Relevant bibliographies by topics / Epigenetic regulator

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  2. Dissertations / Theses
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Academic literature on the topic 'Epigenetic regulator'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Epigenetic regulator"

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Abdullah, Omeima, and Mahmoud Alhosin. "HAUSP Is a Key Epigenetic Regulator of the Chromatin Effector Proteins." Genes 13, no. 1 (December 24, 2021): 42. http://dx.doi.org/10.3390/genes13010042.

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HAUSP (herpes virus-associated ubiquitin-specific protease), also known as Ubiquitin Specific Protease 7, plays critical roles in cellular processes, such as chromatin biology and epigenetics, through the regulation of different signaling pathways. HAUSP is a main partner of the “Epigenetic Code Replication Machinery,” ECREM, a large protein complex that includes several epigenetic players, such as the ubiquitin-like containing plant homeodomain (PHD) and an interesting new gene (RING), finger domains 1 (UHRF1), as well as DNA methyltransferase 1 (DNMT1), histone deacetylase 1 (HDAC1), histone methyltransferase G9a, and histone acetyltransferase TIP60. Due to its deubiquitinase activity and its ability to team up through direct interactions with several epigenetic regulators, mainly UHRF1, DNMT1, TIP60, the histone lysine methyltransferase EZH2, and the lysine-specific histone demethylase LSD1, HAUSP positions itself at the top of the regulatory hierarchies involved in epigenetic silencing of tumor suppressor genes in cancer. This review highlights the increasing role of HAUSP as an epigenetic master regulator that governs a set of epigenetic players involved in both the maintenance of DNA methylation and histone post-translational modifications.
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Albogami, Sarah. "Epigenetic Regulator Signatures in Regenerative Capacity." Current Stem Cell Research & Therapy 14, no. 7 (September 23, 2019): 598–606. http://dx.doi.org/10.2174/1574888x14666190618125111.

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Background:: Regeneration is the process by which body parts lost as a result of injury are replaced, as observed in certain animal species. The root of regenerative differences between organisms is still not very well understood; if regeneration merely recycles developmental pathways in the adult form, why can some animals regrow organs whereas others cannot? In the regulation of the regeneration process as well as other biological phenomena, epigenetics plays an essential role. Objective:: This review aims to demonstrate the role of epigenetic regulators in determining regenerative capacity. Results:: In this review, we discuss the basis of regenerative differences between organisms. In addition, we present the current knowledge on the role of epigenetic regulation in regeneration, including DNA methylation, histone modification, lysine methylation, lysine methyltransferases, and the SET1 family. Conclusion:: An improved understanding of the regeneration process and the epigenetic regulation thereof through the study of regeneration in highly regenerative species will help in the field of regenerative medicine in future.
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Barneda-Zahonero, Bruna, Lidia Roman-Gonzalez, Olga Collazo, Tokameh Mahmoudi, and Maribel Parra. "Epigenetic Regulation of B Lymphocyte Differentiation, Transdifferentiation, and Reprogramming." Comparative and Functional Genomics 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/564381.

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B cell development is a multistep process that is tightly regulated at the transcriptional level. In recent years, investigators have shed light on the transcription factor networks involved in all the differentiation steps comprising B lymphopoiesis. The interplay between transcription factors and the epigenetic machinery involved in establishing the correct genomic landscape characteristic of each cellular state is beginning to be dissected. The participation of “epigenetic regulator-transcription factor” complexes is also crucial for directing cells during reprogramming into pluripotency or lineage conversion. In this context, greater knowledge of epigenetic regulation during B cell development, transdifferentiation, and reprogramming will enable us to understand better how epigenetics can control cell lineage commitment and identity. Herein, we review the current knowledge about the epigenetic events that contribute to B cell development and reprogramming.
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McCoy, Rachel M., Russell Julian, Shoban R. V. Kumar, Rajeev Ranjan, Kranthi Varala, and Ying Li. "A Systems Biology Approach to Identify Essential Epigenetic Regulators for Specific Biological Processes in Plants." Plants 10, no. 2 (February 13, 2021): 364. http://dx.doi.org/10.3390/plants10020364.

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Upon sensing developmental or environmental cues, epigenetic regulators transform the chromatin landscape of a network of genes to modulate their expression and dictate adequate cellular and organismal responses. Knowledge of the specific biological processes and genomic loci controlled by each epigenetic regulator will greatly advance our understanding of epigenetic regulation in plants. To facilitate hypothesis generation and testing in this domain, we present EpiNet, an extensive gene regulatory network (GRN) featuring epigenetic regulators. EpiNet was enabled by (i) curated knowledge of epigenetic regulators involved in DNA methylation, histone modification, chromatin remodeling, and siRNA pathways; and (ii) a machine-learning network inference approach powered by a wealth of public transcriptome datasets. We applied GENIE3, a machine-learning network inference approach, to mine public Arabidopsis transcriptomes and construct tissue-specific GRNs with both epigenetic regulators and transcription factors as predictors. The resultant GRNs, named EpiNet, can now be intersected with individual transcriptomic studies on biological processes of interest to identify the most influential epigenetic regulators, as well as predicted gene targets of the epigenetic regulators. We demonstrate the validity of this approach using case studies of shoot and root apical meristem development.
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Skalnik, David G. "The epigenetic regulator Cfp1." BioMolecular Concepts 1, no. 5-6 (December 1, 2010): 325–34. http://dx.doi.org/10.1515/bmc.2010.031.

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AbstractNumerous epigenetic modifications have been identified and correlated with transcriptionally active euchromatin or repressed heterochromatin and many enzymes responsible for the addition and removal of these marks have been characterized. However, less is known regarding how these enzymes are regulated and targeted to appropriate genomic locations. Mammalian CXXC finger protein 1 is an epigenetic regulator that was originally identified as a protein that binds specifically to any DNA sequence containing an unmethylated CpG dinucleotide. Mouse embryos lacking CXXC finger protein 1 die prior to gastrulation, and embryonic stem cells lacking CXXC finger protein 1 are viable but are unable to achieve cellular differentiation and lineage commitment. CXXC finger protein 1 is a regulator of both cytosine and histone methylation. It physically interacts with DNA methyltransferase 1 and facilitates maintenance cytosine methylation. Rescue studies reveal that CXXC finger protein 1 contains redundant functional domains that are sufficient to support cellular differentiation and proper levels of cytosine methylation. CXXC finger protein 1 is also a component of the Setd1 histone H3-Lys4 methyltransferase complexes and functions to target these enzymes to unmethylated CpG islands. Depletion of CXXC finger protein 1 leads to loss of histone H3-Lys4 tri-methylation at CpG islands and inappropriate drifting of this euchromatin mark into areas of hetero-chromatin. Thus, one function of CXXC finger protein 1 is to serve as an effector protein that interprets cytosine methylation patterns and facilitates crosstalk with histone-modifying enzymes.
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Theys, Claudia, Dorien Lauwers, Claudina Perez-Novo, and Wim Vanden Berghe. "PPARα in the Epigenetic Driver Seat of NAFLD: New Therapeutic Opportunities for Epigenetic Drugs?" Biomedicines 10, no. 12 (November 25, 2022): 3041. http://dx.doi.org/10.3390/biomedicines10123041.

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Nonalcoholic fatty liver disease (NAFLD) is a growing epidemic and the most common cause of chronic liver disease worldwide. It consists of a spectrum of liver disorders ranging from simple steatosis to NASH which predisposes patients to further fibrosis, cirrhosis and even hepatocarcinoma. Despite much research, an approved treatment is still lacking. Finding new therapeutic targets has therefore been a main priority. Known as a main regulator of the lipid metabolism and highly expressed in the liver, the nuclear receptor peroxisome proliferator-activated receptor-α (PPARα) has been identified as an attractive therapeutic target. Since its expression is silenced by DNA hypermethylation in NAFLD patients, many research strategies have aimed to restore the expression of PPARα and its target genes involved in lipid metabolism. Although previously tested PPARα agonists did not ameliorate the disease, current research has shown that PPARα also interacts and regulates epigenetic DNMT1, JMJD3, TET and SIRT1 enzymes. Moreover, there is a growing body of evidence suggesting the orchestrating role of epigenetics in the development and progression of NAFLD. Therefore, current therapeutic strategies are shifting more towards epigenetic drugs. This review provides a concise overview of the epigenetic regulation of NAFLD with a focus on PPARα regulation and highlights recently identified epigenetic interaction partners of PPARα.
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Dey, Anusree, Sheetal Uppal, Jayeeta Giri, and Hari Sharan Misra. "Emerging Roles of Bromodomain Protein 4 in Regulation of Stem Cell Identity." Stem Cells 39, no. 12 (September 25, 2021): 1615–24. http://dx.doi.org/10.1002/stem.3454.

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Abstract Understanding the mechanism of fate decision and lineage commitment is the key step for developing novel stem cell applications in therapeutics. This process is coordinately regulated through systematic epigenetic reprogramming and concomitant changes in the transcriptional landscape of the stem cells. One of the bromo- and extra-terminal domain (BET) family member proteins, bromodomain protein 4 (BRD4), performs the role of epigenetic reader and modulates gene expression by recruiting other transcription factors and directly regulating RNA polymerase II elongation. Controlled gene regulation is the critical step in maintenance of stem cell potency and dysregulation may lead to tumor formation. As a key transcriptional factor and epigenetic regulator, BRD4 contributes to stem cell maintenance in several ways. Being a druggable target, BRD4 is an attractive candidate for exploiting its potential in stem cell therapeutics. Therefore, it is crucial to elucidate how BRD4, through its interplay with pluripotency transcriptional regulators, control lineage commitment in stem cells. Here, we systemically review the role of BRD4 in complex gene regulatory network during three specific states of stem cell transitions: cell differentiation, cell reprogramming and transdifferentiation. A thorough understanding of BRD4 mediated epigenetic regulation in the maintenance of stem cell potency will be helpful to strategically control stem cell fates in regenerative medicine.
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Sarne, Victoria, Sandrina Braunmueller, Lisa Rakob, and Rita Seeboeck. "The Relevance of Gender in Tumor-Influencing Epigenetic Traits." Epigenomes 3, no. 1 (January 28, 2019): 6. http://dx.doi.org/10.3390/epigenomes3010006.

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Tumorigenesis as well as the molecular orchestration of cancer progression are very complex mechanisms that comprise numerous elements of influence and regulation. Today, many of the major concepts are well described and a basic understanding of a tumor’s fine-tuning is given. Throughout the last decade epigenetics has been featured in cancer research and it is now clear that the underlying mechanisms, especially DNA and histone modifications, are important regulators of carcinogenesis and tumor progression. Another key regulator, which is well known but has been neglected in scientific approaches as well as molecular diagnostics and, consequently, treatment conceptualization for a long time, is the subtle influence patient gender has on molecular processes. Naturally, this is greatly based on hormonal differences, but from an epigenetic point of view, the diverse susceptibility to stress and environmental influences is of prime interest. In this review we present the current view on which and how epigenetic modifications, emphasizing DNA methylation, regulate various tumor diseases. It is our aim to elucidate gender and epigenetics and their interconnectedness, which will contribute to understanding of the prospect molecular orchestration of cancer in individual tumors.
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Bithell, Angela. "REST: transcriptional and epigenetic regulator." Epigenomics 3, no. 1 (February 2011): 47–58. http://dx.doi.org/10.2217/epi.10.76.

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Bahia, Ravinder, Xiaoguang Hao, Rozina Hassam, Orsolya Cseh, Danielle Bozek, H. Artee Luchman, and Samuel Weiss. "STEM-18. EPIGENETIC AND MOLECULAR COORDINATION BETWEEN HDAC2 AND SMAD3-SKI IS REQUIRED FOR GROWTH AND STEM CELL CHARACTERISTICS OF BRAIN TUMOUR STEM CELLS." Neuro-Oncology 24, Supplement_7 (November 1, 2022): vii34—vii35. http://dx.doi.org/10.1093/neuonc/noac209.135.

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Abstract Brain tumour stem cell population in glioblastoma (GBM) display key cancer stem cell characteristics of high self-renewal and drug resistance that are maintained by the coordinated functions of epigenetic and molecular regulators. Yet, specific epigenetic mechanisms that, in collaboration with relevant molecular pathways, help maintain a stem-like state in BTSCs remain poorly understood. Here, we identify HDAC2 as a foremost epigenetic regulator in BTSCs that specifically utilizes the transforming growth factor-β (TGF-β) pathway related proteins, SMAD3-SKI, for remodelling BTSC chromatin accessibility and transcriptional programs to facilitate their stemness and tumorigenic potentials. Our initial drug screening revealed that selective inhibition of HDAC1 and 2 with romidepsin was effective in targeting BTSC viability, cell proliferation and self-renewal in vitro. Using CRISPR-cas9 knockout and shRNA knockdown strategies, we further demonstrated that loss of HDAC2 disrupts an epigenetic and molecular coordination between HDAC2 and SMAD-SKI proteins, which negatively impacts BTSC survival, cell proliferation and self-renewal in vitro and improves median survival in orthotopic xenograft mouse models. Loss of HDAC2 showed reduction in the protein abundance of transcriptional regulator, SMAD3 and negative regulator protein, SKI. However, overexpression of SMAD3 in HDAC2 deficient BTSCs could partially rescues their cell functional deficits. These findings suggest that context-specific epigenetic regulations by HDAC2 and its interaction with the critical transcriptional regulators, SMAD3-SKI, maintains the stemness and growth characteristics of BTSCs. Further HDAC2 overexpression increases cell proliferation and self-renewal abilities in normal neural stem cells (NSCs). These findings thus support the role of HDAC2 as a key epigenetic determinant of stemness in normal NSCs and of cancer stem cell characteristics and tumorigenic potential in BTSCs. Collectively, our data raises the potential that disruption of the coordinated mechanisms regulated by HDAC2-SMAD3-SKI axis may be an effective therapeutic approach for targeting GBM BTSCs.
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Dissertations / Theses on the topic "Epigenetic regulator"

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Gocevski, Goran. "Interplay of Mye and Max with Epigenetic Regulator Bmi1." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114264.

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The polycomb group protein Bmi1 is an epigenetic regulator essential for the proliferation of many types of cancers. By impeding the expression of the tumor suppressor p53, Bmi1 is able to prevent apoptosis and senescence. c-Myc, a prominent oncogene, cooperates with Bmi1 to stimulate cellular transformation and tumorigenesis. Further investigation of the basic biological interplay between Bmi1 and c-Myc is crucial for our understanding of their tumorigenic ability. In my project I demonstrated that c-Myc and Bmi1 directly interact with each other and form nuclear foci. Overexpression of Max, a known partner of Myc, disrupts the Bmi1 and c-Myc interaction and prevents the formation of nuclear foci. Similar results were obtained with another member of the Myc family, L-Myc. Additionally, I found that HDAC3 interacts and co-localizes with Myc. HDAC3 also forms nuclear foci with Bmi1 and the addition of Max abrogates this interaction. In addition to the well-established role of Bmi1 as an epigenetic regulator, it has been recently shown that Bmi1 is part of an E3 ubiquitin-ligase complex, known as the Bmi1/RING1A or B complex. This complex controls the stability of many proteins. I showed that Bmi1 induces an L-Myc ubiquitination, which in turn causes the degradation of L-Myc. This data proposes a novel regulatory mechanism for the stability of the Myc oncogenes. The results of this thesis provide new insight into the basic biochemical interplay ofBmi1 with Myc and Max.
La protéine de groupe polycomb Bmi1 est essentielle pour la prolifération de nombreux types de cancers. En freinant l'expression du suppresseur de tumeur p53, Bmi1 est capable de prévenir l'apoptose et la sénescence. c-Myc, une autre oncogène, s'associe à Bmi1 pour stimuler la transformation et la tumorigenèse. Une enquête plus approfondie de l'interaction biologique fondamentale entre Bmi1 et c-Myc est crucial pour notre compréhension de leur capacité à promouvoir la tumorigène. Dans mon projet, j'ai démontré que c-Myc et Bmi1 interagissent directement et forment des foyers nucléaires. La surexpression de Max, un partenaire connu de Myc, perturbe l'interaction entre Bmi1 et c-Myc et empêche la formation de foyers nucléaires. Des résultats similaires ont été obtenus avec un autre membre de la famille Myc, L-Myc. En outre, j'ai constaté que HDAC3 interagi et se co-localise avec Myc. HDAC3 forme aussi des foyers nucléaires avec Bmi1 et l'ajout de Max abroge cette interaction. En plus du rôle bien établi de Bmi1 comme un régulateur épigénétique, il a été démontré récemment que Bmi1 fait partie d'une ubiquitine-ligase E3 complexe, connu sous le nom complexe Bmi1/RING1A ou B. Ce complexe contrôle la stabilité de nombreuses protéines. J'ai démontré que Bmi1 induit l'ubiquitination de L-Myc qui à son tour provoque la dégradation de celle-ci. Ces données proposent un nouveau mécanisme de règlementation pour la stabilité des oncogènes Myc. Les résultats de cette thèse fournissent un nouvel éclairage sur l'interaction biochimique de Bmi1 avec Myc et Max.
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Almoflehi, Sakhar. "Cord Blood CD34+ Expansion Using Vitamin-C: An Epigenetic Regulator." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/41413.

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Vitamin-C (Vit-C) has been shown to modulate hematopoietic stem cells and leukemia stem cell frequency in-vivo. Herein, Vit-C analogue, L-ascorbic acid 2-phosphate (AA2P), was investigated as a new potential HSC expansion agonist. Cord blood CD34+ cells were expanded in cultures with or without AA2P. AA2P induced a 2-fold increase in the expansion of stem and progenitor subsets including lymphoid-primed multi-potential progenitors (p<0.05, n=3) and functional colony forming progenitors. The functional properties of AA2P grafts was evaluated with a xenotransplant model. Superior platelet levels in the periphery (p<0.05) and human bone marrow engraftment (median 75% hCD45+ cells for AA2P Vs. 48% for PBS control at week-22, n=3, p<0.05) was detected in AA2P cohorts Vs. control. In summary, my results demonstrate that AA2P is a new stem and progenitor expansion agonist with AA2P-expanded stem and progenitor cells capable of increased engraftment and higher platelet recovery. These findings may aid to overcome cord blood limitations; thereby, improving clinical relevance.
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Lu, Yizhen. "Physical interation of parathyroid hormone-related protein with the epigenetic regulator Bmi1." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=96929.

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As a cause of malignancy-induced hypercalcemia, PTHrP (parathyroid hormone-related protein) plays an important role in cell growth and differentiation. This peptide is unique in that it not only acts through membrane receptors but also translocates directly to the nucleus. Studies have shown that the repression of target gene expression is achieved through chromatin modifications induced by the PcG complex. As a core protein of the PcG complex, Bmi1 functions as a transcriptional repressor for various genes involved in development and cell proliferation. Recent studies have indicated that the skeletal phenotypes of PTHrP(1-84) knock-in mice are consistent with ones observed in Bmi1-/- mice in vivo. In addition, the down-regulation of Bmi1 expression was detected in PTHrP(1-84) knock-in mice. Both phenotypes indicate that there is correlation between Bmi1 and PTHrP. However, the molecular mechanism involved in correlation of PTHrP and Bmi1 regulation is poorly understood. The aim of this study was to gain insight into the underlying molecular mechanism of the way of PTHrP regulating Bmi1. We focused on the interaction between PTHrP and Bmi1 in vitro and in vivo system and the consequences exerted by this interaction. At first, co-localization of PTHrP and Bmi1 was demonstrated and the N-terminus of PTHrP was found to be responsible for the interaction both in vivo and in vitro. Second, we set up the repression assays in vivo to identify the promoters' activities and cell survival influenced by this direct interaction. As a result, overexpression of PTHrP and Bmi1 in HEK293 cells was shown to have an effect on p19Arf and Gal4 promoter activities in vivo. Thirdly, increased cell proliferation was detected in HEK293 cells and NIH 3T3 cells with overexpressed PTHrP and Bmi1 together. At the same time, I also discovered the elevation of cell survival rate in HEK293 and NIH 3T3 cells when PTHrP and Mel18 were expressed together. This study provides evidence that the hormone PTHrP physically and functionally interacts with Bmi1 and Mel18 to affect the activities of promoters in the nucleus and regulate cell proliferation.
La protéine Parathyroid hormone related-protein (PTHrP) joue un rôle très important dans la croissance et la différentiation cellulaire en plus d'être responsable de l'hypercalcémie induite par la malignité. Ce peptide est unique non seulement parce qu'il agit par l'intermediate de récepteurs transmembranaires, mais aussi parce qu'il est transloqué directement au noyau. Bmi-1, un peptide essentiel du PcG complexe, fonctionne comme un répresseur de transcription pour plusieurs gènes importants dans le développement et de l'organisme de la prolifération cellulaire. Cette fonction répressive régule l'expression des gènes cibles en induisant des modifications sur la chromatine (73). Des études publiées récemment démontrent que PTHrP influence l'expression moléculaire de Bmi-1 (95). Cependant, le mécanisme par lequel Bmi-1 contrôle PTHrP n'est pas encore bien documenté. Mon but premier est d'élucider les mécanismes moléculaires de cette interaction ensuite de trouver quelles conséquences fonctionnelles peuvent résulter de cette interaction. Au départ, la colocalisation de PTHrP et Bmi-1 a été démontrée dans le noyau de cellules HEK293. Ensuite, l'interaction entre Bmi-1 et PTHrP a été illustrée in vivo et in vitro. On a trouvé que c'est le N-Terminal qui est responsable des interactions in vivo et in vitro. De plus, la surexpression de PTHrP et Bmi-1 dans les cellules HEK293 provoque des effets minimes sur l'activité transcriptionelle des gènes et de l'expression du gène P19arf. En outre, la surexpression de PTHrP et Bmi-1 cause une augmentation du niveau de prolifération cellulaire dans les cellules HEK293 et NIH 3T3. En parallèle, j'ai découvert une augmentation du taux de survie des cellules HEK 293 et NIH 3T3 suite à surexpression des peptides PTHrP et Mel18. A été noteé ces études démontrent que l'hormone PTHrP interagit physiquement et est attaché fonctionnellement avec Bmi-1.
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Lubitz, Sandra. "Analysis of an epigenetic regulator in mouse embryonic stem cell self-renewal and differentiation." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2006. http://nbn-resolving.de/urn:nbn:de:swb:14-1139479284063-94996.

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Mammals have two orthologs, Mll and Trx2, for the Drososphila protein Trithorax (TRX), which is the founding member of the trithorax group (TrxG) of epigenetic regulators. TrxG proteins are characterized by an evolutionary conserved SET domain. A major function of all SET domain- containing proteins is to modulate gene activity, but the underlying mechanisms are poorly understood. Apparently TRX, Mll and Trx2 are histone H3 lysine 4 specific methyltransferases. So far all evidence points to roles in expression of specific target genes. However, target genes and function of the epigenetic regulator Trx2 were still unknown. Homozygous trx2 mutant embryos arrest in development because of severe and widespread defects {Glaser, 2005 #296}. Thus mouse embryonic stem (ES) cells carrying a null mutation of trx2 were used as an alternative model system to address the implication of Trx2 in differentiation. This study showed that Trx2 is redundant for ES cell self-renewal. Homozygous trx2 knockout ES cells did not exhibit cell cycle defects. However, loss of Trx2 resulted in reduced proliferation and increased apoptosis rates in trx2-/- ES cells. Due to the fact that differentiation requires an appropriate rate of population growth, trx2-/- cells were affected adversely upon in vitro differentiation. Neurogeneic differentiation of trx2 mutant cells generated fewer mature neurons than wild type cells. Moreover a temporal delay in the developmental progression to differentiation became apparent. Cardiac differentiation of trx2-/- cells confirmed the developmental defect and temporal delay. Notably differentiation of trx2-/- cells was merely delayed or impaired but it was not absent, implying that Trx2 is not required for gene expression programs specific for neurons or cardiac myocytes. We propose that differentiation of trx2-/- ES cells is impaired because apoptosis is disturbing differentiation. Apart from analyzing the phenotype of trx2 mutant cells, this work was focused on the identification of Trx2 target genes. Oligonucleotide expression arrays were used to identify genes whose expression levels were affected by the absence of Trx2. In general, loss of Trx2 function resulted in more genes with decreased than increased expression levels. This is consistent with the hypothesis that Trx2 functions as a transcriptional activator. Comparison of gene expression profiles for constitutive and conditional trx2 mutant cells enabled a distinction between direct and indirect target genes for Trx2. As a result Magoh2 was identified as the key candidate target gene for Trx2. Interaction between Trx2 and Magoh2 suggested a potential regulatory role for Trx2 in alternative splicing. Furthermore this work provided evidence that Trx2 could be involved in the maintenance of CpG island promoter gene expression, thus providing a potent regulatory mechanism for ubiquitously expressed genes.
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Lubitz, Sandra. "Analysis of an epigenetic regulator in mouse embryonic stem cell self-renewal and differentiation." Doctoral thesis, Technische Universität Dresden, 2005. https://tud.qucosa.de/id/qucosa%3A24639.

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Mammals have two orthologs, Mll and Trx2, for the Drososphila protein Trithorax (TRX), which is the founding member of the trithorax group (TrxG) of epigenetic regulators. TrxG proteins are characterized by an evolutionary conserved SET domain. A major function of all SET domain- containing proteins is to modulate gene activity, but the underlying mechanisms are poorly understood. Apparently TRX, Mll and Trx2 are histone H3 lysine 4 specific methyltransferases. So far all evidence points to roles in expression of specific target genes. However, target genes and function of the epigenetic regulator Trx2 were still unknown. Homozygous trx2 mutant embryos arrest in development because of severe and widespread defects {Glaser, 2005 #296}. Thus mouse embryonic stem (ES) cells carrying a null mutation of trx2 were used as an alternative model system to address the implication of Trx2 in differentiation. This study showed that Trx2 is redundant for ES cell self-renewal. Homozygous trx2 knockout ES cells did not exhibit cell cycle defects. However, loss of Trx2 resulted in reduced proliferation and increased apoptosis rates in trx2-/- ES cells. Due to the fact that differentiation requires an appropriate rate of population growth, trx2-/- cells were affected adversely upon in vitro differentiation. Neurogeneic differentiation of trx2 mutant cells generated fewer mature neurons than wild type cells. Moreover a temporal delay in the developmental progression to differentiation became apparent. Cardiac differentiation of trx2-/- cells confirmed the developmental defect and temporal delay. Notably differentiation of trx2-/- cells was merely delayed or impaired but it was not absent, implying that Trx2 is not required for gene expression programs specific for neurons or cardiac myocytes. We propose that differentiation of trx2-/- ES cells is impaired because apoptosis is disturbing differentiation. Apart from analyzing the phenotype of trx2 mutant cells, this work was focused on the identification of Trx2 target genes. Oligonucleotide expression arrays were used to identify genes whose expression levels were affected by the absence of Trx2. In general, loss of Trx2 function resulted in more genes with decreased than increased expression levels. This is consistent with the hypothesis that Trx2 functions as a transcriptional activator. Comparison of gene expression profiles for constitutive and conditional trx2 mutant cells enabled a distinction between direct and indirect target genes for Trx2. As a result Magoh2 was identified as the key candidate target gene for Trx2. Interaction between Trx2 and Magoh2 suggested a potential regulatory role for Trx2 in alternative splicing. Furthermore this work provided evidence that Trx2 could be involved in the maintenance of CpG island promoter gene expression, thus providing a potent regulatory mechanism for ubiquitously expressed genes.
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Grinat, Johanna. "The epigenetic regulator Mll1 is required for Wnt-driven intestinal tumorigenesis and cancer stemness." Doctoral thesis, Humboldt-Universität zu Berlin, 2020. http://dx.doi.org/10.18452/22192.

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Genetisch bedingte Veränderungen im Wnt-Signalweg sind in der Tumorigenese des Darms von zentraler Bedeutung. Mutationen des Wnt-Effektormoleküls β-Catenin in den adulten Stammzellen des Darmepithels führen zu unkontrollierter Proliferation und Expansion der Darmstammzellen und initiieren die Tumorentstehung. Auch in fortgeschrittenen Darmtumoren unterstützt die Wnt-Signalgebung maßgeblich das Tumorwachstum und den Erhalt von Tumorstammzellen. Nach erfolgreicher chemotherapeutischer Behandlung treten oftmals Tumorrezidive auf, für deren Entstehung therapieresistente Tumorstammzellen verantwortlich gemacht werden. Trotz intensiver Forschung fehlen in der Darmkrebstherapie nach wie vor Behandlungsansätze zur gezielten Therapie der Tumorstammzellen. Ziel dieser Dissertation ist es, unser Verständnis der molekularen Regulationsmechanismen in Kolonkarzinomen zu erweitern und die Entwicklung rationaler Behandlungsstrategien zu fördern. Ich konnte die Histonmethyltransferase Mll1 als entscheidenden Faktor in der epigenetischen Regulation humaner und muriner Darmkrebsstammzellen und -tumore identifizieren. Humane Kolonkarzinome weisen eine erhöhte Mll1-Expression auf, die mit dem Level an nukleärem β-Catenin korreliert. Im adulten Darmepithel ist Mll1 insbesondere in den Lgr5+ Stammzellen exprimiert und maßgeblich an der Wnt/β-Catenin-induzierten Stammzellexpansion sowie der Tumorentstehung beteiligt. Der konditionelle Verlust von Mll1 im murinen Darmkrebsmodell verhindert die β-Catenin-induzierte Tumorigenese. Mll1 unterstützt die Selbsterneuerungsfähigkeit und Proliferation der Tumorstammzellen, indem es die Expression von essentiellen Stammzellgenen wie dem Wnt-abhängigen Stammzellmarker Lgr5 aufrechterhält. Eine Inhibition der Mll1-Funktion in der Darmkrebstherapie kann eine gezielte Eliminierung der Tumorstammzellen ermöglichen, wodurch das fortschreitende Tumorwachstum unterbunden und die Bildung von Rezidiven verhindert werden kann.
Genetic mutations inducing aberrant activity of Wnt signalling are causative for intestinal tumorigenesis. Mutations of the Wnt effector molecule β-catenin in adult stem cells of the intestinal epithelium drive uncontrolled proliferation, expand the stem cell pool and initiate tumor formation. In advanced tumors, aberrant Wnt signalling promotes tumor growth and maintains cancer stem cells. The cancer stem cells are highly resistant to conventional chemotherapy and frequently initiate tumor relapse after completion of treatment. Despite extensive research, we are still lacking efficient therapies for colon cancer that specifically eliminate the cancer stem cells. This dissertation aims to expand our knowledge on molecular gene regulatory mechanisms in colon cancer cells to promote the identification and future development of rational therapies for colon cancer patients. I identified the histone methyltransferase Mll1 as an epigenetic regulator in human and mouse intestinal cancer stem cells and tumors. Human colon carcinomas with nuclear β-catenin exhibit high levels of Mll1. In the adult intestinal epithelium of mice, Mll1 is highly expressed in the Lgr5+ stem cells and is a prerequisite for the oncogenic Wnt/β-catenin-mediated stem cell expansion and tumorigenesis. Conditional knockout of Mll1 in an intestinal mouse tumor model prevents the β-catenin-driven intestinal tumorigenesis. Knockdown of Mll1 impairs the self-renewal and proliferation of colon cancer sphere cultures and halts tumor growth in xenografts. Mechanistically, Mll1 sustains the expression of intestinal stem cell genes including the Wnt/β-catenin target gene Lgr5 by antagonizing gene silencing through polycomb repressive complex 2-mediated H3K27 tri-methylation. Interfering with Mll1 function can efficiently eliminate colon cancer stem cells, and has potential as a rational therapy for colon cancer.
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Punnia-Moorthy, Gayathiri. "Defining the functional roles of X-linked epigenetic regulator lysine demethylase 6A (KDM6A) in Melanoma." Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/28897.

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Melanoma is an aggressive form of skin cancer and Australia has one of highest incidences of melanoma in the world. Current treatments for metastatic melanoma are plagued by the resistance melanomas develop against immunotherapies and targeted therapies. Lysine demethylases (KDMs) are epigenetic enzymes that remove methyl groups from the amino acid lysine (K) on histone proteins, which effects gene expression. One of these KDMs is KDM6A (an X-linked gene also known as UTX) that removes methyl groups from histone 3, lysine number 27 (H3K27me3) inducing activation of gene expression. KDM6A has been reported to play roles in the progression of multiple cancers, however the role of KDM6A in melanoma is yet to be investigated. In this study, the effects of KDM6A expression on clinical parameters, including survival, and gene expression patterns were investigated in a cohort of 458 melanoma patients obtained from The Cancer Genome Atlas (TCGA). In addition, the effects of a KDM6 inhibitor GSK-J4 and KDM6A knockout using the CRISPR-Cas9 system in melanoma cells was investigated in vitro using a variety of molecular and cell biology assays. RNA sequencing was used to determine which genes and pathways were significantly upregulated and downregulated in drug treated and KDM6A knockout melanoma cells. Results showed that high KDM6A expression significantly correlated with gender in melanoma patients KDM6A expression was associated with better overall survival in melanoma patients, particularly in females but not in males. High KDM6A expression was associated with upregulation of interferon pathways and downregulation of pro-survival pathways which may prevent melanoma growth. High KDM6A expression was also associated with multiple immune cell infiltration in melanoma patient tumours, especially in females. In addition, KDM6A expression significantly correlated with COMPASS components, an important epigenetic complex in which KDM6A is an essential enzymatic component. In vitro studies showed that KDM6A knockout in melanoma cells significantly increased proliferation and colony formation, hence promoting melanoma cell growth and supporting the role of KDM6A in tumour suppressive function. RNA-seq analysis in KDM6A depleted cells showed significant upregulation of oncogenic pathways and downregulation of tumour suppressive pathways. Surprisingly, GSK-J4 treatment in melanoma cells showed the opposite effect to KDM6A knockdown with increased apoptosis and decreased viability, colony formation and 3D spheroid formation, but had no effect on cell cycle regardless of basal KDM6A expression. In addition, GSK-J4 also targeted other histone markers which include H3K4me3. RNA-seq analysis in drug treated melanoma cells showed a significant upregulation of pathways involved in DNA regulation and significant downregulation of cell metabolic pathways. These results suggest that KDM6A appears to have a protective effect in melanoma patients, especially in females, indicating a potential tumour suppressive role.
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Grinat, Johanna [Verfasser]. "The epigenetic regulator Mll1 is required for Wnt-driven intestinal tumorigenesis and cancer stemness / Johanna Grinat." Berlin : Humboldt-Universität zu Berlin, 2020. http://d-nb.info/1223452255/34.

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Trippel, Franziska Katharina [Verfasser], and Roland [Akademischer Betreuer] Kappler. "The role of NFE2L2 mutations and the epigenetic regulator UHRF1 in hepatoblastoma / Franziska Katharina Trippel. Betreuer: Roland Kappler." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1096162644/34.

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Elangovan, Venkateswaran Ramamoorthi, Sara M. Camp, Gabriel T. Kelly, Ankit A. Desai, Djanybek Adyshev, Xiaoguang Sun, Stephen M. Black, Ting Wang, and Joe G. N. Garcia. "Endotoxin- and Mechanical Stress–Induced Epigenetic Changes in the Regulation of the Nicotinamide Phosphoribosyltransferase Promoter." UNIV CHICAGO PRESS, 2016. http://hdl.handle.net/10150/622492.

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Mechanical ventilation, a lifesaving intervention for patients with acute respiratory distress syndrome (ARDS), also unfortunately contributes to excessive mechanical stress and impaired lung physiological and structural integrity. We have elsewhere established the pivotal role of increased nicotinamide phosphoribosyltransferase (NAMPT) transcription and secretion as well as its direct binding to the toll-like receptor 4 (TLR4) in the progression of this devastating syndrome; however, regulation of this critical gene in ventilator-induced lung injury (VILI) is not well characterized. On the basis of an emerging role for epigenetics in enrichment of VILI and CpG sites within the NAMPT promoter and 5'UTR, we hypothesized that NAMPT expression and downstream transcriptional events are influenced by epigenetic mechanisms. Concomitantly, excessive mechanical stress of human pulmonary artery endothelial cells or lipopolysaccharide (LPS) treatment led to both reduced DNA methylation levels in the NAMPT promoter and increased gene transcription. Histone deacetylase inhibition by trichostatin A or Sirt-1-silencing RNA attenuates LPS-induced NAMPT expression. Furthermore, recombinant NAMPT administration induced TLR4-dependent global H3K9 hypoacetylation. These studies suggest a complex epigenetic regulatory network of NAMPT in VILI and ARDS and open novel strategies for combating VILI and ARDS.
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Books on the topic "Epigenetic regulator"

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Epigenetic regulation of lymphocyte development. Heidelberg: Springer, 2011.

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Jörg, Tost, ed. Epigenetics. Norfolk, UK: Caister Academic Press, 2008.

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Jörg, Tost, ed. Epigenetics. Norfolk, UK: Caister Academic Press, 2008.

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David, Allis C., Jenuwein Thomas, and Reinberg Danny, eds. Epigenetics. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2007.

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Murre, Cornelis, ed. Epigenetic Regulation of Lymphocyte Development. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-24103-1.

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Najafova, Zeynab. Epigenetic regulation of osteoblast differentiation. Göttingen: Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2017.

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A, Russo V. E., Martienssen Robert A, and Riggs Arthur D, eds. Epigenetic mechanisms of gene regulation. Plainview, N.Y: Cold Spring Harbor Laboratory Press, 1996.

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Derek, Chadwick, and Cardew Gail, eds. Epigenetics. Chichester: Wiley, 1998.

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Chan, Yvonne. Epigenetic regulation of enos gene expression. Ottawa: National Library of Canada, 1998.

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Ph, Jeanteur, ed. Epigenetics and chromatin. Berlin: Springer, 2005.

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Book chapters on the topic "Epigenetic regulator"

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Kumar, Sanjay, James A. Stokes, Udai P. Singh, Kumar S. Bishnupuri, and Manoj K. Mishra. "Enhancer of Zeste Homology 2 (Ezh2), an Epigenetic Regulator: A Possibility for Prostate Cancer Treatment." In Epigenetic Advancements in Cancer, 229–44. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-24951-3_10.

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Ganai, Shabir Ahmad. "Epigenetic Regulator Enzymes and Their Implications in Distinct Malignancies." In Histone Deacetylase Inhibitors in Combinatorial Anticancer Therapy, 35–65. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-8179-3_2.

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Raghu, Sukanya, Arathi Bangalore Prabhashankar, Bhoomika Shivanaiah, Ekta Tripathi, and Nagalingam Ravi Sundaresan. "Sirtuin 6 Is a Critical Epigenetic Regulator of Cancer." In Subcellular Biochemistry, 337–60. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-07634-3_10.

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Jog, Ruta, Guohua Chen, Todd Leff, and Jian Wang. "Threonine Catabolism: An Unexpected Epigenetic Regulator of Mouse Embryonic Stem Cells." In Handbook of Nutrition, Diet, and Epigenetics, 1585–604. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-55530-0_103.

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Jog, Ruta, Guohua Chen, Todd Leff, and Jian Wang. "Threonine Catabolism: an Unexpected Epigenetic Regulator of Mouse Embryonic Stem Cells." In Handbook of Nutrition, Diet, and Epigenetics, 1–20. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-31143-2_103-1.

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Paro, Renato, Ueli Grossniklaus, Raffaella Santoro, and Anton Wutz. "Epigenetics and Cancer." In Introduction to Epigenetics, 151–77. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68670-3_8.

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AbstractAlterations in chromatin function and epigenetic mechanisms are a hallmark of cancer. The disruption of epigenetic processes has been linked to altered gene expression and to cancer initiation and progression. Recent cancer genome sequencing projects revealed that numerous epigenetic regulators are frequently mutated in various cancers. This information has not only started to be utilized as prognostic and predictive markers to guide treatment decisions but also provided important information for the understanding of the molecular mechanisms of epigenetic regulation in both physiological and pathological conditions. Furthermore, the reversible nature of epigenetic aberrations has led to the emergence of the promising field of epigenetic therapy that has already provided new therapeutic options for patients with malignancies characterized by epigenetic alterations, laying the basis for new and personalized medicine.
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Skillman, Kristen M., and Manoj T. Duraisingh. "Epigenetic Regulation." In Encyclopedia of Malaria, 1–12. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8757-9_41-1.

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Huang, Yufei. "Epigenetic Regulation." In Encyclopedia of Systems Biology, 665. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_817.

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Minarovits, Janos, Ferenc Banati, Kalman Szenthe, and Hans Helmut Niller. "Epigenetic Regulation." In Patho-Epigenetics of Infectious Disease, 1–25. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-24738-0_1.

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Sato, Shinya, and Yasushi Miyazaki. "Epigenetic Regulator, Re-emerging Antimetabolites with Novel Mechanism of Action (Azacitidine and Decitabine): Clinical Pharmacology and Therapeutic Results." In Chemotherapy for Leukemia, 327–40. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3332-2_19.

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Conference papers on the topic "Epigenetic regulator"

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Gunnell, Andrea, Jessica Downs, Lewis Pennicott, Kay Osborn, Darren Le Grand, Katie Duffell, Hitesh Patel, Jessica Hudson, Jessica R. Booth, and Simon Ward. "Abstract 2907: Targeting the epigenetic regulator KAT2a in cancer." 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.am2018-2907.

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Shields, Cara E., Selma M. Cuya, Sarah K. Chappell, Komal Rathi, Shiv Patel, Sindhu Potlapalli, and Robert W. Schnepp. "Abstract 3838: Targeting epigenetic regulator BMI-1 in alveolar rhabdomyosarcoma." 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.am2019-3838.

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Shields, Cara E., Selma M. Cuya, Sarah K. Chappell, Komal Rathi, Shiv Patel, Sindhu Potlapalli, and Robert W. Schnepp. "Abstract 3838: Targeting epigenetic regulator BMI-1 in alveolar rhabdomyosarcoma." 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.sabcs18-3838.

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Brennan, Donal J., Kirsha Naicker, Sudipto Das, Bruce Moran, Rut Klinger, Fredrik Ponten, Stephen Hewitt, et al. "Abstract 5033: The role of the epigenetic regulator SATB2 in colon cancer progression." 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.sabcs18-5033.

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Brennan, Donal J., Kirsha Naicker, Sudipto Das, Bruce Moran, Rut Klinger, Fredrik Ponten, Stephen Hewitt, et al. "Abstract 5033: The role of the epigenetic regulator SATB2 in colon cancer progression." 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.am2019-5033.

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Mills, Alea A., and Dong-Woo Hwang. "Abstract 2959: The tumor suppressor CHD5 is an epigenetic regulator of neuronal cell fate." 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.am2014-2959.

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Bagheri-Yarmand, Rozita, Sharmistha Lahiri, Xinhai Wan, Nora Navone, Christopher J. Logothetis, Robert F. Gagel, and Krishna M. Sinha. "Abstract 2272: A novel epigenetic regulator histone demethylase NO66 promotes prostate cancer bone metastasis." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2272.

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Faria, Gustavo Hugo de Souza. "The impact of epigenetics on the development of neurodegenerative diseases." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.654.

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Introduction: Neurodegenerative diseases affect thousands of people in Brazil and have been increasing in frequency with the aging population. However, little is known about the molecular mechanisms and biomarkers of these diseases, which leads to a medical approach based on symptomatic and unresolving characteristics. Epigenetics, including DNA methylation, histone modifications, and changes in regulatory RNAs, emerges as a tool for prevention of neurodegenerative diseases. Objectives: To review studies that discuss the role of epigenetics in the development of neurodegenerative diseases. Methodology: This study involved an integrative review of papers published from 2016 to 2021 by searching PubMed and Scopus. Results: The studies showed that there is evidence that epigenetic mechanisms interfere with the development of major neurodegenerative diseases. Huntington’s disease presents an altered gene from birth, but transcriptional dysregulation is characteristic of the pathology that may be correlated to the age of disease onset in the cortex. In Parkinson’s disease dysregulation of expression of a specific protein is believed to play a central role in the disease and occurs through aberrant methylation that controls activation or suppression. In relation to Alzheimer’s disease, it has been found that deregulated DNA methylation and demethylation is linked to the onset and progression of the disease. In addition, these epigenetic factors are interfered with by diet, aging, and exercise. Conclusions: Investment in epigenetic studies is needed to understand possible markers of neurodegenerative diseases, for early diagnosis and the formation of epidrugs with the ability to treat.
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Tu, Yaping, Dennis W. Wolff, Zoran Gatalica, Yan Xie, and Peter W. Abel. "Abstract 1710: Epigenetic repression of regulator of G-protein signaling 2 promotes prostate cancer progression." 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.am10-1710.

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Kang, Sun Kyoung, Tae Soo Kim, Woo Sun Kwon, Jae Kyung Roh, Ho-Yeong Lim, Hyun Cheol Chun, and Sun Young Rha. "Abstract 5069: Inhibition of BET bromodomain, epigenetic regulator, as an effective therapeutic approach for gastric cancer." 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.am2017-5069.

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Reports on the topic "Epigenetic regulator"

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Isaacs, Jennifer S. Extracellular Hsp90 as a Novel Epigenetic Regulator of EMT and Metastatic Risk in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada603247.

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Seale, Maria, R. Salter, Natàlia Garcia-Reyero,, and Alicia Ruvinsky. A fuzzy epigenetic model for representing degradation in engineered systems. Engineer Research and Development Center (U.S.), September 2022. http://dx.doi.org/10.21079/11681/45582.

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Degradation processes are implicated in a large number of system failures, and are crucial to understanding issues related to reliability and safety. Systems typically degrade in response to stressors, such as physical or chemical environmental conditions, which can vary widely for identical units that are deployed in different places or for different uses. This situational variance makes it difficult to develop accurate physics-based or data-driven models to assess and predict the system health status of individual components. To address this issue, we propose a fuzzy set model for representing degradation in engineered systems that is based on a bioinspired concept from the field of epigenetics. Epigenetics is concerned with the regulation of gene expression resulting from environmental or other factors, such as toxicants or diet. One of the most studied epigenetic processes is methylation, which involves the attachment of methyl groups to genomic regulatory regions. Methylation of specific genes has been implicated in numerous chronic diseases, so provides an excellent analog to system degradation. We present a fuzzy set model for characterizing system degradation as a methylation process based on a set-theoretic representation for epigenetic modeling of engineered systems. This model allows us to capture the individual dynamic relationships among a system, environmental factors, and state of health.
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Shrikant, Protul A. Epigenetic Regulation of Ovarian Tumor Immunity. Fort Belvoir, VA: Defense Technical Information Center, November 2010. http://dx.doi.org/10.21236/ada586321.

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Shrikant, Protul A. Epigenetic Regulation of Ovarian Tumor Immunity. Fort Belvoir, VA: Defense Technical Information Center, November 2009. http://dx.doi.org/10.21236/ada589210.

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Ecker, Joseph Robert. Epigenetic Regulation of Hormone-dependent Plant Growth Processes. Office of Scientific and Technical Information (OSTI), November 2016. http://dx.doi.org/10.2172/1332760.

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Shurin, Michael R. Epigenetic Regulation of Chemokine Expression in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2006. http://dx.doi.org/10.21236/ada460756.

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Pawlowski, Wojtek P., and Avraham A. Levy. What shapes the crossover landscape in maize and wheat and how can we modify it. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600025.bard.

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Meiotic recombination is a process in which homologous chromosomes engage in the exchange of DNA segments, creating gametes with new genetic makeup and progeny with new traits. The genetic diversity generated in this way is the main engine of crop improvement in sexually reproducing plants. Understanding regulation of this process, particularly the regulation of the rate and location of recombination events, and devising ways of modifying them, was the major motivation of this project. The project was carried out in maize and wheat, two leading crops, in which any advance in the breeder’s toolbox can have a huge impact on food production. Preliminary work done in the USA and Israeli labs had established a strong basis to address these questions. The USA lab pioneered the ability to map sites where recombination is initiated via the induction of double-strand breaks in chromosomal DNA. It has a long experience in cytological analysis of meiosis. The Israeli lab has expertise in high resolution mapping of crossover sites and has done pioneering work on the importance of epigenetic modifications for crossover distribution. It has identified genes that limit the rates of recombination. Our working hypothesis was that an integrative analysis of double-strand breaks, crossovers, and epigenetic data will increase our understanding of how meiotic recombination is regulated and will enhance our ability to manipulate it. The specific objectives of the project were: To analyze the connection between double-strand breaks, crossover, and epigenetic marks in maize and wheat. Protocols developed for double-strand breaks mapping in maize were applied to wheat. A detailed analysis of existing and new data in maize was conducted to map crossovers at high resolution and search for DNA sequence motifs underlying crossover hotspots. Epigenetic modifications along maize chromosomes were analyzed as well. Finally, a computational analysis tested various hypotheses on the importance of chromatin structure and specific epigenetic modifications in determining the locations of double-strand breaks and crossovers along chromosomes. Transient knockdowns of meiotic genes that suppress homologous recombination were carried out in wheat using Virus-Induced Gene Silencing. The target genes were orthologs of FANCM, DDM1, MET1, RECQ4, and XRCC2.
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Ince, Tan A. Epigenetic Regulation of Normal and Transformed Breast Epithelial Cell Phenotype. Fort Belvoir, VA: Defense Technical Information Center, June 2009. http://dx.doi.org/10.21236/ada514040.

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Millonig, James H. Epigenetic Regulation of the Autism Susceptibility Gene, ENGRAILED 2 (EN2). Fort Belvoir, VA: Defense Technical Information Center, July 2010. http://dx.doi.org/10.21236/ada552004.

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Zhang, Jisheng. Insight into Skin Tumorigenesis Highlighting the Function of Epigenetic Regulators in SCC Formation. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada599253.

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