Готові списки джерел за темами / H3K9ac

Добірка наукової літератури з теми "H3K9ac"

Автор: Grafiati
Опубліковано: 10 травня 2022

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Статті в журналах з теми "H3K9ac":

1

Cui, Long, Jun Miao, Tetsuya Furuya, Xinyi Li, Xin-zhuan Su, and Liwang Cui. "PfGCN5-Mediated Histone H3 Acetylation Plays a Key Role in Gene Expression in Plasmodium falciparum." Eukaryotic Cell 6, no. 7 (April 20, 2007): 1219–27. http://dx.doi.org/10.1128/ec.00062-07.

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ABSTRACT Histone acetylation, regulated by the opposing actions of histone acetyltransferases (HATs) and deacetylases, is an important epigenetic mechanism in eukaryotic transcription. Although an acetyltransferase (PfGCN5) has been shown to preferentially acetylate histone H3 at K9 and K14 in Plasmodium falciparum, the scale of histone acetylation in the parasite genome and its role in transcriptional activation are essentially unknown. Using chromatin immunoprecipitation (ChIP) and DNA microarray, we mapped the global distribution of PfGCN5, histone H3K9 acetylation (H3K9ac) and trimethylation (H3K9m3) in the P. falciparum genome. While the chromosomal distributions of H3K9ac and PfGCN5 were similar, they are radically different from that of H3K9m3. In addition, there was a positive, though weak correlation between relative occupancy of H3K9ac on individual genes and the levels of gene expression, which was inversely proportional to the distance of array elements from the putative translational start codons. In contrast, H3K9m3 was negatively correlated with gene expression. Furthermore, detailed mapping of H3K9ac for selected genes using ChIP and real-time PCR in three erythrocytic stages detected stage-specific peak H3K9ac enrichment at the putative transcriptional initiation sites, corresponding to stage-specific expression of these genes. These data are consistent with H3K9ac and H3K9m3 as epigenetic markers of active and silent genes, respectively. We also showed that treatment with a PfGCN5 inhibitor led to reduced promoter H3K9ac and gene expression. Collectively, these results suggest that PfGCN5 is recruited to the promoter regions of genes to mediate histone acetylation and activate gene expression in P. falciparum.
2

Sahai, Vaibhav, Surabhi Dangi-Garimella, Kazumi Ebine, Krishan Kumar, and Hidayatullah G. Munshi. "Promotion of gemcitabine resistance in pancreatic cancer cells by three-dimensional collagen I through HMGA2-dependent histone acetyltransferase expression." Journal of Clinical Oncology 31, no. 4_suppl (February 1, 2013): 172. http://dx.doi.org/10.1200/jco.2013.31.4_suppl.172.

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172 Background: Pancreatic ductal adenocarcinoma (PDAC) is associated with a pronounced stromal reaction that has been shown to contribute to chemo-resistance. We have previously shown that PDAC cells are resistant to gemcitabine chemotherapy in the collagen microenvironment due to increased expression of the chromatin remodeling protein high mobility group A2 (HMGA2). Methods: Pancreatic TMAs were stained with trichrome and for histone H3K9, H3K27 acetylation (Ac), and histone acetyltransferase (HAT) expression. PDAC cells were plated onto tissue culture plastic or in three-dimensional (3D) collagen gels and protein expression assessed by Western blotting. DNA damage response was assessed by comet and clonogenic assays. Results: PDAC tumors display higher levels of H3K9Ac and H3K27Ac in fibrotic regions. Moreover, PDAC cells upregulate H3K9Ac and H3K27Ac along with GCN5, PCAF and p300 HATs in 3D collagen compared to tissue culture plastic. Knocking down HMGA2 attenuates the effect of collagen on H3K9Ac, H3K27Ac and p300, PCAF and GCN5 expression. We also show that human PDAC tumors with HMGA2 expression demonstrate increased H3K9Ac and H3K27Ac. Additionally, we show that cells in 3D collagen gels demonstrate reduced tailing with the comet assay, increased clonogenic potential and increased γH2AX following gemcitabine treatment, suggesting an increased response and repair to damaged DNA in the 3D collagen microenvironment. Significantly, down-regulation of HMGA2 or p300, PCAF and GCN5 HATs decreases gemcitabine-induced γH2AX detected and attenuates clonogenic potential. Conclusions: Collagen microenvironment limits the effectiveness of gemcitabine through HMGA2-dependent HAT expression. HMGA2 expression is associated with histone acetylation and HAT expression in human PDAC tumors, particularly in area of fibrosis, suggesting that fibrosis may contribute to chemo-resistance through increased HMGA2-HAT signaling. Overall, our results increase our understanding of how the collagen microenvironment contributes to chemo-resistance and identify HATs as potential therapeutic targets against this deadly cancer.
3

Ebrahimi, Azadeh, Jens Schittenhelm, Juergen Honegger, and Hermann Schluesener. "Prognostic relevance of global histone 3 lysine 9 acetylation in ependymal tumors." Journal of Neurosurgery 119, no. 6 (December 2013): 1424–31. http://dx.doi.org/10.3171/2013.9.jns13511.

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Object Ependymal tumors are highly variable in clinical and molecular behavior and affect both children and adults. Regarding the paucity of appropriate experimental models, the underlying molecular mechanisms of their behavioral variability are poorly understood. Considering the increasing evidence of epigenetic changes in various tumors, in addition to the preclinical success of epigenetic-based therapeutics in tumors of the CNS, epigenetic study of ependymal tumors is warranted. Methods Using immunohistochemistry, the authors investigated the patterns of global acetylation of lysine position 9 of histone 3 (H3K9Ac), an epigenetic marker of active gene transcription, in 85 ependymal tumors with various WHO grades and clinicopathological characteristics. Results Most of the nuclei in all ependymal tumors were H3K9Ac negative (mean ± SD 65.9% ± 26.5 vs 34.1% ± 26.5% positive, p < 0.0001). Subependymomas had more H3K9Ac-positive nuclei (67.2% ± 10.2%) than myxopapillary ependymomas, ependymomas, and anaplastic ependymomas (p < 0.05). Additionally, intracranial parenchymal tumors had significantly fewer H3K9Ac-positive nuclei (13.1% ± 21.9%) than tumors of other CNS localizations (p < 0.001), and supratentorial ventricular tumors had the highest number of H3K9Ac-positive nuclei (66.4% ± 11.8%) among CNS ependymal tumors (p < 0.0001). The H3K9Ac pattern in ependymal tumors also revealed prognostic significance such that tumors with less than 20% acetylated nuclei had a higher probability of recurrence than tumors with 20% or more acetylated nuclei (p = 0.0327), and recurrent tumors had significantly fewer H3K9Ac-positive nuclei than primary ones (16% ± 22.5% vs. 38% ± 25.8%; p < 0.0001). However, the effect of tumor location on survival of patients was nonsignificant in a multivariate survival analysis, and H3K9 acetylation levels of tumors contributed independently to the survival of patients. In addition, ependymal tumors with more than or equal to 20% H3K9 acetylated cells had lower MIB-1 expression than those with less than 20% H3K9 acetylated cells (p < 0.01). Conclusions Global H3K9Ac contributes independently to the prognosis of patients with ependymal tumors such that tumors with lower H3K9Ac values have a higher probability of recurrence and are more proliferative. Additionally, subependymomas have a higher H3K9Ac profile than other ependymal tumor subclasses, underlining their benign clinical behavior.
4

Radovani, Ernest, Matthew Cadorin, Tahireh Shams, Suzan El-Rass, Abdel R. Karsou, Hyun-Soo Kim, Christoph F. Kurat, Michael-Christopher Keogh, Jack F. Greenblatt, and Jeffrey S. Fillingham. "The Carboxyl Terminus of Rtt109 Functions in Chaperone Control of Histone Acetylation." Eukaryotic Cell 12, no. 5 (March 1, 2013): 654–64. http://dx.doi.org/10.1128/ec.00291-12.

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ABSTRACT Rtt109 is a fungal histone acetyltransferase (HAT) that catalyzes histone H3 acetylation functionally associated with chromatin assembly. Rtt109-mediated H3 acetylation involves two histone chaperones, Asf1 and Vps75. In vivo , Rtt109 requires both chaperones for histone H3 lysine 9 acetylation (H3K9ac) but only Asf1 for full H3K56ac. In vitro , Rtt109-Vps75 catalyzes both H3K9ac and H3K56ac, whereas Rtt109-Asf1 catalyzes only H3K56ac. In this study, we extend the in vitro chaperone-associated substrate specificity of Rtt109 by showing that it acetylates vertebrate linker histone in the presence of Vps75 but not Asf1. In addition, we demonstrate that in Saccharomyces cerevisiae a short basic sequence at the carboxyl terminus of Rtt109 (Rtt109C) is required for H3K9ac in vivo . Furthermore, through in vitro and in vivo studies, we demonstrate that Rtt109C is required for optimal H3K56ac by the HAT in the presence of full-length Asf1. When Rtt109C is absent, Vps75 becomes important for H3K56ac by Rtt109 in vivo . In addition, we show that lysine 290 (K290) in Rtt109 is required in vivo for Vps75 to enhance the activity of the HAT. This is the first in vivo evidence for a role for Vps75 in H3K56ac. Taken together, our results contribute to a better understanding of chaperone control of Rtt109-mediated H3 acetylation.
5

Tsurubuchi, Takao, Shunsuke Ichi, Kyu-won Shim, William Norkett, Elise Allender, Barbara Mania-Farnell, Tadanori Tomita, David G. McLone, Norman Ginsberg, and C. Shekhar Mayanil. "Amniotic fluid and serum biomarkers from women with neural tube defect–affected pregnancies: a case study for myelomeningocele and anencephaly." Journal of Neurosurgery: Pediatrics 12, no. 4 (October 2013): 380–89. http://dx.doi.org/10.3171/2013.7.peds12636.

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Object The authors sought to identify novel biomarkers for early detection of neural tube defects (NTDs) in human fetuses. Methods Amniotic fluid and serum were drawn from women in the second trimester of pregnancy. The study group included 2 women pregnant with normal fetuses and 4 with fetuses displaying myelomeningocele (n = 1), anencephaly (n = 1), holoprosencephaly (n = 1), or encephalocele (n = 1). Amniotic fluid stem cells (AFSCs) were isolated and cultured. The cells were immunostained for the stem cell markers Oct4, CD133, and Sox2; the epigenetic biomarkers H3K4me2, H3K4me3, H3K27me2, H3K27me3, H3K9Ac, and H3K18Ac; and the histone modifiers KDM6B (a histone H3K27 demethylase) and Gcn5 (a histone acetyltransferase). The levels of 2 markers for neural tube development, bone morphogenetic protein–4 (BMP4) and sonic hedgehog (Shh), were measured in amniotic fluid and serum using an enzyme-linked immunosorbent assay. Results The AFSCs from the woman pregnant with a fetus affected by myelomeningocele had higher levels of H3K4me2, H3K4me3, H3K27me2, and H3K27me3 and lower levels of KDM6B than the AFSCs from the women with healthy fetuses. The levels of H3K9ac, H3K18ac, and Gcn5 were also decreased in the woman with the fetus exhibiting myelomeningocele. In AFSCs from the woman carrying an anencephalic fetus, levels of H3K27me3, along with those of H3K9Ac, H3K18ac, and Gcn5, were increased, while that of KDM6B was decreased. Compared with the normal controls, the levels of BMP4 in amniotic fluid and serum from the woman with a fetus with myelomeningocele were increased, whereas levels of Shh were increased in the woman pregnant with a fetus displaying anencephaly. Conclusions The levels of epigenetic marks, such as H3K4me, H3K27me3, H3K9Ac, and H3K18A, in cultured AFSCs in combination with levels of key developmental proteins, such as BMP4 and Shh, are potential biomarkers for early detection and identification of NTDs in amniotic fluid and maternal serum.
6

Wei, Wenbin, Yuemin Liu, Yating Qiu, Minjie Chen, Yiwen Wang, Zixiang Han, and Ying Chai. "Characterization of Acetylation of Histone H3 at Lysine 9 in the Trigeminal Ganglion of a Rat Trigeminal Neuralgia Model." Oxidative Medicine and Cellular Longevity 2022 (May 4, 2022): 1–13. http://dx.doi.org/10.1155/2022/1300387.

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Trigeminal neuralgia (TN) is a chronic neuropathic pain disorder characterized by spontaneous and elicited paroxysms of electric-shock-like or stabbing pain in a region of the face. The epigenetic regulation of TN is still obscure. In current study, a rat TN model subject to carbamazepine (CBZ) treatment was established, and transcriptome- and genome-scale profiling of H3K9ac and HDAC3 was performed by RNA-seq and ChIP-seq. We observed that H3K9ac levels in the trigeminal ganglion were lower in the TN rats compared with those in the control, and CBZ treatment led to recovery of H3K9ac levels. Further, we found that HDAC3 was overactivated, which interfered with H3K9 acetylation due to higher phosphorylation in TN compared with that in the control. Finally, the phosphokinase leucine-rich repeat kinase 2 (LRRK2) was demonstrated to contribute to HDAC3 activity via the MAPK signaling pathway. Taken together, we identified a regulatory mechanism in which the phosphate groups transferred from activated ERK and LRRK2 to HDAC3 caused genome-scale deacetylation at H3K9 and resulted in the silencing of a large number of genes in TN. The kinases or important enzymes within this regulatory axis may represent important targets for TN therapy and prevention.
7

Ispada, Jessica, Aldcejam Martins da Fonseca Junior, Otávio Luiz Ramos Santos, Camila Bruna de Lima, Erika Cristina dos Santos, Vinicius Lourenço da Silva, Fernanda Nascimento Almeida, Saul de Castro Leite, Pablo Juan Ross, and Marcella Pecora Milazzotto. "Metabolism-driven post-translational modifications of H3K9 in early bovine embryos." Reproduction 162, no. 3 (September 1, 2021): 181–91. http://dx.doi.org/10.1530/rep-21-0134.

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Metabolic and molecular profiles were reported as different for bovine embryos with distinct kinetics during the first cleavages. In this study, we used this same developmental model (fast vs slow) to determine if the relationship between metabolism and developmental kinetics affects the levels of acetylation or tri-methylation at histone H3 lysine 9 (H3K9ac and H3K9me3, respectively). Fast and slow developing embryos presented different levels of H3K9ac and H3K9me3 from the earliest stages of development (40 and 96 hpi) and up to the blastocyst stage. For H3K9me3, both groups of embryos presented a wave of demethylation and de novo methylation, although it was more pronounced in fast than slow embryos, resulting in blastocysts with higher levels of this mark. The H3K9ac reprogramming profile was distinct between kinetics groups. While slow embryos presented a wave of deacetylation, followed by an increase in this mark at the blastocyst stage, fast embryos reduced this mark throughout all the developmental stages studied. H3K9me3 differences corresponded to writer and eraser transcript levels, while H3K9ac patterns were explained by metabolism-related gene expression. To verify if metabolic differences could alter levels of H3K9ac, embryos were cultured with sodium-iodoacetate (IA) or dichloroacetate (DCA) to disrupt the glycolytic pathway or increase acetyl-CoA production, respectively. IA reduced H3K9ac while DCA increased H3K9ac in blastocysts. Concluding, H3K9me3 and H3K9ac patterns differ between embryos with different kinetics, the second one explained by metabolic pathways involved in acetyl-CoA production. So far, this is the first study demonstrating a relationship between metabolic differences and histone post-translational modifications in bovine embryos.
8

Chacón, Liliana, Martha C. Gómez, Jill A. Jenkins, Staley P. Leibo, Gemechu Wirtu, Betsy L. Dresser, and C. Earle Pope. "Effect of cryopreservation and in vitro culture of bovine fibroblasts on histone acetylation levels and in vitro development of hand-made cloned embryos." Zygote 19, no. 3 (July 7, 2010): 255–64. http://dx.doi.org/10.1017/s0967199410000316.

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SummaryIn this study, the relative acetylation levels of histone 3 in lysine 9 (H3K9ac) in cultured and cryopreserved bovine fibroblasts was measured and we determined the influence of the epigenetic status of three cultured (C1, C2 and C3) donor cell lines on the in vitro development of reconstructed bovine embryos. Results showed that cryopreservation did not alter the overall acetylation levels of H3K9 in bovine fibroblasts analysed immediately after thawing (frozen/thawed) compared with fibroblasts cultured for a period of time after thawing. However, reduced cleavage rates were noted in embryos reconstructed with fibroblasts used immediately after thawing. Cell passage affects the levels of H3K9ac in bovine fibroblasts, decreasing after P1 and donor cells with lower H3K9ac produced a greater frequency of embryo development to the blastocyst stage. Cryopreservation did not influence the total cell and ICM numbers, or the ICM/TPD ratios of reconstructed embryos. However, the genetic source of donor cells did influence the total number of cells and the trophectoderm cell numbers, and the cell passage influenced the total ICM cell numbers.
9

Hezroni, Hadas, Badi Sri Sailaja, and Eran Meshorer. "Pluripotency-related, Valproic Acid (VPA)-induced Genome-wide Histone H3 Lysine 9 (H3K9) Acetylation Patterns in Embryonic Stem Cells." Journal of Biological Chemistry 286, no. 41 (August 17, 2011): 35977–88. http://dx.doi.org/10.1074/jbc.m111.266254.

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Embryonic stem cell (ESC) chromatin is characterized by a unique set of histone modifications, including enrichment for H3 lysine 9 acetylation (H3K9ac). Recent studies suggest that histone deacetylase (HDAC) inhibitors promote pluripotency. Here, using H3K9ac ChIP followed by high throughput sequencing analyses and gene expression in E14 mouse ESCs before and after treatment with a low level of the HDAC inhibitor valproic acid, we show that H3K9ac is enriched at gene promoters and is highly correlated with gene expression and with various genomic features, including different active histone marks and pluripotency-related transcription factors. Curiously, it predicts the cellular location of gene products. Treatment of ESCs with valproic acid leads to a pervasive genome-wide and time-dependent increase in H3K9ac, but this increase is selectively suppressed after 4 h in H3K4me3/H3K27me3 bivalent genes. H3K9ac increase is dependent on the promoter's chromatin state and is affected by the binding of P300, various transcription factors, and active histone marks. This study provides insights into the genomic response of ESCs to a low level of HDAC inhibitor, which leads to increased pluripotency. The results suggest that a mild (averaging less than 40%) but global change in the chromatin state is involved in increased pluripotency and that specific mechanisms operate selectively in bivalent genes to maintain constant H3K9ac levels. Our data support the notion that H3K9ac has an important role in ESC biology.
10

Steilmann, C., A. Paradowska, M. Bartkuhn, M. Vieweg, H. C. Schuppe, M. Bergmann, S. Kliesch, W. Weidner, and K. Steger. "Presence of histone H3 acetylated at lysine 9 in male germ cells and its distribution pattern in the genome of human spermatozoa." Reproduction, Fertility and Development 23, no. 8 (2011): 997. http://dx.doi.org/10.1071/rd10197.

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During spermatogenesis, approximately 85% of histones are replaced by protamines. The remaining histones have been proposed to carry essential marks for the establishment of epigenetic information in the offspring. The aim of the present study was to analyse the expression pattern of histone H3 acetylated at lysine 9 (H3K9ac) during normal and impaired spermatogenesis and the binding pattern of H3K9ac to selected genes within ejaculates. Testicular biopsies, as well as semen samples, were used for immunohistochemistry. Chromatin immunoprecipitation was performed with ejaculated sperm chromatin. HeLa cells and prostate tissue served as controls. Binding of selected genes was evaluated by semiquantitative and real-time polymerase chain reaction. Immunohistochemistry of H3K9ac demonstrated positive signals in spermatogonia, spermatocytes, elongating spermatids and ejaculated spermatozoa of fertile and infertile men. H3K9ac was associated with gene promoters (CRAT, G6PD, MCF2L), exons (SOX2, GAPDH, STK11IP, FLNA, PLXNA3, SH3GLB2, CTSD) and intergenic regions (TH) in fertile men and revealed shifts of the distribution pattern in ejaculated spermatozoa of infertile men. In conclusion, H3K9ac is present in male germ cells and may play a role during the development of human spermatozoa. In addition, H3K9ac is associated with specific regions of the sperm genome defining an epigenetic code that may influence gene expression directly after fertilisation.
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Статті в журналах Дисертації

Дисертації з теми "H3K9ac":

1

Hache, Antoine. "Molecular basis of transcriptional dysregulations in the spinocerebellar ataxia type 7, a neurodegenerative polyglutamine disorder." Thesis, Strasbourg, 2020. http://www.theses.fr/2020STRAJ083.

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SCA7 est une maladie génétique dont l’un des principaux symptômes est une perte progressive d’acuité visuelle pouvant aller jusqu’à la cécité. La mutation responsible de cette pathologie est une expansion instable d’un triplet CAG au sein de l’ATXN7, gene codant une sous-unité du complexe SAGA, un co-activateur de l’ARN polymerase de type II. Des études réalisées sur modèles de souris transgéniques mirent en évidence une perte d’identité des photorécepteurs au niveau morphologique, fonctionnel, et moléculaire. Au cours de ma thèse la caractérisation d’un nouveau modèle knock-in de SCA7 fut réalisée. Ce modèle, qui exprime le gène muté à un niveau endogène récapitule les atteintes rétiniennes observées dans les modèles transgéniques et chez les patients. Une étude transcriptomique (RNA-seq) et épigénomique (ChIP-seq) de ce modèle fut réalisée et mis en évidence des défauts globaux de l’acétylation des lysines 9 et 27 de l’histone H3 (H3K9 et H3K27ac). De plus une étude plus poussée des ARNs non codants mit en évidence l’existance d’ARN enhancer (eRNA) encore non répertoriés au niveau des loci de gènes uniquement exprimés dans les photorécepteurs comme Rho, ces même eRNAs sont retrouvés dérégulés chez les animaux développant la rétinopathie SCA7
SCA7 is a genetic disorder whose one of its main symptoms is a progressive loss of visual acuity which can ultimately lead to blindness. The mutation responsible for this disease is an unstable CAG expansion within ATXN7, a gene encoding a subunit of the SAGA complex, a co-activator of the RNA polymerase II. Previous studies performed on transgenic mouse models highlighted a neuronal identity loss of the photoreceptors at the morphological, functional and molecular levels. During my PhD a characterization of a new SCA7 knock-in mouse model was performed. This model, which expresses the mutated genes at endogenous level recapitulates the retinal impairments observed in transgenic models and in patients. A transcriptomic (RNA-seq) and epigenomic (ChIP-seq) analyses were performed on this model and highlight global acetylation defects on lysine 9 and 27 of histone H3 (H3K9ac and H3K27ac). Moreover, investigations on non-coding RNAs identified the presence of enhancer RNAs (eRNAs) on photoreceptor specific genes such as Rho. These eRNAs, which were never described before, undergo a downregulation in symptomatic SCA7 mice
2

Beyer, Susanne [Verfasser], and Udo [Akademischer Betreuer] Jeschke. "Immunhistochemische Untersuchung der Expression von H3K9ac, H3K4me3 und GR an Zervix-Karzinom-Präparaten sowie deren prognostische Analyse / Susanne Beyer ; Betreuer: Udo Jeschke." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2020. http://d-nb.info/1209472627/34.

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3

Rifai, Khaldoun. "Etude des modifications épigénétiques en fonction de l'agressivité du cancer sporadique du sein : l'implication de l'histone désacétylase SIRT1 dans la progression tumorale." Thesis, Université Clermont Auvergne‎ (2017-2020), 2018. http://www.theses.fr/2018CLFAS011/document.

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Avec 59 000 nouveaux cas en 2017, le cancer du sein est le cancer le plus fréquemment diagnostiqué chez les femmes françaises, et pose un réel problème de santé publique en France, mais aussi au niveau mondial. Il est bien établi que la complexité de la carcinogenèse implique des modifications épigénétiques profondes qui contribuent au processus du développement tumoral. La dérégulation des marques d'histones acétylées H3 et H4 font partie de ces modifications. L'acétylation et la désacétylation des protéines sont des modifications posttraductionnelles majeures qui régulent l'expression des gènes liés au cancer et à l'activité d'une myriade d'oncoprotéines. Ainsi, une activité désacétylase aberrante peut alors favoriser ou supprimer la tumorigenèse dans différents types de cancers humains, y compris le cancer du sein. La désacétylase SIRT1 et l’acétyltransférase TIP60 sont 2 enzymes épigénétiques antagonistes qui sont impliquées dans l'apoptose, la régulation des gènes, la stabilité génomique, la réparation de l'ADN, et le développement du cancer. Dans le cadre de cette thèse, nous avons étudié la dérégulation des profils d’acétylation des histones H3 et H4 dans les différents sous-types moléculaires du cancer du sein, et investigué l’implication de SIRT1 et de TIP60 dans la progression tumorale de cancer du sein. Tout d’abord, nous avons signalé les rôles de SIRT1 et de TIP60 comme des biomarqueurs pronostiques potentiels en révélant leurs expressions différentielles en fonction de l’agressivité du cancer. Ensuite, nous avons montré leur régulation épigénétique différentielle des cibles histones en fonction du sous-type moléculaire, ainsi que leur modulation de la marque activatrice H3K4ac. En outre, l’inhibition de ces 2 enzymes par des Épidrogues s’est avérée comme une stratégie efficace dans le traitement du cancer. Ces travaux mettent en relief alors, SIRT1 et TIP60 comme des cibles thérapeutiques potentielles du cancer sporadique du sein
With 59,000 new cases in 2017, breast cancer is the most frequently diagnosed cancer among French women, and poses a real public health problem in France, but also worldwide. It is well established that the complexity of carcinogenesis involves profound epigenetic deregulations that contribute to the tumorigenesis process. Deregulated H3 and H4 acetylated histone marks are amongst those alterations. Acetylation and deacetylation are major post-translational protein modifications that regulate gene expression and the activity of a myriad of oncoproteins. Aberrant deacetylase activity can promote or suppress tumorigenesis in different types of human cancers, including breast cancer. The deacetylase SIRT1 and the acetyltransferase TIP60 are 2 antagonistic epigenetic enzymes that are well implicated in apoptosis, gene regulation, genomic stability, DNA repair, and cancer development. In this manuscript, we identified the dysregulation of the histones H3 and H4 acetylation profiles in different molecular subtypes of sporadic breast cancer, and investigated the involvement of SIRT1 and TIP60 in breast tumorigenesis. First, we highlighted the roles of SIRT1 and TIP60 as potential prognostic biomarkers by revealing their differential expression patterns depending on breast cancer aggressiveness. Then, we demonstrated their differential epigenetic regulation of histone targets according to molecular subtype, and revealed their modulation of the H3K4ac epigenetic marker. Moreover, Epi-drugs mediated inhibition of these 2 enzymes has proven to be an effective strategy in the treatment of cancer. Thus, this work highlights the potential use of SIRT1 and TIP60 as epigenetic therapeutic targets for sporadic breast cancer
4

Audergon, Pauline Nicole Clotilde Beatrice. "Restricted epigenetic inheritance of H3K9 methylation." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/16212.

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In most eukaryotes methylation of histone H3 on lysine 9 (H3K9me) is the key post-translational modification required for the assembly of constitutive heterochromatin at centromeres and other chromosomal regions. H3K9me is bound by the chromodomain proteins HP1/Swi6 and the Suv39/Clr4 H3K9 methyltransferase itself suggesting that, once established, H3K9me might act as an epigenetic mark that can transmit the chromatin state independently of the initiator signal. However, it has not been demonstrated that H3K9me does indeed act as an epigenetic mark. Fission yeast represents an excellent system to address this question since S. pombe lacks DNA methylation and H3K9me is catalysed by the unique, non-essential H3K9 methyltransferase Clr4. To determine whether H3K9me carries epigenetic properties it is important to uncouple H3K9me from genomic domains that have the intrinsic ability to recruit the heterochromatin machinery. One way to solve this problem is to isolate H3K9me from its original context and investigate whether at an ectopic site H3K9me can self-propagate through cell division. To accomplish this, we tethered regulatable TetR-Clr4 fusion protein at euchromatic loci in fission yeast. This resulted in the assembly of an extensive domain of H3K9me-dependent heterochromatin that is rapidly disassembled following TetR-Clr4 release. Strikingly, the inactivation of Epe1, a putative histone demethylase, is sufficient to maintain the silent H3K9me-dependent heterochromatin at the tethering sites through mitotic and meiotic cell divisions in absence of TetR-Clr4. These results indicate that H3K9me acts as an epigenetic mark to maintain heterochromatin domains; however, a regulatory mechanism dependent on Epe1 exists to actively remove H3K9me and thus prevent heterochromatin from being transmitted when assembled at inappropriate regions of the genome.
5

Ferguson, Fleur Marcia. "Molecular recognition in the BAZ2B bromodomain: histone H3K14ac complex : biophysical studies and fragment-based targeting." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708479.

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6

Audonnet, Laure. "Caractérisation fonctionnelle de JMJ24, une déméthylase d’histone de la famille JUMONJI, chez Arabidopsis thaliana." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA112033/document.

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Cette dernière décennie a vu augmenter le nombre d’études portant sur la caractérisation des protéines JUMONJI (JMJ) et montrant leur rôle prépondérant dans la régulation des gènes et le développement des organismes. Ces protéines sont capables de déméthyler certains résidus des queues des histones et ont été organisées en groupes phylogénétiques en fonction de la conservation de leur domaine catalytique. Pour chaque clade entre un et trois substrats spécifiques ont pu être identifiés. De la sous famille KDM3, dont le résidu cible est H3K9, seul un membre, IBM1, a été caractérisé chez Arabidopsis. Cette étude montre que la mutation de JMJ24, un autre membre de ce groupe, entraine une augmentation de la taille des racines, cotylédons et organes floraux, suggérant un rôle dans le contrôle du développement à différents stades. De plus, l’analyse de l’expression tissulaire indique que JMJ24 est exprimé dans le phloème, en cohérence avec l’effet pléiotropique de sa mutation. Enfin, nos données suggèrent une interaction entre JMJ24 et d’autres protéines JMJ, telles JMJ14 et IBM1, mais aussi une interaction avec les protéines DCL, impliquées dans la régulation des gènes et des éléments transposables
Numerous studies over the last decade have reported the characterization of the JUMONJI (JMJ) proteins, showing their critical importance in regulating genes and organism’s development. These proteins are able to demethylate a subset of histone tail residues and were clustered into distinct groups using a phylogenetic analysis based on their catalytic domain conservation. Furthermore, modification of one to three specific residues has been attributed to each JMJ group. Within the KDM3 subfamily, of which target is the H3K9 residue, only one member, IBM1, was first characterized in Arabidopsis. In this report, we showed that the mutation of JMJ24, another member of this subfamily, resulted in an increase of the root length, cotyledon and floral organ size, suggesting that JMJ24 functions is needed at different developmental stage. In addition, the analysis of the tissue-specific expression of JMJ24 indicated that the gene is expressed within the phloem of all organs, correlating with the pleiotropic effect of the gene mutation. Last, our data also suggested that JMJ24 interacts with other JMJ protein like JMJ14 and IBM1, but also with the DCL proteins knowing to be involved in genes and transposable elements regulation
7

Sklias, Athéna. "Epigenetic regulation by estrogen receptor in breast cancer cells." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1149/document.

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Les travaux épidémiologiques et expérimentaux effectués à ce jour sur le cancer du sein ont montré que les oestrogènes - comme l’eostradiole (E2) - et leur récépteur (ER) - un facteur de transcription les liants - sont fortement impliqués dans au moins 70% des cas de cancer du sein. Cette implication est d’autant plus visible que les patients, suite à une thérapie anti-oestrogénique, ont tendance à développer une résistance endocrinienne au traitement. Pendant longtemps, l’ER a été étudié en tant que facteur indépendant liant directement une séquence ADN spécifique sur le génome. Aujourd’hui le paradigme a profondément changé. Il est bien connu que ER s’associe avec de nombreux autres facteurs de transcription et protéines régulant la chromatine afin de réguler l’expression des gènes. Cependant, nos connaissances concernant la fonction de modifications épigénétiques suite à l’activation de ER - notamment la méthylation de l’ADN et l’acétylation des histones - sont encore limitées. Dans cette étude, j’ai mis en place un protocole de culture cellulaire adapté à l’étude de la privation et à la re-stimulation d’E2 stricto sensu. Dans un premier temps, ce protocole a été évalué à l’aide de la toute dernière technologie de puce permettant la lecture du méthylome et couvrant la liste complète des éléments amplificateurs. Dans un deuxième temps, j’ai mesuré le transcriptome et les profiles d’acétylation de l’histone H3 (H3K27ac) afin de déterminer la capacité de ER à réguler l’expression des gènes J’ai découvert que, suite à la privation de E2, les niveaux de méthylation de l’ADN et de H3K27ac changent et que ces changements s’accentuent avec le temps, en particulier au niveau des éléments amplificateurs. Une analyse d’enrichissement des facteurs de transcription et des séquences de liaison spécifiques a révélé que les facteurs de transcriptions des familles AP-1 et FOX sont des intermédiaires favorisants la liaison de ER aux éléments amplificateurs. Finalement, la re-stimulation des cellules par de l’E2 a montré que la majorité des changements épigénétiques observé sont réversibles mais que certains éléments amplificateurs restent hyperméthylés et déacétylés. Ceci pourrait indiquer que les traitements anti-oestrogéniques sont efficaces mais pourrait également indiquer un marqueur de résistance endocrinienne. Cette étude apporte des informations nouvelles quant aux effets de l’inhibition et l’activation de ER sur la méthylation de l’ADN et l’acétylation de l’histone H3 à l’échelle du génome et renforce l’importance du rôle d’autres facteurs au niveau des amplificateurs
Previous epidemiological and experimental studies have strongly implicated estrogens in breast cancer risk and Estrogen Receptor (ER), the transcription factor to which estrogen binds, is considered as the major molecular driver of around 70% breast cancers. The importance of the deregulated estrogen signalling is further highlighted by increasing evidence that current chemopreventive and therapeutic strategies that target hormonally responsive breast cancers frequently result in the development of resistance to anti-estrogens and metastatic progression, highlighting the need for understanding the molecular underlying mechanisms. While until recently, ER was believed to act as a stand-alone transcription factor, which can directly bind its motifs in DNA, it is now accepted that ER activity is a complex and dynamic process that requires highly concerted actions of a dozen transcriptional cofactors and various chromatin regulators at DNA. Recent studies focused on characterising ER-associated cofactors and their role in opening the chromatin provided a remarkable insight into transcriptional regulation mediated by ER. However DNA methylation and histone acetylation are poorly understood in the context of ER’s dynamic binding. In this thesis, I combined a cell culture protocol adapted for studying estradiol (E2) deprivation and re-stimulation in stricto sensu in ER-positive breast cancer cells with the latest methylation array, that allowed a genome-wide interrogation of DNA methylation (including a comprehensive panel of enhancers). I further investigated histone acetylation (ChIP-seq) and transcriptome (RNA-seq) after E2 deprivation and re-stimulation to better characterise the ability of ER to coordinate gene regulation. I found that E2 deprivation and re-stimulation result in time-dependent DNA methylation changes and in histone acetylation across diverse genomic regions, many of which overlap with enhancers. Further enrichment analysis of transcription factor (TF) binding and motif occurrence highlights the importance of ER tethering mainly through two partner TF families, AP-1 and FOX, in the proximity of enhancers that are differentially methylated and acetylated. This is the first study that comprehensively characterized DNA methylation at enhancers in response to inhibition and activation of ER signalling. The transcriptome and genome occupancy data further reinforced the notion that ER activity may orchestrate a broad transcriptional programme through regulating a limited panel of critical enhancers. Finally, the E2 re-stimulation experiments revealed that although the majority of the observed epigenetic changes induced by E2 deprivation could be largely reversed when the cells were re-stimulated we show that DNA hypermethylation and H3K27 acetylation at enhancers as well as several gene expression changes are selectively retained. The partial reversibility can be interpreted as a sign of treatment efficiency but also as a mechanism by which ER activity may contribute to endocrine resistance. This study provides entirely new information that constitutes a major advance in our understanding of the events by which ER and its cofactors mediate changes in DNA methylation and chromatin states at enhancers. These findings should open new avenues for studying role of the deregulated estrogen signalling in the mechanism underlying the “roots” of endocrine resistance that commonly develops in response to anti-estrogen therapy
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Battisti, Valentine. "Rôle d'histones methyltransférases spécifiques de H3K9 dans l'équilibre prolifération et différenciation cellulaire." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T092/document.

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Chez les eucaryotes, l’expression des gènes dépend en partie du degré de compaction de la chromatine. La structure chromatinienne est régulée par des marques dites épigénétiques,telles que les modifications post-traductionnelles des protéines structurelles de la chromatine, les histones. Ainsi, la méthylation de la lysine 9 de l’histone H3 (H3K9) sur le promoteur des gènes est essentiellement associée à la répression de la transcription. H3K9 est méthylée par différentes enzymes appelées lysine méthyltransférases (KMTs). L’objectif principal de mon projet de thèse a été de mieux comprendre le rôle de principales KMTs de H3K9, que sontG9a, GLP, Suv39h1 et SETDB1, dans la régulation de l’équilibre entre prolifération et différenciation terminale. Pour cela, j’ai utilisé le modèle de différenciation terminale de cellules du muscle squelettique. En effet, durant la différenciation terminale, les myoblastes arrêtent de proliférer et fusionnent entre eux pour former de longues cellules multi nucléées que sont les myotubes. Ce processus implique, d’une part, l’expression des gènes de différenciation musculaire et, d’autre part, la répression irréversible des gènes associés à la prolifération cellulaire. L’introduction bibliographique de ce travail de thèse est séparée en trois chapitres. Le premier chapitre porte sur la chromatine et ses modifications post-traductionnelles. Le second s’attache à décrire les rôles de la méthylation de H3K9 et, en particulier, des quatre KMTs sur lesquelles j’ai travaillé durant ma thèse : G9a, GLP, SETDB1 et Suv39h1. Dans le troisième chapitre, je présente le modèle de la différenciation terminale du muscle squelettique. Dans la partie "Résultats", je décris deux des principales études que j’ai menées durant ma thèse. La première porte sur les rôles antagonistes de G9a et GLP. La seconde porte sur le rôle de SETDB1 durant la différenciation musculaire. Les résultats que j’ai obtenus sont discutés dans cette partie. Je conclus ce manuscrit en discutant mes résultats de manière plus générale et en proposant des perspectives à long terme. Enfin, une annexe présentera les autres articles de recherche auxquels j’ai participé pendant ma thèse
In eukaryotes, gene expression partly relies on chromatin compaction degree. Chromatin status is controlled by epigenetic marks, such as histones (chromatin structural proteins) posttranslational modifications. As an example, histone H3 lysine 9 (H3K9) methylation on gene promoters is mainly associated with transcriptional repression. H3K9 is methylated by several enzymes called lysine methyltransferases (KMTs). The aim of my thesis project was to understand the role of the H3K9 KMTs, G9a, GLP, Suv39h1 and SETDB1 in regulating the balance between proliferation and terminal differentiation. For this purpose, I used skeletal muscle terminal differentiation as model. Upon muscle terminal differentiation, myoblasts exit, in an irreversible way, from the cell cycle and under go differentiation where cells fusion and form myotubes. During this process, cell cycle genes are permanently silenced and muscle specific genes are activated. Thesis introduction is divided into three chapters. The first chapter focuses on chromatin and post-translational modifications. The second chapter describes H3K9 methylation characteristics and the role of the four KMTs that I studied during my thesis project: G9a,GLP, Suv39h1 and SETDB1. In the third chapter, the skeletal muscle terminal differentiation model is described in details. Results section reports my two major studies outcomes and their discussion. The first concerns the antagonistic roles of G9a and GLP regarding the muscle terminal differentiation and the second focuses on the role of SETDB1 during muscle differentiation. Finally, I conclude this manuscript by a plainer discussion followed by long term perspectives and an appendix presents other research articles, in which I collaborated during my PhD
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Malik, Athar Naveed. "Genome-Wide Identification and Characterization of Stimulus-Responsive Enhancers in the Nervous System." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11026.

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During development, intrinsic genetic programs give rise to distinct cellular lineages through the establishment of cell type specific chromatin states. These distinct chromatin states instruct gene expression primarily through the genome-wide demarcation of enhancers. In addition to maintaining cellular identity, the chromatin state of a cell provides a platform for transcriptional responses to environmental signals. However, relatively little is known about the influence of extracellular stimuli on chromatin state at enhancers, and it is not clear which enhancers among the tens of thousands that have been recently identified function to drive stimulus-responsive transcription. In the nervous system, the chromatin state of terminally differentiated neurons not only maintains neuronal identity but also provides a platform for sensory experience-dependent gene expression, which plays a critical role in the development and refinement of neural circuits and in long-lasting changes in neuronal function that underlie learning, memory, and behavior. Using chromatin-immunoprecipitation followed by high through put sequencing (ChIP-Seq), we determined the effects of neuronal stimuli on the active chromatin landscape of mouse cortical neurons. We discover that stimulation with neuronal activity and brain derived neurotrophic factor (BDNF) cause rapid, widespread, and distinct changes in the acetylation of histone H3 lysine 27 (H3K27Ac) at thousands of enhancers throughout the neuronal genome. We find that functional stimulus-responsive enhancers can be identified by stimulus- inducible H3K27Ac, and we use this dynamic chromatin signature to discover neuronal enhancers that respond to neuronal activity, BDNF, or both stimuli. Finally, we investigate the transcriptional mechanisms underlying the function of stimulus responsive enhancers. We show that a subset of stimulus-responsive enhancers in the nervous system require the coordinated action of the stimulus-general transcription factor activator protein 1 (AP1) with additional stimulus-specific factors. Our studies reveal the genome-wide basis for transcriptional specificity in response to distinct neuronal stimuli. Furthermore, the comprehensive identification of neuronal activity and BDNF-dependent enhancers in cortical neurons provides a critical resource for elucidating the role of stimulus-responsive transcription in synaptic plasticity, learning and memory, behavior, and disease. Finally, the epigenetic signature of stimulus-inducible H3K27Ac may aid in the identification and study of stimulus- regulated enhancers in other tissues.
10

Leung, Danny Chi Yeu. "Transcriptional silencing of endogenous retroviruses : interplay between histone H3K9 methylation and DNA methylation." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/38966.

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Endogenous retroviruses (ERVs) are found in genomes of all higher eukaryotes. As retrotransposition is deleterious, pathways have evolved to repress these retroelements. While DNA methylation transcriptionally represses ERVs in differentiated cells, this epigenetic mark is dispensable for maintaining proviral silencing during early stages of mouse embryogenesis and in embryonic stem cells (mESCs). Studies in diverse species have found histone H3K9 methylation and DNA methylation to function together to repress retrotransposons. However, until recently, little was known about the role of this histone modification in proviral silencing in mESCs. Interestingly, our analysis of mESCs lacking G9a, an H3K9-specific lysine methyltransferase (KMTase) revealed that although ERVs lost H3K9 di-methylation (me2) and DNA methylation, they remained silent. Strikingly, the levels of H3K9 tri-methylation (me3) remained unaltered, suggesting that this mark may instead be responsible for maintaining these parasitic elements transcriptionally inactive. The first stage of my research focused on identifying the enzyme depositing H3K9me3 at ERVs and on determining its role in proviral silencing. I discovered that Setdb1, another H3K9-specific KMTase, was indeed depositing H3K9me3 at a subset of ERVs and was required for maintaining transcriptional repression. Interestingly, this silencing pathway operated independently of DNA methylation. Through collaboration, we also discovered that this pathway played a diminished role in differentiated cells. Taken together, these findings indicate the existence of a DNA methylation-independent proviral silencing pathway in mESCs. The second stage of my research focused on the establishment of transcriptional repression of newly integrated proviruses. By employing an exogenous retroviral construct, I discovered a dramatic silencing defect in mESCs lacking G9a, which phenocopied cells depleted of the de novo DNA methyltransferases. Furthermore, efficient DNA methylation of proviruses required G9a-mediated H3K9me2. These findings reveal that histone modifications and DNA methylation function in concert to defend the genome against invading retroviral elements in mESCs. Taken together with discoveries regarding the mechanism of DNA demethylation in early embryos, I propose that cells undergoing DNA methylation reprogramming predominantly employ histone modification-based pathways to maintain these parasitic elements in a silent state; however, the establishment of transcriptional repression for newly integrated elements also requires de novo DNA methylation.
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Частини книг з теми "H3K9ac":

1

Minh, N. T., N. B. Tu, N. T. T. Tram, H. T. Bui, and N. Van Thuan. "Histone Deacetylase Inhibitor Corrects Histone H3K9 Modification in Round Spermatid DNA at the 2-Cell Stage and Increases the Development of ROSI Embryos." In 6th International Conference on the Development of Biomedical Engineering in Vietnam (BME6), 877–81. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4361-1_149.

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2

"H3K9." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 885. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_7691.

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3

Nestorov, Peter, Mathieu Tardat, and Antoine H. F. M. Peters. "H3K9/HP1 and Polycomb." In Current Topics in Developmental Biology, 243–91. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-416027-9.00008-5.

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4

Yang, Xu, Wei Li, Hangyuan He, Yongjian Qi, Jacques Magdalou, Hui Wang, and Liaobin Chen. "H3K9 Acetylation Level of 11β-HSD2 in Human Wharton’s Jelly-Derived Mesenchymal Stem Cells: A Potential Biomarker for Evaluating Susceptibility to Multiple Chronic Diseases in Adulthood." In Stem Cells and Regenerative Medicine. IOS Press, 2021. http://dx.doi.org/10.3233/bhr210009.

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Objective: A large number of studies have suggested that low birth weight fetuses were susceptible to fetal-originated diseases in adulthood. The purpose of this study was to investigate whether the histone 3 Lysine 9 (H3K9) acetylation level of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) in human Wharton’s jelly-derived mesenchymal stem cells (WJ-MSCs) was an early warning marker for the susceptibility of multiple chronic diseases in adulthood. Methods: The epigenetic and expressional abnormality of 11β-HSD2 in human WJ-MSCs induced by a variety of prenatal adverse xenobiotic factors were analyzed by real-time quantitative PCR (RT-qPCR), chromatin immunoprecipitation (ChIP) and western blotting (WB). The expression of insulin-like growth factor 1 (IGF1) in human WJ-MSCs after overexpression or knockdown of 11β-HSD2 gene was analyzed by RT-qPCR. Finally, immunofluorescence and ChIP-PCR were used to analyze the H3K9 acetylation level and expression of 11β-HSD2 in the human umbilical cord with intrauterine growth retardation (IUGR). Results: The mRNA and protein expression of 11β-HSD2 in WJ-MSCs were decreased after treatment with caffeine, nicotine, and ethanol. The histone acetylation level in 11β-HSD2 promoter region (H3K9) was significantly reduced simultaneously. In the proliferation model of WJ-MSCs, 300 nM of cortisol promoted the gene expression of the IGF1 pathway, while 1200 nM inhibited the gene expression of the IGF1 pathway. The expression of IGF1 treated with cortisol at 300 nM was decreased after overexpression of 11β-HSD2, while the expression of IGF1 was increased after treatment with 1200 nM cortisol. After knockdown of 11β-HSD2, the expression of IGF1 was decreased after treatment with 300 nM cortisol, and IGF1 gene expression decreased further after treatment with 1200 nM cortisol. Besides, the expression and H3K9 acetylation level of 11β-HSD2 in the IUGR-derived human umbilical cord was also reduced. Conclusion: The decreased expression and H3K9 acetylation level of 11β-HSD2 in WJ-MSCs induced by multiple xenobiotics exposures may mediate the decreased expression of IGF1. The H3K9 acetylation level of 11β-HSD2 in the human umbilical cord might be an early warning biomarker for evaluating susceptibility to multiple chronic diseases in adulthood.
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Sidhaye, Aniket R., Shunichi Matsumoto, Rong Huang, Shonoi Barnett, Philip A. Cole, and Fredric E. Wondisford. "Thyroid Hormone–Induced Changes in H3K4 Methylation and H3K9 Acetylation in the TSHB Promoter Region Suggest a Role for Epigenetic Modifications in TSHB Gene Regulation." In BASIC - Hypothalamic-Pituitary-Thyroid Axis: Thyroid Hormone Metabolism, Cellular Uptake & Action, P1–646—P1–646. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p16.p1-646.

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Тези доповідей конференцій з теми "H3K9ac":

1

Berger, L., T. Kolben, S. Meister, T. M. Kolben, E. Schmoeckel, D. Mayr, S. Mahner, U. Jeschke, N. Ditsch, and S. Beyer. "Expression von H3K4me3 und H3K9ac in Brustkrebs." In 94. Kongress der Bayerischen Gesellschaft für Geburtshilfe und Frauenheilkunde e. V. (BGGF). Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1713965.

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2

Estevan, Mariana, Pablo Vargas, Gleyson Amaral-Silva, Vivian Wagner, Bruno Mariz, Alan Santos-Silva, Marcio Lopes, and Oslei Almeida. "Evaluation of the H3K9ac immunoexpression in lip carcinogenesis." In Congresso de Iniciação Científica UNICAMP. Universidade Estadual de Campinas, 2019. http://dx.doi.org/10.20396/revpibic2720192623.

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3

Berger, L., T. Kolben, S. Meister, TM Kolben, E. Schmoeckel, D. Mayr, S. Mahner, U. Jeschke, N. Ditsch, and S. Beyer. "Expression of H3K4me3 and H3K9ac in breast cancer." In Kongressabstracts zur Tagung 2020 der Deutschen Gesellschaft für Gynäkologie und Geburtshilfe (DGGG). © 2020. Thieme. All rights reserved., 2020. http://dx.doi.org/10.1055/s-0040-1717839.

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4

Meister, S., L. Hahn, S. Beyer, C. Kuhn, M. Jegen, V. von Schönfeldt, S. Corradini, et al. "Die epigenetische Modifikation durch H3K4me3 und H3K9ac ist in Präeklampsieplazenten reduziert." In Kongressabstracts zur Gemeinsamen Jahrestagung der Österreichischen Gesellschaft für Gynäkologie und Geburtshilfe (OEGGG) und der Bayerischen Gesellschaft für Geburtshilfe und Frauenheilkunde e.V. (BGGF). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1730489.

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Meister, S., L. Hahn, S. Beyer, C. Paul, S. Mitter, C. Kuhn, V. von Schönfeldt та ін. "Die Expression von PPARγ in der Präeklampsie reguliert die Histonmodifikationen H3K4me3 und H3K9ac". У Kongressabstracts zur Gemeinsamen Jahrestagung der Österreichischen Gesellschaft für Gynäkologie und Geburtshilfe (OEGGG) und der Bayerischen Gesellschaft für Geburtshilfe und Frauenheilkunde e.V. (BGGF). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1730490.

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Wehrmann, M., T. Kolben, S. Meister, T. M. Kolben, E. Schmoeckel, D. Mayr, A. Burges, et al. "Gal-8, Gal-9, H3K9ac, H3K4me3 und der Glukokortikoidrezeptor als prognostische Marker im Endometriumkarzinom." In 94. Kongress der Bayerischen Gesellschaft für Geburtshilfe und Frauenheilkunde e. V. (BGGF). Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1713967.

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7

Fong, Pui Kwan, and Nung Kion Lee. "Improved H3K27ac histone mark prediction using k-mer proximity feature." In 2015 9th International Conference on IT in Asia (CITA). IEEE, 2015. http://dx.doi.org/10.1109/cita.2015.7349830.

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Tang, Chunlao, Vipin Yadav, Hui-Rong Qian, Jason B. Cunningham, Hong Gao, Yushi Liu, Jason C. Ting, et al. "Abstract 1446: Super-enhancer identification via Bru/BrUV-Seq and H3K27Ac ChIP-Seq." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1446.

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Kellner, I., S. Beyer, S. Corradini, N. Rogenhofer, TM Kolben, U. Hasbargen, A. Hester, et al. "Epigenetische Modifikationen durch H3K4me3 und H3K9acan der fetomaternalen Grenzzone der Plazenta im Abortgeschehen." In Kongressabstracts zur Gemeinsamen Jahrestagung der Österreichischen Gesellschaft für Gynäkologie und Geburtshilfe (OEGGG) und der Bayerischen Gesellschaft für Geburtshilfe und Frauenheilkunde e.V. (BGGF). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1730484.

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Giannikou, Krinio, Clemens K. Probst, Mahsa Zarei, Xintao Qiu, Melissa Duarte, Nikolas Kesten, Zachary Hebert, et al. "Abstract PO-010: Kidney angiomyolipomas are defined by a unique transcriptomic profile and H3K27ac chromatin state." In Abstracts: AACR Special Virtual Conference on Epigenetics and Metabolism; October 15-16, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.epimetab20-po-010.

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