell cycle arrest in the G2/M checkpoint during stress response, process that has been related to SirT2-dependent regulation of H4K2Omel. However, the mechanisms behind the cell cycle arrest are still undefined. In the present work we aimed to elucidate the function of SirT2 in G2/M transition and its coordination with the checkpoint regulatory machinery. Our results seem indicate that SirT2 drives the G2/M checkpoint activation through the regulation of H4K16Ac, H4K2Omel and the control of the expression of cell cycle related genes. We also describe for the first time, a complementary mechanism whereby SirT2 regulates the levels of H4K16Ac during mitosis. We observe that SirT2 not only deacetylates MOF during G2/M, suppressing its acetyltransferase activity, but also induces both chromatin eviction and degradation of MOF. This in turn, results in H4K16 hypoacetylation and subsequent monomethylation of H4K20. Additionally, we show that MOF inhibits PR-SETT chromatin localization, maintaining the appropriate levels of H4K2Omel before entering mitosis and avoiding premature chromosome condensation. Our study suggests that the crosstalk between MOF and SirT2 is directly involved in the epigenetic control of the cell cycle, contributing to the maintenance of genome stability.
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Sessa, Luca. "Epigenetic control of human HOX clusters." Thesis, Open University, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.402692.

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Deraze, Jérôme. "Epigenetic control of ribosome biogenesis homeostasis." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066342/document.

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La traduction est une activité cellulaire essentielle, réalisée par les ribosomes. Ces particules sont synthétisées dans le nucléole, ce qui nécessite l'expression coordonnée de 4 ARN ribosomaux, 80 protéines ribosomales, et plus de 200 facteurs d'assemblage. Leur biogenèse est complexe et sollicite plus de la moitié de l'énergie des cellules en prolifération. La quantité de ribosomes varie selon les conditions environnementales et métaboliques et de ce fait, leur synthèse est modulée en réponse à de nombreux stimuli. Plusieurs mécanismes coordonnent la biogenèse des ribosomes avec l'homéostasie cellulaire. L'un d'eux est la capacité des protéines ribosomiques à réguler l'expression des gènes à plusieurs niveaux. Ces fonctions effectuées hors du ribosome sont dites extraribosomales. Notre équipe a mis en évidence l'une de ces fonctions de la protéine ribosomale uL11 chez la Drosophile. Quand sa lysine 3 est triméthylée (uL11K3me3), elle interagit avec Corto, un facteur de transcription de la famille des Enhancers de Trithorax et Polycomb. L'étude de leur fixation à la chromatine montre que ces protéines se répartissent différemment à l'échelle du génome, et que uL11K3me3 est présente au niveau de gènes actifs enrichis en composants du ribosome. Nous avons généré les premiers allèles génétiques du gène uL11 chez la Drosophile, et décrivons la stratégie de crible moléculaire employée pour leur isolation. Finalement, nous avons étudié les allèles de uL11 dont la lysine 3 est mutée. Leurs phénotypes ressemblent à ceux des mutants Minute, suggérant que le domaine N-terminal de uL11 possède une fonction essentielle, mais peut-être indépendante d'une interaction avec Corto
Translation is an essential metabolic activity carried by ribosomes. These complexes are synthetized in the nucleolus, and require the coordinated expression of 4 ribosomal RNA, 80 ribosomal proteins, and more than 200 assembly factors. Indeed, their biogenesis is complex and expensive, consuming more than half of the energy in proliferating cells. As the cellular need for ribosomes varies with environmental or metabolic conditions, their synthesis is tightly regulated in response to a number of cues. Many mechanisms ensure that the intensity of ribosome biogenesis is coupled to cell homeostasis. Such is the ability of ribosomal proteins to regulate gene expression at many levels, from translation specificity to activation or repression of transcription. Many such functions are carried off the ribosome, and are thus termed extraribosomal. Our team discovered a new extraribosomal function of ribosomal protein uL11 in Drosophila. Indeed, when trimethylated on lysine 3 (uL11K3me3), it associates with Corto, a transcription factor of the Enhancers of Trithorax and Polycomb family. By studying their genome-wide binding profile on chromatin, we show that these proteins are distributed along different patterns, and that uL11K3me3 specifically binds a subset of active genes enriched in ribosome biogenesis components. Additionally, we generated the first genetic alleles for Drosophila uL11 and describe the molecular screening method that we employed. Last, we studied the uL11 alleles that delete or replace lysine 3. We describe that their Minute-like phenotypes suggest an essential role for the N-terminal domain of uL11, though it may be independent of its association with Corto
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Martucci, Mariane Ferracin. "Impactos das biotécnicas reprodutivas no controle epigenético de genes imprinted." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/10/10132/tde-20102015-082930/.

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Técnicas de reprodução assistida (TRAs) são utilizadas tanto na medicina humana quanto na medicina veterinária com o objetivo principal de corrigir infertilidades adquiridas ou herdadas. A transferência nuclear de célula somática (TNCS) ocupa um lugar de destaque na veterinária pela possibilidade de geração de indivíduos geneticamente idênticos, permitindo a produção de rebanhos homogêneos de alto mérito genético e servindo como modelo de estudo para técnicas de reprogramação. Porém, a utilização de TRAs, e em especial da TNCS, é considerada responsável pelo aumento na geração de conceptos portadores de alterações durante e após o desenvolvimento embrionário e fetal. A provável causa principal é a alteração na regulação da reprogramação epigenética devido à manipulação de gametas e embriões no período inicial do desenvolvimento, levando a alterações na regulação epigenética de genes imprinted. O presente estudo teve como objetivo principal avaliar marcas epigenéticas e expressão de genes imprinted no desenvolvimento de conceptos bovinos produzidos por TNCS ou inseminação artificial (IA). Para tal, foram coletadas amostras de tecido muscular e membranas corioalantoideana e amniótica de animais na fase pré natal (fetal) e tecidos muscular, nervoso e hepático na fase pós natal (animais nascidos saudáveis adultos ou não) de animais derivados de IA ou TNCS. Foi analisada a expressão dos genes imprinted H19, IGF2, IGF2R e Airn quando possível, assim como a metilação do DNA no locus H19/IGF2 na fase pós natal. Foi observado que na fase pré natal não foi detectada expressão do IGF2, enquanto que a expressão de H19 é aumentada em relação ao IGF2R, porém, sem diferenças entre os grupos nos tecidos estudados. Na fase pós natal, o padrão de expressão dos genes IGF2, H19 e IGF2R indica diminuição da expressão gênica relativa no fígado de animais TNCS e no aumento da expressão gênica do H19 na musculatura de animais adultos (saudáveis) bovinos produzidos por TNCS, apesar de o padrão de metilação dos genes imprinted IGF2/H19 não ser diferente entre organismos considerados saudáveis e não saudáveis. Os resultados deste projeto contribuem para o entendimento dos mecanismos epigenéticos relacionados ao desenvolvimento embrionário e fetal, em especial aqueles relacionados à dinâmica das alterações epigenéticas envolvidas no imprinting genômico
Assisted reproductive technologies (ARTs) are usually used in both human and veterinary medicine aiming the correction of heritable or acquired infertilities. The somatic cell nuclear transfer technique (SCNT) is of particular importance in veterinary as it enables the generation of genetically identical organisms, allowing the production of homogeneous genetically improved herds, and also serving as a model for reprogramming studies. However, the use of TRAs, SCNT in special, may be responsible for the increase of developmental-related abnormalities in the conceptuses. Such phenotypes are probably caused by a disruption during the epigenetic reprogramming due to the manipulation of gametes and embryos during the early development period, and therefore leading to disturbances in the epigenetic regulation of imprinted genes. The present study aimed to evaluate epigenetic marks and expression of imprinted genes in different developmental periods of cattle generated by SCNT or artificial insemination (AI). For that, corionic/alantoic and amniotic membranes from fetuses and muscular, nervous and hepatic tissues from born animals, healthy (adult) or not, produced by SCNT or AI were collected. The expression of the imprinted genes H19, IGF2, IGF2R and Airn was analyzed as well as the DNA methylation at locus H19/IGF2 in post-natal period. It was observed that IGF2 was not detected during pre-natal period, whereas H19 expression is increased when compared to IGF2R in the groups studied herein. At post-natal period the IGF2, H19 and IGF2R expression patterns infers the decrease of relative gene expression in the liver and the increase of H19 expression in the muscle of SCNT adult animals. The methylation pattern of IGF2/H19 locus, however, did not differ between healthy or not animals. The results described herein may contribute to the understanding of the epigenetic mechanisms related to embryonic and fetal development, and in special, to those related to the epigenetic dynamics during genomic imprinting
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Freyer, Jennifer Sandra Silvia. "Regulation und funktionelle Rolle des murinen Transkriptionsfaktors Foxp3 in T-Zellen." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2008. http://dx.doi.org/10.18452/15841.

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In dieser Arbeit wurde die funktionelle Rolle und Regulation des murinen Transkriptionsfaktor Foxp3 untersucht. Der erste wesentliche Teil zur Analyse der funktionellen Rolle war dabei die Erzeugung einer BAC- transgenen Maus. Hierfür wurde ein Zielgenvektor mit der kodierenden Region des eYFPs und einer dualen Selektionskassette sowie die Methode des ET- Klonierens verwendet. Leider war die homologe Rekombination des Zielgenvektors in den BAC nicht erfolgreich. Es kam zu einer ungeklärten Rekombination mit Fremd- DNS. Die Erzeugung der transgenen Maus wurde nach diesem Ergebnis eingestellt, und es wurde mit einer von unserem Kooperationspartner zur Verfügung gestellten BAC- transgenen Maus weitergearbeitet. Diese Maus, die DEREG- Maus, wurde nach dem gleichen Prinzip erstellt, wie die in dieser Arbeit gestartete transgene Maus, an Stelle des eYFPs trägt die DEREG- Maus die kodierenden Region des GFPs und des Diphtheria- Toxin- Rezeptors. Mit dieser Maus wurden erste Analysen zur Überprüfung der transgenen Maus unternommen. Es wurde die Koexpression von GFP und Foxp3, sowie die Depletion der Foxp3+ T- Zellen mittels Diphtheria- Toxin analysiert. Als nächstes wurde die funktionelle Rolle des Transkriptionsfaktors Foxp3 analysiert. Als einer der ersten Schritte wurde die Stabilität von Foxp3 in vivo überprüft und gezeigt, dass T- Zellen, die das Foxp3- Protein exprimieren, bis zu 14 Tage in vivo stabil sind. Weiterhin wurde die Stabilität der Foxp3- Expression in in vitro Kulturen nach Induktion durch TGF-beta untersucht. Die induzierten Tregs zeigten keine stabile Foxp3- Expression und auch bei der Methylierungsanalyse der TSDR zeigten diese T- Zellen nicht das für ex vivo isolierte Foxp3+ T- Zellen beschriebene Methylierungsmuster. Die Stabilität scheint mit der Demethylierung der TSDR zu korrelieren. Die induzierten Tregs zeigten neben dem nicht stabilen Foxp3- Phänotyp auch eine von der Foxp3- Expression abhängige Suppression von naiven Zellen im in vitro Proliferations- Test. Im dritten Teil der Arbeit wurde die Struktur und Regulation des Transkriptionsfaktors Foxp3 untersucht. Der Lokus wurde auf konservierte Regionen im Vergleich zu den Spezies Maus, Mensch, Ratte, Huhn, Schimpanse, Hund und Frosch untersucht. Die in Floess*, Freyer* et al. (63) gefundenen Region TSDR enthält einen hochkonservierten Bereich. Die Region wurde auf mögliche Transkriptionsfaktor- Bindungsstellen hin analysiert, und ebenfalls wurden in diesem Bereich Histon- Modifikationen für die Acetylierung der Histone H3 und H4, sowie Tri- Methylierung des Lysin4 des Histons H3 gefunden. Die TSDR wurde in Luciferase- Tests auf ihre transkriptionelle Aktivität hin getestet und zeigte einem Enhancer ähnliche unterstützende Aktivität. Die Methylierung der TSDR in den Luciferase- Tests führte zu einer Reduktion der transkriptionellen Aktivität. Deletionsmutanten der TSDR konnten den Bereich für die transkriptionelle Aktivität weiter einschränken und zeigten ein 275pb großes Fragment auf, in welchem viele interessante, mögliche Transkriptionsfaktor- Bindungsstellen und auch die größte Anzahl der differentiell methylierten CpG- Motive liegen.
The aim of the study was to analyze the function and regulation of the transcription factor Foxp3. In a first step we designed a BAC-transgenic mouse with eYFP under the control of the Foxp3 promoter. For creating these mice we use the ET- cloning method. The step of homologous recombination of the target vector into the BAC failed. Because of that, we decided to work in cooperation with the group of Tim Sparwasser from Munich and their BAC- transgenic mouse called DEREG- mouse. This mouse expresses the coding region of eGFP fused to the diphtheria- toxin- receptor under the control of the Foxp3 promoter. Therefore Foxp3+ T cells can be easily detected by eGFP expression and can even be depleted by diphtheria- toxin- application. We confirmed the co- expression of Foxp3 and eGFP and furthermore tested the functionality of the depletion- process of Foxp3+ T cells by treatment with diphtheria- toxin. In a second study, we analyzed the stability of Foxp3 expressing cells in vivo. Therefore we transferred Foxp3+ T cells in syngenic mice and analyzed these cells after 14 days for their Foxp3- expression. Furthermore, we tested the induction of Foxp3 expression through TGF-beta and the suppressive activity of these cells. We also analyzed those cells for their methylation pattern, comparing cells, which showed an induction of Foxp3- expression after one week of culture with TGF-beta to cells, which received TGF-beta for one week and were then restimulated in the absence of TGF-beta. The stability of Foxp3 expression seems to correlate with the demethylated state of the TSDR (Treg Specific Demethylated Region). To get a closer look on the region called TSDR in the murine foxp3 locus, we decided to analyze this region under different aspects. First, we checked for putative binding sites of transcription factors by database analysis of the TSDR. We also analysed histon modifications, such as acetylation of histon H3 and H4 and tri- methylation of lysine 4 at histon3, in this region. Presence of these modifications hinted an epigenetic regulation of Foxp3 involving the TSDR. In a last step, the transcriptional activity of TSDR was tested to delineate whether the TSDR serves as an alternative promoter or acts as a regulative element like an enhancer. Luciferase assays showed that TSDR is a regulative enhancer element, which loses transcriptional activity when methylated. Deletion mutants determined the most important fragment of the TSDR.
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Ferreira, Mónica Alexandra dos Santos. "Epigenetic control of the male progenitor germline by the protein phosphatase PP1-NIP." Doctoral thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/22814.

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Doutoramento em Biologia
NIPP1, for nuclear inhibitor of protein phosphatase 1 (PP1), is a multifunctional scaffold protein that regulates cell signaling, pre-mRNA splicing and transcription by targeting PP1 to specific nuclear substrates. The global deletion of NIPP1 in mice is embryonic lethal at the onset of gastrulation, precluding its functional analysis in adult tissues. This prompted us to generate a tamoxifen-inducible NIPP1 knockout (iKO) mouse model. Unexpectedly, the deletion of NIPP1 was not efficient in the examined organs except for testis. The loss of NIPP1 caused an age-dependent progressive loss of testicular germ cells, culminating in a Sertoli cells-only phenotype. iKO testis showed a decreased proliferation of (un)differentiated spermatogonia and an increased level of apoptosis. Likewise, neonatal iKO testis exhibited an almost complete loss of gonocyte-derived (un)differentiated spermatogonia during the first wave of spermatogenesis. In addition, GFRA1+ progenitor cells isolated from induced iKO testis displayed a reduced proliferation potential. These data suggest that NIPP1 is required for the maintenance of undifferentiated spermatogonia. We also found that the observed phenotype was associated with the deregulation of genes that are implicated in the control of cell proliferation and survival. At the molecular level, the deletion of NIPP1 was associated with the loss of core components of the Polycomb Repressive Complex 2 (PRC2), which affects gene expression through trimethylation of histone H3 at Lys 27. The loss of PRC2 components could be explained by the hyperphosphorylation and degradation of EZH2, the catalytic subunit of the PRC2 complex, resulting in the destabilization of other PRC2 core components. The testis phenotype of the iKOs could be phenocopied by the chemical inhibition of EZH1/2 in organotypic testis cultures. Overall, our study uncovers a key function for PP1-NIPP1 in the regulation of EZH2 phosphorylation and stability, which is essential for the maintenance of germ cells.
NIPP1, inhibidor nuclear da protein phosphatase 1 (PP1), é uma proteina multifuncional que regula a sinalização celular, splicing do pre-mRNA e transcrição mediante o direcionamento da PP1 para substratos nucleares específicos. A deleção global da NIPP1 é letal durante o desenvolvimento embrionário no início da gastrulação, impedindo assim a sua análise funcional em tecidos de adultos. Este facto incitou-nos a gerar um modelo de ratinho knockout induzível (iKO) para a NIPP1. Inesperadamente, a remoção da NIPP1 não foi eficiente na maioria dos órgãos analisados, com exceção do testículo. A deleção da NIPP1 causou uma perda progressiva de células germinativas do testículo dependente da idade, culminando num fenótipo denominado Sertoli cells-only phenotype. O testículo adulto nos ratinhos iKO apresentaram uma diminuição na proliferação das espermatogónias (in)diferenciadas e aumento dos níveis de apoptose. De modo análogo, o testículo dos neonatos exibiu uma perda quase completa das espermatogónias (in)diferenciadas derivadas de gonócitos, durante o primeiro ciclo de espermatogénese. Adicionalmente, culturas celulares enriquecidas em células progenitoras GFRA1+ isoladas do testículo dos ratinhos iKO apresentaram uma diminuição do seu potencial proliferativo. Estes resultados sugerem que a NIPP1 é necessária para a manutenção das espermatogónias indiferenciadas. Demonstrámos também que fenótipo observado está associado à desregulação de genes implicados no controlo da proliferação e viabilidade celular. No que concerne o mecanismo molecular, a deleção da NIPP1 resultou na perda dos componentes centrais do complexo PRC2 (Polycomb Repressive Complex 2), o que afetou a expressão genética através da trimetilação da histone H3 no resíduo Lys27 (H3K27me3). A perda dos componentes integrantes do complexo PRC2 foi explanada pela hiperfosforilação e degradação da proteína EZH2, o componente catalítico central do complexo PRC2, resultando na subsequente destabilização de outros componentes deste complexo. Em conformidade, o fenótipo foi reproduzido através da inibição química da proteína EZH1/2 em culturas organotípicas de testículos. De modo geral, este estudo revela a importância da fosfatase PP1-NIPP1 para a regulação da fosforilação e estabilização da proteína EZH2, essencial para a manutenção das células germinativas.
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Hitchcock, Robert Arthur. "Epigenetic control of the kinetoplastid spliced leader RNA." Diss., Restricted to subscribing institutions, 2009. http://proquest.umi.com/pqdweb?did=1998392041&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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Herranz, Martín Nicolás. "New insights in the epigenetic control of EMT." Doctoral thesis, Universitat Pompeu Fabra, 2011. http://hdl.handle.net/10803/80660.

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The epithelial to mesenchymal transition (EMT) is a highly conserved cellular program that allows well-­‐differentiated epithelial cells to convert to motile mesenchymal cells. EMT is critical for appropriate embryogenesis and plays a crucial role in tumorigenesis and cancer progression. At this regard, it has become increasingly evident that, in addition to genetic alterations, tumour development involves the alteration of gene expression patterns owing to epigenetic changes. Taking this into account, this thesis mainly addresses the description of new molecular epigenetic mechanisms underlying one of the hallmark processes governing EMT, the Snail1-­‐mediated E-­‐cadherin repression. Indeed, our results demonstrate that both Polycomb group (PcG) proteins and the LOXL2 protein are involved in this process. Apart from providing novel insights into the significance of these proteins in tumor progression, our work uncovers the characterization of a new epigenetic modification carried out by LOXL2; H3K4 deamination.
La transició epiteli-­‐mesènquima (EMT) és un programa cel·lular molt conservat que permet a les cèl·lules epitelials convertir-­‐se en cèl·lules mesenquimals indiferenciades. La EMT és un procés crucial pel desenvolupament embrionari i per la progressió tumoral. A aquest respecte, ha esdevingut cada cop més evident que el desenvolupament tumoral no només està associat a alteracions genètiques, sinó també a l'alteració de l’expressió gènica causada per canvis epigenètics. Tenint això en compte, aquesta tesi es centra en la descripció de nous mecanismes moleculars en l’àmbit de l’epigenètica associats a un dels processos clau en la EMT, la repressió de la E-­‐ cadherina mitjançada pel factor de transcripció Snail1. De fet, els nostres resultats demostren que tant les proteïnes del grup Polycomb (PcG) com la proteïna LOXL2 estan implicades en aquest procés. A part de proporcionar nova informació respecte la importància d'aquestes proteïnes en la progressió tumoral, la nostra feina ha permès la caracterització d'una nova modificació epigenètica duta a terme per la proteïna LOXL2; la deaminació de H3K4.
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Goncharevich, Alexander. "Epigenetic control of Wnt signalling in CNS remyelination." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648183.

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Books on the topic "Epigentic control"

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Grafi, Gideon, and Nir Ohad, eds. Epigenetic Memory and Control in Plants. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-35227-0.

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Mukesh, Verma, Dunn Barbara K, Umar Asad, and National Cancer Institute (U.S.). Division of Cancer Prevention., eds. Epigenetics in cancer prevention: Early detection and risk assessment. New York: New York Academy of Sciences, 2003.

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Epigenetic Memory And Control In Plants. Springer-Verlag Berlin and Heidelberg GmbH &, 2013.

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Grafi, Gideon, and Nir Ohad. Epigenetic Memory and Control in Plants. Springer, 2013.

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Grafi, Gideon, and Nir Ohad. Epigenetic Memory and Control in Plants. Springer, 2015.

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Wolffe, Alan P., and Fyodor Urnov. Epigenetics: Principles of Eukaryotic Genome Control. Wiley-Liss, 2008.

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Qiu, Xuan. Epigenetic Control of Tumor Suppressor Genes in Lung Cancer. INTECH Open Access Publisher, 2012.

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Cabej, Nelson R. Neural Control of Development: The Epigenetic Theory of Heredity. Albanet, 2005.

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Cabej, Nelson R. Neural Control of Development: The Epigenetic Theory of Heredity. 2nd ed. Albanet, 2005.

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Yang, Jin, Pei Han, Wei Li, and Ching-Pin Chang. Epigenetics and post-transcriptional regulation of cardiovascular development. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0032.

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Cardiac organogenesis requires the control of gene expression at distinct developmental windows in order to organize morphogenetic steps in the correct sequence for heart development. This is facilitated by concerted regulation at three levels: chromatin, transcription, and post-transcriptional modifications. Epigenetic regulation at the chromatin level changes the chromatin scaffold of DNA to regulate accessibility of the DNA sequence to transcription factors for genetic activation or repression. At the genome, long non-coding RNAs work with epigenetic factors to alter the chromatin scaffold or form DNA-RNA complexes at specific genomic loci to control the transcription of genetic information. After RNA transcription, the expression of genetic information can be further modified by microRNAs. Each layer of gene regulation requires the participation of many factors, with their combinatorial interactions providing variations of genetic expression at distinct pathophysiological phases of the heart. The major functions of chromatin remodellers and non-coding RNAs are discussed.
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Book chapters on the topic "Epigentic control"

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Helmbold, Heike, Wolfgang Deppert, and Wolfgang Bohn. "Epigenetic Control in Cellular Senescence." In Cancer Epigenetics, 25–44. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118005743.ch3.

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Bronner, Christian, Mayada Achour, Thierry Chataigneau, and Valérie B. Schini-Kerth. "Epigenetic Control of Gene Transcription." In Cancer Epigenetics, 57–99. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118005743.ch5.

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Lopez-Granados, Eduardo. "Epigenetic Control of Lymphocyte Differentiation." In Epigenetic Contributions in Autoimmune Disease, 26–35. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-8216-2_3.

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van den Elsen, Peter J., Marja C. J. A. van Eggermond, and Rutger J. Wierda. "Epigenetic Control in Immune Function." In Epigenetic Contributions in Autoimmune Disease, 36–49. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-8216-2_4.

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Razin, Aharon, and Ruth Shemer. "Epigenetic Control of Gene Expression." In Results and Problems in Cell Differentiation, 189–204. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-540-69111-2_9.

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Guénet, Jean-Louis, Fernando Benavides, Jean-Jacques Panthier, and Xavier Montagutelli. "Epigenetic Control of Genome Expression." In Genetics of the Mouse, 187–220. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-44287-6_6.

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Van Wynsberghe, Priscilla M., and Eleanor M. Maine. "Epigenetic Control of Germline Development." In Germ Cell Development in C. elegans, 373–403. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4015-4_13.

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Saijo, Yusuke, and Eva-Maria Reimer-Michalski. "Epigenetic Control of Plant Immunity." In Epigenetic Memory and Control in Plants, 57–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-35227-0_4.

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Zografou, Theo, and Franziska Turck. "Epigenetic Control of Flowering Time." In Epigenetic Memory and Control in Plants, 77–105. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-35227-0_5.

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Houben, Andreas, Dmitri Demidov, and Raheleh Karimi-Ashtiyani. "Epigenetic Control of Cell Division." In Epigenetic Memory and Control in Plants, 155–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-35227-0_8.

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Conference papers on the topic "Epigentic control"

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Young, Richard A. "Abstract IA01: Transcriptional and epigenetic control of oncogenes." In Abstracts: AACR Special Conference on Chromatin and Epigenetics in Cancer - June 19-22, 2013; Atlanta, GA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.cec13-ia01.

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Zakarya, Razia, Hui Chen, Corey-Anke Brandsma, Ian M. Adcock, and Brian G. G. Oliver. "Epigenetic control of TGFβ induced fibrosis in COPD." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa961.

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Bailly, David, Pierre Andry, and Philippe Gaussier. "Learning anticipatory motor control." In 2012 IEEE International Conference on Development and Learning and Epigenetic Robotics (ICDL). IEEE, 2012. http://dx.doi.org/10.1109/devlrn.2012.6400850.

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Talbott, Walter A., He Crane Huang, and Javier Movellan. "Infomax models of oculomotor control." In 2012 IEEE International Conference on Development and Learning and Epigenetic Robotics (ICDL). IEEE, 2012. http://dx.doi.org/10.1109/devlrn.2012.6400823.

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Zeng, Guihua, Fu-Sen Liang, and Lina Cui. "Abstract 5234: Epigenetic control of heparanase expression through CRISPR/dCas9." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-5234.

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Maitland, Norman James, and John Packer. "Abstract B23: Epigenetic control of prostate epithelial stem cell differentiation." In Abstracts: AACR Special Conference on Developmental Biology and Cancer; November 30 - December 3, 2015; Boston, Massachusetts. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.devbiolca15-b23.

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Li, Qunfang, and Michael A. Tainsky. "Abstract 4002: Epigenetic control of a checkpoint for miRNA tolerance." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4002.

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Koss, Brian, Bradley D. Shields, Erin M. Taylor, Aaron J. Storey, Stephanie D. Byrum, Allen J. Gies, Charity L. Washam, et al. "Abstract 1029: Epigenetic control of tumor-infiltrating lymphocyte metabolic-exhaustion." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-1029.

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Zeng, Guihua, Fu-Sen Liang, and Lina Cui. "Abstract 5234: Epigenetic control of heparanase expression through CRISPR/dCas9." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-5234.

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Chen, Zixin, Guihua Zeng, Xiaogang Li, Fu-Sen Liang, and Lina Cui. "Abstract 2112: Epigenetic control of heparanase expression using CRISPR/dCas9." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2112.

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Reports on the topic "Epigentic control"

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Williams, Kristin P. Epigenetic Control of Tamoxifen-Resistant Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2013. http://dx.doi.org/10.21236/ada581650.

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Williams, Kristin P. Epigenetic Control of Tamoxifen-Resistant Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2014. http://dx.doi.org/10.21236/ada601260.

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Case, Adam J., and Frederick E. Domann. Epigenetic Control of Prolyl and Asparaginyl Hydroxylases in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2010. http://dx.doi.org/10.21236/ada542700.

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Case, Adam J. Epigenetic Control of Prolyl and Asparaginyl Hydroxylases in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada511993.

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Franceschi, Renny T. Epigenetic Control of Prostate Cancer Metastasis: Role of Runx2 Phosphorylation. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada580104.

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Case, Adam. Epigenetic Control of Prolyl and Asparaginyl Hydroxylases in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada552430.

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Franceschi, Renny T. Epigenetic Control of Prostate Cancer Metastasis: Role of Runx2 Phosphorylation. Fort Belvoir, VA: Defense Technical Information Center, May 2015. http://dx.doi.org/10.21236/ada620609.

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Martínez-Balbás, Marian. La epigenética controla el desarrollo del sistema nervioso (Especial Premio FBBVA 2013). Sociedad Española de Bioquímica y Biología Molecular (SEBBM), July 2014. http://dx.doi.org/10.18567/sebbmdiv_rpc.2014.07.1.

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