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Auswahl der wissenschaftlichen Literatur zum Thema „Epigenetic switch“
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Zeitschriftenartikel zum Thema "Epigenetic switch"
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Linquist, Stefan, und Brady Fullerton. „Transposon dynamics and the epigenetic switch hypothesis“. Theoretical Medicine and Bioethics 42, Nr. 3-4 (August 2021): 137–54. http://dx.doi.org/10.1007/s11017-021-09548-x.
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AbstractThe recent explosion of interest in epigenetics is often portrayed as the dawning of a scientific revolution that promises to transform biomedical science along with developmental and evolutionary biology. Much of this enthusiasm surrounds what we call the epigenetic switch hypothesis, which regards certain examples of epigenetic inheritance as an adaptive organismal response to environmental change. This interpretation overlooks an alternative explanation in terms of coevolutionary dynamics between parasitic transposons and the host genome. This raises a question about whether epigenetics researchers tend to overlook transposon dynamics more generally. To address this question, we surveyed a large sample of scientific publications on the topics of epigenetics and transposons over the past fifty years. We found that enthusiasm for epigenetics is often inversely related to interest in transposon dynamics across the four disciplines we examined. Most surprising was a declining interest in transposons within biomedical science and cellular and molecular biology over the past two decades. Also notable was a delayed and relatively muted enthusiasm for epigenetics within evolutionary biology. An analysis of scientific abstracts from the past twenty-five years further reveals systematic differences among disciplines in their uses of the term epigenetic, especially with respect to heritability commitments and functional interpretations. Taken together, these results paint a nuanced picture of the rise of epigenetics and the possible neglect of transposon dynamics, especially among biomedical scientists.
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Holding, Cathy. „Epigenetic switch for Igf2“. Genome Biology 5 (2004): spotlight—20040728–01. http://dx.doi.org/10.1186/gb-spotlight-20040728-01.
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Domann, Frederick E., und Bernard W. Futscher. „Flipping the Epigenetic Switch“. American Journal of Pathology 164, Nr. 6 (Juni 2004): 1883–86. http://dx.doi.org/10.1016/s0002-9440(10)63748-0.
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Socolovsky, Merav. „Systems Biology and Epigenetic Mechanisms in Erythropoiesis“. Blood 122, Nr. 21 (15.11.2013): SCI—11—SCI—11. http://dx.doi.org/10.1182/blood.v122.21.sci-11.sci-11.
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Abstract Irreversible rapid cellular decisions are often controlled by network motifs known as bistable switches. We identified a cell-cycle regulated bistable switch that controls activation of the erythroid transcriptional program during early S phase of the last generation of erythroid colony-forming-unit progenitors (CFUe). This switch drives a rapid, multi-layered commitment event that activates GATA-1 transcription, renders the cells dependent on erythropoietin, and brings about chromatin reconfiguration at erythroid gene loci. In addition, it triggers an unusual process of genome-wide DNA demethylation, the first known example of such a process in somatic cell development. Approximately 25 to 30 percent of all methylation marks are lost from essentially all genomic elements during erythroid terminal differentiation. The bistable switch activating erythroid transcription consists of two linked double-negative feedback interactions of the erythroid transcriptional repressor PU.1, which antagonizes both S phase progression, and the erythroid master transcriptional regulator GATA-1. During operation of the switch, a rapid S phase-dependent decline in PU.1 activates GATA-1 transcription. The dependence of this switch on S phase progression coincides with a dramatic change in the nature of S phase itself, which becomes shorter and 50 percent faster. The accelerated intra-S phase DNA synthesis rate is essential for the loss of genome-wide DNA methylation, which in turn is required for the rapid induction of erythroid genes. Disclosures: No relevant conflicts of interest to declare.
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Pedini, Giorgia, und Claudia Bagni. „Epigenetic switch controls social actions“. Neuron 110, Nr. 7 (April 2022): 1085–87. http://dx.doi.org/10.1016/j.neuron.2022.03.028.
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Attar, Naomi. „SMRT-seq reveals an epigenetic switch“. Nature Reviews Microbiology 14, Nr. 9 (01.08.2016): 546. http://dx.doi.org/10.1038/nrmicro.2016.122.
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Song, J., A. Angel, M. Howard und C. Dean. „Vernalization - a cold-induced epigenetic switch“. Journal of Cell Science 125, Nr. 16 (15.08.2012): 3723–31. http://dx.doi.org/10.1242/jcs.084764.
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Fawal, Mohamad-Ali, und Alice Davy. „Impact of Metabolic Pathways and Epigenetics on Neural Stem Cells“. Epigenetics Insights 11 (Januar 2018): 251686571882094. http://dx.doi.org/10.1177/2516865718820946.
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Balancing self-renewal with differentiation is crucial for neural stem cells (NSC) functions to ensure tissue development and homeostasis. Over the last years, multiple studies have highlighted the coupling of either metabolic or epigenetic reprogramming to NSC fate decisions. Metabolites are essential as they provide the energy and building blocks for proper cell function. Moreover, metabolites can also function as substrates and/or cofactors for epigenetic modifiers. It is becoming more evident that metabolic alterations and epigenetics rewiring are highly intertwined; however, their relation regarding determining NSC fate is not well understood. In this review, we summarize the major metabolic pathways and epigenetic modifications that play a role in NSC. We then focus on the notion that nutrients availability can function as a switch to modify the epigenetic machinery and drive NSC sequential differentiation during embryonic neurogenesis.
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Li, Xudong, und Ye Zheng. „Treg identity protection by an epigenetic switch“. Cell Cycle 13, Nr. 20 (15.10.2014): 3159–60. http://dx.doi.org/10.4161/15384101.2014.969996.
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Dai, Xiaofeng, Xinyu Lv, Erik W. Thompson und Kostya (Ken) Ostrikov. „Histone lactylation: epigenetic mark of glycolytic switch“. Trends in Genetics 38, Nr. 2 (Februar 2022): 124–27. http://dx.doi.org/10.1016/j.tig.2021.09.009.
Der volle Inhalt der QuelleDissertationen zum Thema "Epigenetic switch"
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Octavio, Leah M. (Leah Mae Manalo). „Molecular systems analysis of a cis-encoded epigenetic switch“. Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/68433.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Computational and Systems Biology Program, 2011.Cataloged from PDF version of thesis.
Includes bibliographical references.
An ability to control the degree of heterogeneity in cellular phenotypes may be important for cell populations to survive uncertain and ever-changing environments or make cell-fate decisions in response to external stimuli. Cells may control the degree of gene expression heterogeneity and ultimately levels of phenotypic heterogeneity by modulating promoter switching dynamics. In this thesis, I investigated various mechanisms by which heterogeneity in the expression of FLO 11 in S. cerevisiae could be generated and controlled. First, we show that two copies of the FLOJ1 locus in S. cerevisiae switch between a silenced and competent promoter state in a random and independent fashion, implying that the molecular event leading to the transition occurs in cis. Through further quantification of the effect of trans regulators on both the slow epigenetic transitions between a silenced and competent promoter state and the fast promoter transitions associated with conventional regulation of FLO11, we found different classes of regulators affect epigenetic, conventional, or both forms of regulation. Distributing kinetic control of epigenetic silencing and conventional gene activation offers cells flexibility in shaping the distribution of gene expression and phenotype within a population. Next, we demonstrate how multiple molecular events occurring at a gene's promoter could lead to an overall slow step in cis. At the FLO] 1 promoter, we show that at least two pathways that recruit histone deacetylases to the promoter and in vivo association between the region -1.2 kb from the ATG start site of the FLO11 ORF and the core promoter region are all required for a stable silenced state. To generate bimodal gene expression, the activator Msnlp forms an alternate looped conformation, where the core promoter associates with the non-coding RNA PWR1's promoter and terminator regions, located at -2.1 kb and -3.0 kb from the ATG start site of the FLO]1 ORF respectively. Formation of the active looped conformation is required for Msnlp's ability to stabilize the competent state without destabilizing the silenced state and generate a bimodal response. Our results support a model where multiple stochastic steps at the promoter are required to transition between the silenced and active states, leading to an overall slow step in cis. Finally, preliminary investigations of heterozygous diploids revealed possible transvection occurring at FLO] 1, where a silenced allele of FLO 11 appeared to transfer silencing factors to a desilenced FLO11 allele on the homologous chromosome. These observations suggest a new mechanism through which heterogeneity in FL011 expression could be further controlled, in addition to the molecular events at the FL011 promoter we elucidated previously.
by Leah M. Octavio.
Ph.D.
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JnBaptiste, Courtney K. (Courtney Kenneil). „Dicer loss induces an oncogenic epigenetic switch in mesenchymal stem cells“. Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/103163.
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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2016.This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis. Vita.
Includes bibliographical references.
MicroRNAs (miRNAs) are post-transcriptional regulators that tune gene expression. Despite the modest 2-fold repression that miRNA activity generally confers on a target, miRNAs are critical for many biological processes including development and differentiation. Due to this mild repression directly conferred by miRNA activity, miRNAs coordinate with other regulators such as transcription factors to shape the gene expression landscape and phenotypes of a cell. To understand the function of global miRNA activity in regulating the specification of the somatic state, we deleted Dicer in a murine mesenchymal stem cell model. Upon exploring the consequences of Dicer deletion, we identify a specific let-7 regulated mid-embryonic program within the global de-repression of miRNA targets accompanying Dicer loss. We further observe within the landscape of let-7 regulated targets, an activation of greater than 50-fold of known oncofetal (Igf2bp1/2/3) genes, an effect much greater than that typically reported for miRNA-mRNA interactions. This suggests a requirement of let-7 for the continual suppression of mid-embryonic programs in adult cells. To investigate the regulation of these oncofetal genes, we restored miRNAs through re-expression of Dicer. Despite complete reconstitution of the posttranscriptional activity of miRNAs, the activated oncofetal genes are incompletely suppressed. Igf2bp1-3 are components of a larger set of irreversible oncogenes whose chromatin signature indicate that they are transcriptionally activated upon Dicer deletion. This transcriptional activation is maintained, despite miRNA restoration in Dicer rescued cells. Consistent with this expression pattern, Dicer rescued cells are able to form tumors in mice, a phenotype absent in the parental wild-type and Dicer knockout cells. Moreover, the irreversible gene set is amplified in human cancers and is predictive of patient survival indicating that our observations are relevant to human disease. Finally, we develop a computational method to decipher the indirect, transcription factor mediated effects of miRNAs on gene expression. Through comprehensive analysis of ChIP-Seq, CLIP-Seq and RNA-Seq datasets, we quantitatively assess the relative contributions of direct posttranscriptional miRNA activity and transcriptional activity on gene expression changes resulting from Dicer deletion. We find that transcriptional changes contribute significantly to perturbations in gene expression resulting from global miRNA loss upon Dicer deletion. In summary, our work expands the current knowledge of fundamental roles for miRNAs in differentiated mammalian cells. As further work builds on our observations, the increased understanding of miRNA-mediated regulation will inform therapeutic strategies for human disease.
by Courtney K. JnBaptiste.
Ph. D.
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ZENOBI, ALESSANDRO. „CHARACTERIZATION OF MOLECULAR MECHANISMS DRIVING EPIGENETIC CONVERSION AND PHENOTYPE SWITCH OF FIBROBLASTS INTO INSULIN SECRETING CELLS“. Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/548193.
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La conversione epigenetica è una tecnica promettente che consente ad una cellula somatica matura di passare ad un fenotipo funzionale diverso ed alternativo rispetto a quello di origine. Questo risultato viene perseguito senza alcuna modificazione transgenica e senza l'acquisizione di uno stato di pluripotenza stabile e irreversibile, caratteristiche che rendono questo approccio molto prezioso per la medicina rigenerativa. Il protocollo di conversione epigenetica è robusto, riproducibile e assicura una buona efficienza ed il conseguimento di un fenotipo funzionale. Tuttavia, le cellule ottenute non sono completamente mature e differenziate ed è necessario identificare le migliori condizioni per realizzare uno “scale-up” che permetta l’applicazione in studi preclinici. Lo scopo del presente progetto di dottorato è stato quello di individuare condizioni di coltura fisiologiche, limitando le differenze tra l’ambiente in vitro e quello in vivo, al fine di aumentare l'efficienza del processo di differenziamento. Più precisamente, sono state testate concentrazioni fisiologiche di ossigeno e di glucosio per poter valutare l’efficienza di conversione cellulare nei diversi ambienti. Parallelamente, è stato valutato l'uso di sistemi di coltura tridimensionale (3D), con lo scopo di studiare il loro impatto sull’efficienza di conversione e sull'acquisizione di un fenotipo funzionale e maturo. I dati ottenuti suggeriscono che il “background genetico” ha un effetto significativo sulla risposta cellulare alle diverse condizioni di ossigeno durante il processo di differenziamento. D’altro canto, l'efficienza di conversione è risultata strettamente dipendente dalle concentrazioni di glucosio utilizzate durante l’isolamento delle cellule dal tessuto di origine. Inoltre, l’utilizzo di sistemi di coltura 3D, che riflettono la rigidità e l’elasticità proprie dell'organo in vivo, ha dimostrato un effetto positivo per l'acquisizione di un fenotipo pancreatico maturo, tipico delle cellule terminalmente differenziate. Infine, le informazioni molecolari ottenute dagli esperimenti di “genome editing” (ancora in corso) dovrebbero ulteriormente chiarire e corroborare i dati ottenuti.
Complessivamente, i risultati di questa tesi possono fornire informazioni utili sia per la comprensione dei meccanismi di base che regolano la crescita e il differenziamento cellulare, così come per la messa a punto di un protocollo di “scale-up” da utilizzare nella realizzazione di studi preclinici finalizzati alla medicina rigenerativa del diabete.Epigenetic conversion is a powerful technique that allows a mature somatic cell to switch into a different and alternative functional phenotype. The result is acquired without any transgenic modification, nor the acquisition of a stable and irreversible pluripotent state, making this approach very valuable for regenerative medicine. The protocol is robust, reproducible and ensures good functional efficiency, however, cells obtained are not completely mature and the optimal scale up conditions are needed for clinical translation. Aim of the present PhD project was to investigate whether the use of ambient conditions that try to closely mimic the physiological milieu, and limit the differences between in vitro and in vivo situations, may generate terminally differentiated cells and boost efficiency. To this purpose, physiological oxygen and different glucose concentrations were tested in order to assess cell responses and conversion ability in the different environments. In parallel, the use of three-dimensional (3D) culture systems was investigated, with the specific aim to study the impact of stiffness on epigenetic conversion and the acquisition of a functional, mature phenotype. The data obtained suggest that genetic background has a profound effect on the response to oxygen during the differentiation process and that conversion efficiency is strictly dependent on the glucose concentrations applied at cell isolation from the original tissue. 3D culture systems that match the stiffness typical of the original organ were able to increase differentiation and favored the acquisition of a mature pancreatic phenotype, distinctive of terminally differentiated cells. Last but not least, key molecular informations deriving from the ongoing gene editing experiments are expected to further clarify and substantiate the data obtained. Altogether, the information derived in this PhD project may find useful applications in order to design the best in vitro conditions and obtain a powerful scale-up protocol for pre-clinical studies and regenerative medicine of diabetes.
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Cardoso, e. Castro Inês Sofia [Verfasser], und Thomas [Akademischer Betreuer] Rudel. „Epigenetic switch induced by MYC in Non-Small-Cell Lung Cancer / Inês Sofia Cardoso e Castro. Betreuer: Thomas Rudel“. Würzburg : Universitätsbibliothek der Universität Würzburg, 2013. http://d-nb.info/1032482656/34.
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Castro, Inês Sofia Cardoso e. [Verfasser], und Thomas [Akademischer Betreuer] Rudel. „Epigenetic switch induced by MYC in Non-Small-Cell Lung Cancer / Inês Sofia Cardoso e Castro. Betreuer: Thomas Rudel“. Würzburg : Universitätsbibliothek der Universität Würzburg, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-76713.
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Stolz, Anne. „Molecular mechanisms involved in the expansion of Tet2-/- hematopoietic stem cells upon stresses“. Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL092.
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L'hématopoïèse clonale à potentiel in déterminé (CHIP) est définie par l'expansion de cel lules souches hématopoïétiques (CSH) portant des mutations somatiques dans des gènes couramment mutés dans les leucémies myéloïdes, sans être as sociées à une maladie hématologique. L'expansion de clones mutés est notamment observée dans un contexte inflammatoire lié à l'âge, et en réponse à différents stress. La CHIP induit un état pré leucémique et un risque accru de développer des leucémies. Cependant, la plupart des porteurs de CHIP ne développeront jamais de tumeurs malignes. Il est donc primordial de comprendre les mécan ismes par lesquels les mutations CHIP déclenchent l'expansion des CSH et l'émergence du clone pré leucémique. Deux hypothèses non exclusives pour raient expliquer l'expansion des clones mutés CHIP avec l'âge et en réponse au stress : 1- un désa vantage des cellules non mutées, et/ou 2- un avan tage compétitif pour les cellules mutées. Il est donc crucial d'étudier l'effet du vieillissement et du stress sur les cellules mutées et non mutées. Les gènes les plus fréquemment mutés dans la CHIP codent pour des facteurs épigénétiques tels que TET2, qui joue un rôle à la fois dans la méthylation de l'ADN et dans les modifications des histones. La réorgan isation de l'hétérochromatine est l'un des change ments les plus fréquemment observés dans le vieil lissement. L'hétérochromatine, par le biais de la méthylation de l'ADN et de la triméthylation de la ly sine 9 de l'histone H3 (H3K9me3), joue un rôle cru cial dans le contrôle des éléments transposables (TE). Lorsqu'ils sont déréprimés, les TE peuvent induire des dommages à l'ADN, une inflammation et des altéra tions transcriptomiques dans les CSH. Notre équipe a récemment montré une perte de H3K9me3 associée à une augmentation des L1 Md, les sous-familles les plus récentes des Long Interspersed Eléments LINE-1, lors du vieillissement ou suite à des stress tels que les radiations ionisantes (IR), qui induisent un vieillissement prématuré dans les CSH. Nous avons montré que la dérépression de L1 Md est impliquée dans la perte de fonction des CSH par l'accumulation de dommages à l'ADN et des altérations su transcriptome. Les principaux objectifs de ma thèse étaient les suivants : 1/étudier si la perte d'hétérochromatine au niveau des TE peut également être impliquée dans la perte de fonction des CSH dans le contexte d'une inflammation chronique, 2/étudier l'impact des changements d'hétérochromatine au niveau des TE sur l'expansion clonale des CSH Tet2-/- en réponse à l'irradiation et à l'inflammation chronique. Par des expériences de CUTTag H3K9me3, nous montrons que des injections chroniques de lipopolysaccharide (LPS) à faible dose réduisent la marque H3K9me3 aux L1Md dans les CSH WT, comme cela a été ob servé précédemment lors de l'IR. Ce phénomène est associé à l'accumulation de dommages à l'ADN, ob servée par des foyers H2AX en immunofluorescence. En utilisant des inhibiteurs de la reverse transcrip tase, nous avons montré que les dommages à l'ADN induits par le LPS dépendent des L1. Inversement, nous avons montré que le LPS induit une augmentation de H3K9me3 aux L1Md dans les CSH Tet2- /- , et n'induit pas de dommages à l'ADN. Les CSH Tet2-/- semblent donc être protégées de l'effet de l'inflammation chronique par rapport à leurs homo logues WT. Cela pourrait expliquer leur expansion en cas d'inflammation. Pour tester cette hypothèse, nous avons réalisé des tests de compétition in vitro et in vivo entre les CSH Tet2-/- et les CSH WT transduites avec un sh-contrôle ou un sh-LI. De manière intéres sante, nous avons montré que la dégradation de L1 dans les CSH WT empêche l'expansion des CSH Tet2- /- en réponse à l'inflammation. Dans l'ensemble, ces données suggèrent que l'expansion des CSH Tet2-/- dépend des transcrits L1 et de leurs effets délétères sur les CSH WTClonal hematopoiesis of indeterminiate potential (CHIP) is defined by the expansion of he matopoietic stem cells (HSCs) harboring somatic mutations in genes commonly mutated in myeloid leukemia, without being associated with a hémato logie disease. Expansion of mutated clones is no- tably observed in an inflammatory context such as aging, and in response to different stresses. CHIP induces a pre-leukemic State and an increa- sed risk of developing leukemia. However, most CHIP carriers will never develop malignancies. It is thus of major interest to understand the me chanisms by which CHIP mutations trigger HSC expansion and the emergence of the pre-leukemic clone. Two non-exclusive hypothèses could explain the expansion of CHIP-mutated clones with âge and in response to stress : 1- a disadvantage of non-mutated cells, and/or 2- a compétitive ad- vantage of mutated cells. It is therefore crucial to study the effect of aging and stress on both mu tated and non-mutated cells. The most frequently mutated genes in CHIP encode for epigenetic fac tors such as TET2, which plays a rôle in both DNA méthylation and histone modifications. Reor- ganization of heterochromatin is one of the most commonly reported changes in aging. Heterochro matin, through DNA méthylation and the trime- thylation of lysine 9 of histone H3 (H3K9me3), is also crucial in controlling transposable element (TE). When derepressed, TEs can induce DNA damage, inflammation, and transcriptomic altera tions in HSCs. Our team recently showed a loss of H3K9me3, associated with an upregulation of LIMd, the most recent subfamilies of Long Interspersed Eléments LINE-1, in HSC upon aging or stress inducing a prématuré aging such as ioni- zing radiation. We showed that LIM d derepression is involved in HSC loss of function through DNA damage accumulation and transcriptomic changes. The main objectives of my thesis were 1/to investi- gate if loss of heterochromatin at TEs may also be involved in the loss of HSC function upon chronic inflammation, 2/-to decipher the impact of hete rochromatin changes at TEs on Tet2-/- clonal ex pansion upon IR and inflammatory stresses. Using H3K9me3 CUTandTag experiments, we show that chronic injections of low-dose lipopolysaccharide (LPS) reduce H3K9me3 at LIMd in W T HSCs, as previously observed upon IR. This is associa ted with DNA damage accumulation, as observed by H2AX foci through immunofluorescence. Using reverse transcriptase inhibitors, we further showed that LPS-induced DNA damages are dépendent on L1 expression. Inversely, we showed that LPS induced an increase of H3K9me3 at LIMd in Tet2-/- HSCs, and did not induce damages. Tet2-/- HSCs thus seem to be protected from the effect of chro nic inflammation as compared to their W T coun- terparts. This may explain their expansion upon inflammation. To test this hypothesis, we perfor- med some in vitro and in vivo compétitive assays between Tet2-/- HSCs and W T HSCs transduced with either an sh-control or a sh-LI. Interestingly, we were able to show that L1 dégradation in W T HSCs prevent Tet2-/- HSCs expansion upon in flammation. Altogether, these data suggest that Tet2-/- HSCs expansion is dépendent on L1 trans- cripts and their deleterious effects on W T HSCs
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Farhat, Dayana. „MORC, un régulateur épigénétique au carrefour des trajectoires développementales du parasite T. gondii A MORC-driven transcriptional switch controls Toxoplasma developmental trajectories and sexual commitment“. Thesis, Université Grenoble Alpes, 2020. http://www.theses.fr/2020GRALV014.
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Toxoplasma gondii est l’agent pathogène responsable de la toxoplasmose, une maladie sans gravité lorsqu'elle est contractée chez un sujet immunocompétent ou en dehors d'une grossesse. Lorsqu’elle est congénitale, la toxoplasmose peut se manifester par des malformations neurologiques sévères et une atteinte de la rétine, pouvant conduire à la cécité. La toxoplasmose peut être aussi gravissime chez le malade immunodéprimé (SIDA - greffes d'organes - thérapies anticancéreuses). Les principaux modes de contamination sont d’origine alimentaire. L’homme se contamine habituellement en ingérant les kystes présents dans les viandes, ou des oocystes provenant des matières fécales d’un chat infecté et souillant les légumes, les fruits ou l’eau. Si la reproduction sexuée constitue un élément central dans la pathogénèse de la toxoplasmose et la transmission du parasite entre les animaux, cette étape clé du cycle parasitaire reste encore mal étudiée à l’échelle moléculaire, en partie dû à la difficulté à cultiver in vitro les formes sexuées ; pour des raisons évidentes d’éthique, l’utilisation de chats est quant à elle restreinte par la législation. Le destin cellulaire d’un parasite est apparemment prédéterminé par des mécanismes épigénétiques modifiant de manière réversible, transmissible et adaptative, l'expression des gènes sans en changer la séquence d’ADN. Nous avons montré que l’épi-drogue FR235222 en inhibant l’enzyme HDAC3 modifie les trajectoires développementales et promeut l’apparition dans les cultures in vitro des formes latentes et sexuées. Au cours de ma thèse j’ai étudié protéine Microrchidia (MORC), initialement identifiée comme un partenaire de HDAC3. Les protéines MORC interviennent dans la réponse aux dommages à l'ADN et la répression des transposons et bien que conservées chez les eucaryotes restent peu étudiées. Nous avons résolu l’interactome spécifique de MORC qui réunit HDAC3 mais aussi plusieurs facteurs de transcription apetala (AP2). L’immunoprécipitation de chromatine de la protéine MORC, couplée au séquençage massif (ChIP-seq), a montré que la protéine MORC co-localise parfaitement avec HDAC3 à la chromatine au voisinage de plus de 1600 gènes dont l’expression est connue pour être restreintes au stades sexués et latents (sporozoites et bradyzoite). L’épuisement de la protéine MORC de manière inductible par le système dégron induit à l’auxine (AID) confirme la répression par MORC des gènes susmentionnés et de leurs protéines. Le phénomène de transition vers les stades sexués est quasi exhaustif et très peu de gènes échappent à cette régulation par MORC. Nous avons montré que MORC est nécessaire à l’adressage à la chromatine de HDAC3, et émettons l’hypothèse que les facteurs AP2 co-purifiés apportent la spécificité de reconnaissante à l’ADN. Nos données montrent également un schéma de régulation beaucoup plus complexe puisque la déplétion de MORC dans les parasites conduit à l’induction de facteurs AP2 dits secondaires qui aurait pour mission de guider les trajectoires développementales et de garantir l’unidirectionnalité du cycle parasitaire, un élément clé de la persistance et de la transmission entre les hôtes définitifs/intermédiaires de Toxoplasma gondiiToxoplasma gondii has a complex life cycle that is typified by asexual development that takes place in vertebrates, and sexual reproduction, which occurs exclusively in felids and is therefore less studied. The developmental transitions rely on changes in the patterns of gene expression, and recent studies have assigned roles for chromatin shapers, including histone modifications, in establishing specific epigenetic programs for each given stage. Here, we identified the T. gondii microrchidia (MORC) protein as an upstream transcriptional repressor of sexual commitment. MORC, in a complex with Apetala 2 (AP2) transcription factors, was shown to recruit the histone deacetylase HDAC3, thereby impeding the accessibility of chromatin at the genes that are exclusively expressed during sexual stages. We found that MORC-depleted cells underwent marked transcriptional changes, resulting in the expression of a specific repertoire of genes, and revealing a shift from asexual proliferation to sexual differentiation. MORC acts as a master regulator that directs the hierarchical expression of secondary AP2 transcription fac- tors, and these transcription factors potentially contribute to the unidirectionality of the life cycle. Thus, MORC plays a cardinal role in the T. gondii life cycle, and its conditional depletion offers a method to study the sexual development of the parasite in vitro, and is proposed as an alternative to the requirement of T. gondii infections in cats
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Nordor, Akpéli. „Toward the identification of cancer/placenta epigenetic switches“. Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB097.
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Les cellules placentaires portent un génome différent du génome maternel, puisque 50% de leurs gènes proviennent du génome paternel. Cependant, comme les cellules cancéreuses après la transformation néoplasique, elles réussissent à envahir les tissus de leur hôte, échapper à son système immunitaire et induire une angiogenèse afin d’établir la grossesse. Les cellules cancéreuses et placentaires arborent aussi une différence majeure : alors que de tels mécanismes typiques des cancers sont incontrôlés dans les cellules cancéreuses, ils sont spatialement et temporairement contrôlés dans les cellules placentaires saines. Ainsi, le recherche sur le « concept cancer/placenta » – l’utilisation du placenta pour mieux comprendre le cancer – peut aboutir à l’identification de biomarqueurs et d’approches thérapeutiques innovantes en oncologie, tout comme en gynécologie-obstétrique. Par exemple, les efforts de recherche portant sur l’expression des gènes CGB, codant pour la sous-unité ß de l’hormone chorionique gonadotrope humaine, dans les cellules cancéreuses et placentaires a mené au développement d’un biomarqueur largement utilisé pour la prise en charge de multiples cancers. Il est aussi intéressant de noter que ce même biomarqueur est aussi utilisé pour le dépistage d’aneuploïdies fœtales. De même, le clonage d’INSL4, codant pour le précurseur du peptide placentaire précoce ressemblant à l’insuline (pro-EPIL), dans des cellulaires placentaires précoces, a mené au développement d’un biomarqueur faisant actuellement l’objet d’études cliniques. Avec l’émergence de l’épigénétique, des études de la méthylation de l’ADN, la caractéristique épigénétique la mieux comprise, ont montré que les loci de gènes CGB et INSL4 sont hypométhylés dans les cellules cancéreuses et placentaires ; ce qui pourrait refléter l’hypométhylation globale caractéristique de ces deux types cellulaires. Par conséquent, le projet doctoral présenté dans cette thèse a exploré les modifications des paysages épigénétiques des cellules placentaires au cours de la grossesse et des cellules cancéreuses au cours de la transformation néoplasique. Ce projet a contribué initialement au développement d’un test d’immunoanalyse qui détecte l’hCGß de type II, spécialement codée par un sous-groupe de gènes CGB et détectée dans le sérum de patients atteints de cancers non-placentaires et de trisomie 21 fœtale. Ce test d’immunoanalyse, avec un test similaire développé pour la détection de pro-EPIL, a aussi été utilisé pour des études de preuve de concept précoces quant à l’effet de la méthylation de l’ADN sur l’expression de l’hCGß de type II et de pro-EPIL dans des surnageants de culture cellulaire. En fin de compte, ce projet a mené à la première comparaison directe et pan-génomique de la méthylation de l’ADN dans des cellules cancéreuses au cours de la transformation néoplasique et dans des cellulaires placentaires au cours de la grossesse. Cette étude a porté sur des données, disponibles publiquement, générées à partir de biopsies de 13 types de tumeurs, de villosités choriales (tissus placentaires) et d’autres tissus sains. Elle a également porté sur des données originales générées par nos soins à partir d’échantillons placentaires uniques : des cellules cytotrophoblastiques isolées de villosités choriales ex vivo. Toutes les données inclus dans cette étude ont été générées sur une plateforme de puces à ADN pour la mesure de la méthylation au niveau de 485 512 sites CpG pour chaque échantillon. En combinant, des logiciels innovants reposant sur la puissance d’algorithmes de lissage statistique et sur un solide rationnel biologique, cette étude a ainsi contribué à l’identification de motifs d’hypométhylation à l’échelle du mégabase distinguant les cellules placentaires du début de la grossesse de celles de la fin de la grossesse tout comme ils distinguent les cellules cancéreuses des cellules normales. (...)Placental cells carry a genome different from the maternal genome, as 50% of it originate from the paternal genome. However, like cancer cells after neoplastic transformation, they successfully invade their host tissues, escape its immune system and induce angiogenesis in order to establish the pregnancy. Cancer and placental cells also display a major discrepancy: while such hallmarks of cancer mechanisms are uncontrolled in cancer cells, they are spatially and temporally controlled in healthy placental cells. Thus, research on the “cancer/placenta concept” – the use of the placenta to better understand cancer – can lead to innovative biomarkers and therapeutic approaches in oncology as well as in gynecology and obstetrics. For example, research efforts on the expression of the CGB genes, encoding for the human chorionic gonadotropin beta subunit (hCGß), in cancer and placental cells have led to the development of a biomarker widely used for the management of various cancers. Interestingly, this same biomarker is also used for the screening of fetal aneuploidies. Likewise, the cloning of INSL4, encoding for the precursor of the early placenta insulin-like peptide (pro-EPIL) in early pregnancy placental cells, has led to the development of a biomarker currently investigated in the clinical setting. Following the rise of epigenetic, studies on DNA methylation, the most well understood epigenetic mark, showed that the loci of CGB genes and INSL4 are hypomethylated in cancer and placental cells, which may reflect a global hypomethylation also characteristic of these cells. Therefore, the doctoral project presented in this dissertation had explored modifications in the epigenetic landscape of placental cells throughout pregnancy and cancer cells throughout neoplastic transformation. This project initially contributed to the development of an immunoassay detecting type II hCGß, specifically encoded by a subset of CGB genes and detected in the serum of patients with non-placental cancers and fetal Down Syndrome. This immunoassay, along with another one directed to pro-EPIL, was also used for an early proof of concept study regarding the effect of DNA methylation on the expression of type II hCGß and pro-EPIL in cell culture supernatants. Ultimately, this project led to the first direct genome-wide comparison of DNA methylation in cancer cells throughout neoplastic transformation and in placental cells throughout pregnancy. It included publically available data generated from biopsies of 13 types of tumors, chorionic villi (placental tissues) and other normal tissues. It also included original data generated from unique placental samples: villous cytotrophoblastic cells isolated ex vivo from chorionic villi. All datasets were generated on a microarray platform measuring DNA methylation at 485,512 CpG sites in each sample. Combining innovative software that leverages the power of statistical smoothing algorithms and a strong biological rationale, this study thus contributed to the identification of megabase-scale patterns of hypomethylation distinguishing early pregnancy from late pregnancy placenta cells as they distinguish normal from cancers cells. Strikingly, the affected genomic regions encompassed genes related to hallmarks of cancer mechanisms such as epithelial-mesenchymal transition (EMT), innate and acquired immune response, and hypoxia. Taken together, these results suggest the hypothesis that patterns of DNA methylation might contribute to “cancer/placenta epigenetic switches” allowing placental implantation and neoplastic transformation when turned “on”, while preventing the placenta to degenerate into an aggressive tumor when turned “off”
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Oudinet, Chloé. „Mécanismes transcriptionnels et épigénétiques dans la régulation de l'expression du locus IgH murin au cours du développement des lymphocytes B“. Thesis, Toulouse 3, 2020. http://www.theses.fr/2020TOU30106.
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Les lymphocytes B sont les seules cellules du système immunitaire capables de produire des immunoglobulines (Ig). La vaste diversité et la haute spécificité des Ig produites sont l'aboutissement de multiples mécanismes cellulaires et moléculaires incluant des processus recombinationnels et mutationnels au sein des loci des chaînes lourdes et légères des immunoglobulines. Ces loci sont soumis à de multiples niveaux de régulation tout au long du développement des cellules B impliquant des mécanismes épigénétiques et transcriptionnels qui orchestrent l'activation progressive et ordonnée de ces loci. Au cours de ma thèse, je me suis intéressée à deux processus recombinationnels dans le locus des chaînes lourdes des Ig (locus IgH) : la recombinaison V(D)J et la commutation de classe (CSR). Les deux processus requièrent la transcription des séquences cibles. Cette transcription, dite transcription germinale, joue un rôle important dans la régulation de l'accessibilité des séquences cibles aux enzymes initiant les deux processus. Spécifiquement, j'ai étudié 3 aspects de la régulation de l'expression du locus IgH murin au cours du développement précoce et tardif des cellules B : 1) Le rôle de la transcription germinale dans la régulation de la recombinaison V(D)J. La recombinaison V(D)J est initiée au sein de "centres de recombinaison" riches en activité transcriptionnelle, mais la relation causale entre transcription et recombinaison demeure controversée. En utilisant un modèle murin et un système d'analyse de la transcription et de la recombinaison au niveau de la cellule unique, j'ai montré que la recombinaison V(D)J pouvait se produire au sein des centres de recombinaison en l'absence de transcription détectable, suggérant fortement que ces deux processus sont contrôlés par des mécanismes distincts. 2) Le rôle de la méthylation de l'ADN dans la transcription germinale associée à la CSR. Le rôle précis de cette modification épigénétique dans la régulation de la transcription germinale est inconnu. J'ai effectué une analyse longitudinale des profils de méthylation de différents éléments cis-régulateurs du locus IgH dans des cellules primaires de différentes lignées murines. J'ai montré que dans la lignée B, les profils de méthylation de la majorité de ces éléments étaient établis et maintenus indépendamment de l'activation des cellules B ou de la transcription germinale, et que certains promoteurs étaient hypométhylés tôt au cours du développement embryonnaire, bien avant l'apparition du lignage B, suggérant un rôle potentiel de la méthylation de l'ADN dans le pré-marquage épigénétique du locus plutôt que dans la régulation de son expression. Les bases moléculaires de la spécificité de la séquence Sµ. La CSR implique une recombinaison entre la séquence Sµ, site donneur universel de commutation, et une séquence partenaire en aval. Plusieurs données suggèrent que la séquence Sµ a des propriétés qui la distinguent des autres séquences S, mais les bases moléculaires de cette spécificité sont inconnues. J'ai utilisé un modèle murin où une séquence S en aval a été placée sous le contrôle des éléments qui régulent la transcription de la région Sµ. J'ai montré que parmi les différents facteurs impliqués dans la spécificité de Sµ, la proximité d'un enhancer jouait un rôle important et suffisait à conférer à la séquence S en aval la fonction de site donneur de CSRB lymphocytes have the unique ability to produce immunoglobulins (Ig). The vast Ig diversity and exquisite specificity of Igs result from various cellular and molecular mechanisms including recombinational and mutational processes within Ig heavy and light chain loci. These loci are subjected to multiple layers of regulation during B cell development involving epigenetic and transcriptional mechanisms that orchestrate the stepwise and ordered activation of these loci. During my thesis, I was interested in two recombinational processes that take place within the Ig heavy chain locus (IgH locus) : V(D)J recombination and class switch recombination (CSR). Both processes require transcription of target sequences. This transcription, called germline transcription, plays an important role in the regulation of target sequence accessibility to the enzymes that initiate these processes. Specifically, I studied three aspects of the murine IgH locus expression regulation during early and late B cell development: 1) The role of germline transcription in the regulation of V(D)J recombination. V(D)J recombination initiates within "recombination centres" that are highly enriched in transcriptional activity, but the causal relationship between transcription and recombination remains controversial. By using a mouse model and single-cell analyses of transcription and recombination, I showed that V(D)J recombination could occur in the absence of detectable transcription within recombination centres, strongly suggesting that the two processes involve distinct mechanisms. 2) The role of DNA methylation in CSR-associated germline transcription. The precise role of this epigenetic mark in the control of germline transcription is presently unknown. I determined the methylation patterns of various IgH cis-acting elements in primary cells of different mouse lines. I showed that in B cells, the methylation patterns of most cis-elements were established and maintained independently of B cell activation or germline transcription, and that specific promoters were hypomethylated early during embryonic development, before B cell commitment, pointing to a role of DNA methylation in the epigenetic pre-marking of the locus rather than in the regulation of its expression. Molecular basis of Sµ specificity. CSR involves recombination between Sµ region, the universal switch donor, and a downstream partner S region. Numerous studies suggest that Sµ displays specific features that distinghuish it from the other S regions, but the molecular basis of this specificity is unknown. By using a mouse model in which a downstream S region was placed under the control of elements that regulate Sµ region transcription, I showed that, among the different factors involved in Sµ specificity, the proximity of a particular enhancer was important and sufficient to confer the CSR donor site function to the downstream S region
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Schenkelberger, Marc [Verfasser], und Albrecht [Akademischer Betreuer] Ott. „Cooperative biomolecular binding : high specificity of competitive single stranded DNA hybridization, influence of DNA methylation on the duplex stability, and epigenetic regulation of in vitro gene switches / Marc Schenkelberger. Betreuer: Albrecht Ott“. Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2014. http://d-nb.info/1053982453/34.
Der volle Inhalt der QuelleBuchteile zum Thema "Epigenetic switch"
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Hernday, Aaron, Bruce Braaten und David Low. „The Intricate Workings of a Bacterial Epigenetic Switch“. In Advances in Experimental Medicine and Biology, 83–89. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-8861-4_7.
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Müller, Natascha. „Chapter 5. Parameter setting in multilingual children with special reference to acceleration in French“. In Language Acquisition in Romance Languages, 114–43. Amsterdam: John Benjamins Publishing Company, 2024. http://dx.doi.org/10.1075/bpa.18.05mul.
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Linguistic theorizing has revised the switch metaphor of parameters as being part of Universal Grammar. Within an epigenetic approach to language (Biberauer et al., 2014; Roberts, 2019), parameters result from the interaction of innate (linguistic) knowledge and universal non-language-specific cognitive optimization strategies, which are set in relation to the child’s experience. Languages vary at different levels of granularity (Baker, 2014), which is expressed in a parameter taxonomy, more particularly in parameter hierarchies (Roberts, 2019) distinguishing macro-, meso-, micro-, and nanoparameters (Biberauer et al., 2014). In the context of multilingualism, Mac Swan (2000) has argued that some components of the architecture of the language faculty are duplicated in multilingual children, while others are not. Parameter hierarchies, defined as previously, belong to the non-duplicated components. Therefore, multilingual children set the parameters simultaneously for all their different languages at the relevant level of variation. Taken together, these assumptions can account for acceleration effects exceeding monolingual limits in multilingual French as a non-null-subject language, if (one of) the other language(s) is a null-subject language like Italian or Spanish for example. The results reported come from longitudinal studies of balanced as well as unbalanced multilingual children during early stages of language development (from 1;6 until the age of 5) and cross-sectional studies of multilingual children at similar ages.
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Kanno, Yuka, Steven Witte und John J. O’Shea. „Lymphocyte Identity and Genomic Switches“. In Epigenetics - A Different Way of Looking at Genetics, 41–52. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27186-6_3.
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Flavell, R. B., M. O'Dell und M. Metzlaff. „Transgene-Promoted Epigenetic Switches of Chalcone Synthase Activity in Petunia Plants“. In Novartis Foundation Symposia, 144–67. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515501.ch9.
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Yuan, Guo-Cheng. „Prediction of Epigenetic Target Sites by Using Genomic DNA Sequence“. In Handbook of Research on Computational and Systems Biology, 187–201. IGI Global, 2011. http://dx.doi.org/10.4018/978-1-60960-491-2.ch008.
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Epigenetic regulation provides an extra layer of gene control in addition to the genomic sequence and is critical for the maintenance of cell-type specific gene expression programs. Significant changes of epigenetic patterns have been linked to developmental stages, environmental exposure, ageing, and diet. However, the regulatory mechanisms for epigenetic recruitment, maintenance, and switch are still poorly understood. Computational biology provides tools to deeply uncover hidden connections and these tools have played a major role in shaping the current understanding of gene regulation, but its application in epigenetics is still in the infancy. This chapter reviews some recent developments of computational approaches to predict epigenetic target sites.
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Sato, Kosei, und Daisuke Yamamoto. „An Epigenetic Switch of the Brain Sex as a Basis of Gendered Behavior in Drosophila“. In Epigenetic Shaping of Sociosexual Interactions - From Plants to Humans, 45–63. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-800222-3.00003-6.
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Lucchesi, John C. „Nuclear reprogramming and induced pluripotency“. In Epigenetics, Nuclear Organization & Gene Function, 205–12. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198831204.003.0018.
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Four core transcription factors known to maintain the pluripotent state in embryonic stem cells (ESCs)—Oct4, Sox2, Klf4 and c-Myc—were used to induce pluripotent stem cells in adult-derived fibroblasts. Induced pluripotent stem cells (iPSCs), like ESCs, have less condensed and more transcriptionally active chromatin than differentiated cells. The number of genes with bivalent promoter marks increases during reprogramming, reflecting the switch of differentiation-specific active genes to an inactive, but poised, status. The levels of DNA methyl transferases and demethylases are increased, underlying the changes in the pattern of DNA methylation that occur late during reprogramming. The potential therapeutic applications of iPSCs include reprogramming a patient’s own cells to avoid the problem of rejection following injection to restore tissue or organ function. iPSCs derived from individuals at risk of developing late-onset neurological diseases could be differentiated in culture to predict the future occurrence of the disease. Caveats involve the fact that long-term culturing often results in genomic mutations that may, by chance, involve tumor suppressors or oncogenes.
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Suchy, Frederick J. „The Environment and Liver Disease in Children“. In Textbook of Children's Environmental Health, 707–18. 2. Aufl. Oxford University PressNew York, 2024. http://dx.doi.org/10.1093/oso/9780197662526.003.0052.
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Abstract Injury to the liver caused by toxic chemicals in the environment can produce a wide spectrum of illness that includes asymptomatic elevation of liver function tests, fatty liver, hepatitis, liver cancer, and even fulminant hepatic failure. Some agents are well known to produce cellular injury and even necrosis in the liver following absorption into the body. Among infants and children, immaturity of metabolic pathways for biotransformation and gene polymorphisms may influence vulnerability of the liver to toxic chemicals in the environment. Toxic chemicals and other environmental factors such as stress, diet, behavior, and disease can cause epigenetic changes that influence susceptibility to liver injury by activating chemical switches such as DNA methylations and histone tail modifications that regulate gene expression. Recognition is increasing that exposures to certain toxic chemicals that have become widespread in the modern environment—chemical obesogens such as the organotins and plasticizers—are likely contributing to the global epidemic of obesity and to its complications such as diabetes and nonalcoholic fatty liver disease. Exposures to these compounds in early life may cause long-lasting metabolic disruption at low doses that do not produce acute signs of toxicity.
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Parrington, John. „Genome and Epigenome“. In Mind Shift, 80–91. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780198801634.003.0006.
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This chapter focuses on the role that genes play in the formation of human consciousness. While the genome has generally been defined as the sum of the genes in an organism, the more we study real genomes, the more we realise that viewing them in this way is a major oversimplification of their true complexity. Perhaps the most surprising outcome of the Human Genome Project was the realization that genes only represent a small fraction of the total DNA sequence. More recently, evidence has been accumulating to show that a significant proportion of the ‘non-coding’ DNA plays key roles in gene regulation—that is, determining which genes get switched on or off and when. In addition, instead of DNA being seen as the sole controller of cellular function, there is now growing recognition that RNA also plays a key role. Meanwhile, the new science of ‘epigenetics’ is revealing that the DNA ‘recipe’ for each organism appears far more responsive to the environment than previously thought, both to changes in the cellular environment, and those outside the organism itself. These new ways of looking at the genome have important implications for the understanding of how the human brain works, and of some of the factors that might make it unique compared to those of other species.
Konferenzberichte zum Thema "Epigenetic switch"
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Di, Lijun, Alfonso Fernandez und Kevin Gardner. „Abstract 1116: Epigenetic control of the BRCA1 expression by a metabolic switch“. 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.am10-1116.
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Banerjee, Amrita, Chandrima Das und Dipak Dasgupta. „Abstract B44: Mithramycin exhibits dual binding mode and acts as an epigenetic switch“. 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-b44.
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Ohtani, Hitoshi, Minmin Liu, Wanding Zhou, Gangning Liang und Peter A. Jones. „Abstract 2993: A switch in epigenetic silencing mechanisms of endogenous retroviruses during human genome evolution“. 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.am2018-2993.
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Abadie, Kathleen, Elisa C. Clark, Rajesh Valanparambil, Obinna Ukogu, Wei Yang, Riza Daza, Kenneth Ng et al. „949 Flexible control of T cell memory and self-renewal by a reversible epigenetic switch“. In SITC 38th Annual Meeting (SITC 2023) Abstracts. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/jitc-2023-sitc2023.0949.
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Osuka, Satoru, Liquan Yang, Dan Zhu, Hideharu Hashimoto, Narra S. Devi und Erwin G. Van Meir. „Abstract 1996: Epigenetic reactivation of BAI1/ADGRB1 suppresses tumor invasion by preventing TGFβ1-induced mesenchymal switch in glioblastoma“. 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.sabcs18-1996.
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Osuka, Satoru, Liquan Yang, Dan Zhu, Hideharu Hashimoto, Narra S. Devi und Erwin G. Van Meir. „Abstract 1996: Epigenetic reactivation of BAI1/ADGRB1 suppresses tumor invasion by preventing TGFβ1-induced mesenchymal switch in glioblastoma“. 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.am2019-1996.
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Seo, Hyungseok. „442-H IL-21 on/off switch CAR-T enhance anti-tumor effects by epigenetic and transcriptional regulation“. In SITC 38th Annual Meeting (SITC 2023) Abstracts Supplement 2. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/jitc-2023-sitc2023.0442-h.
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Li, Liping, Jung-Hyun Kim, Wenyan Lu, Donna Marie Williams, Lingling Xian, Joseph Kim, Ophelia Rogers et al. „Abstract 2666: HMGA1: An epigenetic switch required for MPN progression by inducingGATA-2and cell cycle progression through enhancer rewiring“. 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.am2021-2666.
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Chang, Jichun, und Ruiqi Wang. „An epigenetic switch involving a positive feedback loop linking inflammation to cancer effected by Myc and miRNA-17-92 microRNA cluster“. In 2014 8th International Conference on Systems Biology (ISB). IEEE, 2014. http://dx.doi.org/10.1109/isb.2014.6990755.
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Lin, Jora Meng-Ju, Jacqueline Shay, Jian-Liang Chou, Pearlly S. Yan, Tim H. M. Huang, Hung Cheng Lai und Michael W. y. Chan. „Abstract 2318: The role of EZH2 as an epigenetic switch of the TGF-β/SMAD4 targets in regulating EMT in ovarian cancer“. In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2318.
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