subject:(DNMT)

1. Preethi, Devanand. Epigenetic regulation of BTG2/TIS21/PC3 and its tumor suppressive role in invasive human cancers.

Degree: 2018, Ajou University

URL: http://repository.ajou.ac.kr/handle/201003/16536 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000027461

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B cell translocation gene 2 (BTG2/TIS21/PC3) belongs to the family of antiproliferative (APRO) genes and reported as a tumor suppressor by our group and others.… (more)

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B cell translocation gene 2 (BTG2/TIS21/PC3) belongs to the family of antiproliferative (APRO) genes and reported as a tumor suppressor by our group and others. Expression of BTG2 is significantly reduced in cancers developed in various organs and tissues. EJ (bladder carcinoma cells), MKN-1 (gastric cancer cells) are highly invasive and metastatic cells with very less endogenous BTG2 expression due to epigenetic regulation. Significantly lower endogenous expression of BTG2 was observed in human muscle-invasive bladder cancers (MIBC) than matched normal tissues and non-muscle invasive bladder cancers (NMIBC). BTG2 expression was inversely correlated with increased expression of the DNA methyltransferases DNMT1 and DNMT3a in MIBC, but not NMIBC, suggesting a potential role for BTG2 expression in muscle invasion of bladder cancer. Over 90% of tumor tissues revealed strong methylation at CpG islands of the BTG2 gene, compared with no methylation in the normal tissues, implying epigenetic regulation of BTG2 expression in bladder carcinogenesis. BTG2 is constitutively expressed in mucous epithelium and parietal cells of gastric glands in stomach, and the expression was increased in mucous epithelium with H. pylori infection as opposed to loss in human gastric adenocarcinoma. Indeed, adenoviral transduction of BTG2 significantly inhibited Tipα activity in MKN-1 and MGT-40, human and mouse gastric cancer cells, respectively, thereby downregulated TNFα expression and Erk1/2 phosphorylation via reducing nucleolin, Tipα receptor, expression. Chromatin immunoprecipitation proved that BTG2 inhibited Sp1 expression and it’s binding to the promoter of nucleolin gene. In addition, BTG2 expression significantly reduced membrane localized nucleolin expression in cancer cells and the loss of BTG2/TIS21 expression rather induced cytoplasmic nucleolin availability in gastric cancer tissues, evidenced by immunoblot and immunohistochemistry. The higher expression of BTG2 and the lower nucleolin expression accompanied with the better overall survival of the poorly differentiated gastric cancer patients.

B cell translocation gene 2(BTG2/TIS21/PC3)는 antiproliferative gene(APRO) 계열에 속하며 본 연구팀을 포함한 많은 연구자들에 의해 BTG2 의 암억제 기능이 연구되어 왔다. BTG2 는 여러 조직과 기관에서 발생한 암에서 그 발현이 감소되어 있고, 특히 침윤(invasion)과 전이(metastasis)를 잘하는 암세포인 EJ (bladder carcinoma cells)와 MKN-1 (gastric cancer cells)에서도 후성유전학적(epigenetic regulation)으로 BTG2 발현이 매우 감소되어 있다. 최근 사람에서, 이런 침윤성과 전이성이 높은 암에서 BTG2 가 침윤을 억제하고 침윤을 조장하는 단백질과 mRNA 발현과는 음의 상관도를 보인다는 보고가 많기에, 본 저자는 BTG2 가 어떤 기전으로 침윤성 암을 조절하는지를 중점적으로 연구하였다. 사람의 근육침범 방광암(muscleinvasive bladder cancers, MIBC)에서 비-근육침범 방광암(non-muscle invasive bladder cancers, NMIBC)보다 BTG2 의 발현이 현저히 감소되어 있다는 것을 발견하였다. 이런 MIBC 에서의 BTG2 의 감소는 반대로 DNA 메틸기전달효소 DNMT1 과 DNMT3a 의 증가와 연관이 있었고, 이런 음의 상관관계는 NMIBC 에서는 발견되지 않음으로써 BTG2 이 방광암의 근육 침범에 분명한 역할을 하고 있다는 가능성을 보였다. 방광암 조직들의 90%에서 BTG2 유전자의 CpG 섬에 강한 메틸화를 보였고, 반대로 정상 방광조직에서는 메틸화가 발견되지 않음으로써, 방광암발생과정에서 BTG2 이 후성학적 조절을 받는다는 사실도 증명했다. 한편, BTG2 는 위 점막의 상피세포와 위샘의 벽세포(Parietal cell)에서 기본적으로 발현되고 있으며, 이 유전자의 발현은…

Advisors/Committee Members: 대학원 의생명과학과, 201024529, Preethi, Devanand.

Subjects/Keywords: BTG2; 침윤성 암; DNMT; H. pylori; TNFα

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APA (6^th Edition):

Preethi, D. (2018). Epigenetic regulation of BTG2/TIS21/PC3 and its tumor suppressive role in invasive human cancers. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/16536 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000027461

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Preethi, Devanand. “Epigenetic regulation of BTG2/TIS21/PC3 and its tumor suppressive role in invasive human cancers.” 2018. Thesis, Ajou University. Accessed January 16, 2021. http://repository.ajou.ac.kr/handle/201003/16536 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000027461.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Preethi, Devanand. “Epigenetic regulation of BTG2/TIS21/PC3 and its tumor suppressive role in invasive human cancers.” 2018. Web. 16 Jan 2021.

Vancouver:

Preethi D. Epigenetic regulation of BTG2/TIS21/PC3 and its tumor suppressive role in invasive human cancers. [Internet] [Thesis]. Ajou University; 2018. [cited 2021 Jan 16]. Available from: http://repository.ajou.ac.kr/handle/201003/16536 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000027461.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Preethi D. Epigenetic regulation of BTG2/TIS21/PC3 and its tumor suppressive role in invasive human cancers. [Thesis]. Ajou University; 2018. Available from: http://repository.ajou.ac.kr/handle/201003/16536 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000027461

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

2. Dahlet, Thomas. Méthylation de l'ADN : fonctions et ciblage au cours du développement chez la souris : DNA methylation : functions and recruitment during mouse development.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2019, Université de Strasbourg

URL: http://www.theses.fr/2019STRAJ075

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La méthylation des cytosines est une modification épigénétique catalysée par la famille des ADN méthyltransférases (DNMTs). C’est une marque répressive lorsqu’elle est adressée sur les… (more)

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La méthylation des cytosines est une modification épigénétique catalysée par la famille des ADN méthyltransférases (DNMTs). C’est une marque répressive lorsqu’elle est adressée sur les îlots CpG des promoteurs de gènes. Le développement embryonnaire murin est caractérisé par une reprogrammation de la méthylation de l’ADN qui est critique pour le développement de l’embryon. Cependant, la contribution des différentes DNMTs dans la méthylation du génome ainsi que les mécanismes qui ciblent la méthylation de l'ADN vers certains gènes durant le développement embryonnaires sont mal connus. En combinant des approches de cartographie génomique avec des lignées génétiquement modifiées de souris, mes travaux de Thèse ont permis de clarifier la contribution des différentes DNMTs dans la méthylation du génome dans l’embryon : DNMT3A et DNMT3B sont strictement impliqués dans la méthylation de novo, et DNMT1 est strictement impliqué dans son maintien au cours des divisions cellulaires. De plus, l’analyse d’embryons globalement déméthylés a révélé de nombreuses fonctions de la méthylation de l’ADN dans le maintien de l'intégrité transcriptomique de l'embryon en réprimant des gènes gamétiques, des gènes du développement, des promoteurs cryptiques ainsi qu’un large panel de transposons. Dans un deuxième temps, j’ai étudié le rôle du facteur de transcription E2F6 dans le ciblage de la méthylation de l'ADN in vivo chez la souris. Mes résultats démontrent que E2F6 facilite l’acquisition de la méthylation de l’ADN au niveau du promoteurs des gènes gamétiques et est nécessaire pour initier leur répression à long terme au cours de l'embryogenèse. Dans leur ensemble, ces travaux contribuent à mieux comprendre les fonctions et mécanismes de ciblage de la méthylation de l'ADN au cours de l'embryogenèse des mammifères.

Cytosine methylation is an epigenetic modification catalyzed by the family of DNA methyltransferases (DNMTs). This modification is involved in gene repression when it is addressed to CpG islands in gene promoters. Global DNA methylation reprogramming occurs in mice during the early phases of embryogenesis, which is critical for proper embryo development. However, the contribution of different DNMTs in genome methylation and the mechanisms that target DNA methylation to specific genes during embryonic development are poorly understood. By combining genomic mapping with genetically modified mouse lines, my Thesis work clarified the contribution of the different DNMTs in genome methylation in the embryo: DNMT3A and DNMT3B are strictly involved in de novo methylation, and DNMT1 is strictly involved in the maintenance of DNA methylation during cellular divisions. In addition, the analysis of globally demethylated embryos revealed numerous functions of DNA methylation in maintaining the transcriptomic intergrity of the embryo by repressing germline genes, developmental genes, cryptic promoters as well as a large panel of transposons.  In the second part of my…

Advisors/Committee Members: Weber, Michaël (thesis director).

Subjects/Keywords: Épigénitique; Développement; DNMT; Méthylation de l’ADN; Epigenetics; Development; DNMT; DNA methylation; 572.8

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dahlet, T. (2019). Méthylation de l'ADN : fonctions et ciblage au cours du développement chez la souris : DNA methylation : functions and recruitment during mouse development. (Doctoral Dissertation). Université de Strasbourg. Retrieved from http://www.theses.fr/2019STRAJ075

Chicago Manual of Style (16^th Edition):

Dahlet, Thomas. “Méthylation de l'ADN : fonctions et ciblage au cours du développement chez la souris : DNA methylation : functions and recruitment during mouse development.” 2019. Doctoral Dissertation, Université de Strasbourg. Accessed January 16, 2021. http://www.theses.fr/2019STRAJ075.

MLA Handbook (7^th Edition):

Dahlet, Thomas. “Méthylation de l'ADN : fonctions et ciblage au cours du développement chez la souris : DNA methylation : functions and recruitment during mouse development.” 2019. Web. 16 Jan 2021.

Vancouver:

Dahlet T. Méthylation de l'ADN : fonctions et ciblage au cours du développement chez la souris : DNA methylation : functions and recruitment during mouse development. [Internet] [Doctoral dissertation]. Université de Strasbourg; 2019. [cited 2021 Jan 16]. Available from: http://www.theses.fr/2019STRAJ075.

Council of Science Editors:

Dahlet T. Méthylation de l'ADN : fonctions et ciblage au cours du développement chez la souris : DNA methylation : functions and recruitment during mouse development. [Doctoral Dissertation]. Université de Strasbourg; 2019. Available from: http://www.theses.fr/2019STRAJ075

3. Menon, Yoann. Etude des effets pharmacologiques d'inhibiteurs non nucléosidiques de la méthylation de l'ADN : Study of the pharmacological effects of non-nucleoside inhibitors of DNA methylation.

Degree: Docteur es, Pharmacologie, 2016, Université Toulouse III – Paul Sabatier

URL: http://www.theses.fr/2016TOU30004

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Les modifications épigénétiques participent au contrôle de l'expression génique. Il a été montré que la méthylation des désoxycytidines (dC) de l'ADN joue un rôle clé… (more)

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Les modifications épigénétiques participent au contrôle de l'expression génique. Il a été montré que la méthylation des désoxycytidines (dC) de l'ADN joue un rôle clé dans la régulation épigénétique chez les mammifères. Cette modification correspond à la marque épigénétique la plus stable. Elle a lieu sur des résidus CpG regroupés en ilôts, essentiellement situés au niveau des séquences promotrices, des séquences répétées et des séquences encadrants les ilôtsCpG. L'hyperméthylation des promoteurs induit une inhibition de l'expression des gènes, tandis qu'une hypométhylation est associée à une expression. Les enzymes responsables de la méthylation de l'ADN sont les méthyltransférases d'ADN (DNMTs). Deux familles de DNMTscatalytiquement actives ont été identifiées: on distingue la DNMT1, principalement responsable de la maintenance de la méthylation de l'ADN lors de la réplication, et les DNMT3A et 3B, qui sont responsables d'une méthylation de l'ADN dite de novo. L'altération des profils de méthylation de l'ADN conduit à diverses maladies telles que le cancer. Les cellules cancéreuses présentent souvent un profil de méthylation de l'ADN différent des cellules saines, on observe en particulier une hyperméthylation spécifique des gènes dits suppresseurs de tumeur. Une restauration de leur expression par l'inhibition de la méthylation de l'ADN représente ainsi une stratégie thérapeutique attrayante. Plusieurs inhibiteurs de DNMTs ont été décrits et deux analogues de nucléosides sont approuvés par la FDA pour traiter certaines leucémies: la 5-azacytidine (VidazaTM) et la 5-azadeoxycytidine (Dacogene(r)). Notre laboratoire développe depuis plusieurs années de nouveaux inhibiteurs non nucléosidiques de DNMTs qui ciblent leur site catalytique. J'ai étudié ici les effets pharmacologiques de ces inhibiteurs catalytiques des DNMTs, en utilisant plusieurs lignées cellulaires cancéreuses (issues d'une leucémie, d'un lymphome et d'un cancer du côlon). J'ai utilisé pour cela différentes technologies permettant d'analyser la méthylation de l'ADN, l'accessibilité de la chromatine, les modifications des histones et l'expression des gènes. Ces nouvelles thérapies épigénétiques visent à la reprogrammation des cellules cancéreuses, c'est pourquoi j'ai exploré les modifications à long terme induites par ces nouveaux composés. Nous avons montré que ces composés sont des inhibiteurs puissants de DNMT3A et qu'ils sont capables d'induire l'expression d'un gène raporteur (la luciférase) sous le contrôle du promoteur CMV, par une déméthylation de ce promoteur et une ouverture de la chromatine. Enfin, ces nouveaux inhibiteurs de DNMTs déméthylent la région promotrice de gènes suppresseurs de tumeurs et induisent leur ré-expression.

Epigenetic modifications participate to the control of gene expression. Methylation of deoxycytidines (dC) in the DNA was shown to play a key role in epigenetic regulation in mammals. It is the most stable epigenetic mark and occurs at CpG sites, which are grouped in islands and essentially located in promoters,…

Advisors/Committee Members: Arimondo, Paola Barbara (thesis director).

Subjects/Keywords: Epigénétique; Méthylation de l'ADN; Inhibiteurs de DNMT; Flavanones; Epigenetic; DNA methylation; DNMT inhibitors; Flavanones

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Menon, Y. (2016). Etude des effets pharmacologiques d'inhibiteurs non nucléosidiques de la méthylation de l'ADN : Study of the pharmacological effects of non-nucleoside inhibitors of DNA methylation. (Doctoral Dissertation). Université Toulouse III – Paul Sabatier. Retrieved from http://www.theses.fr/2016TOU30004

Chicago Manual of Style (16^th Edition):

Menon, Yoann. “Etude des effets pharmacologiques d'inhibiteurs non nucléosidiques de la méthylation de l'ADN : Study of the pharmacological effects of non-nucleoside inhibitors of DNA methylation.” 2016. Doctoral Dissertation, Université Toulouse III – Paul Sabatier. Accessed January 16, 2021. http://www.theses.fr/2016TOU30004.

MLA Handbook (7^th Edition):

Menon, Yoann. “Etude des effets pharmacologiques d'inhibiteurs non nucléosidiques de la méthylation de l'ADN : Study of the pharmacological effects of non-nucleoside inhibitors of DNA methylation.” 2016. Web. 16 Jan 2021.

Vancouver:

Menon Y. Etude des effets pharmacologiques d'inhibiteurs non nucléosidiques de la méthylation de l'ADN : Study of the pharmacological effects of non-nucleoside inhibitors of DNA methylation. [Internet] [Doctoral dissertation]. Université Toulouse III – Paul Sabatier; 2016. [cited 2021 Jan 16]. Available from: http://www.theses.fr/2016TOU30004.

Council of Science Editors:

Menon Y. Etude des effets pharmacologiques d'inhibiteurs non nucléosidiques de la méthylation de l'ADN : Study of the pharmacological effects of non-nucleoside inhibitors of DNA methylation. [Doctoral Dissertation]. Université Toulouse III – Paul Sabatier; 2016. Available from: http://www.theses.fr/2016TOU30004

New Jersey Institute of Technology

4. Rana, Jagruti. Synthetic approaches to the understanding of DNA nucleobase methylation.

Degree: PhD, Chemistry and Environmental Science, 2015, New Jersey Institute of Technology

URL: https://digitalcommons.njit.edu/dissertations/107

► DNA methylation is a major source of genetic variation and cancer. Methylation occurs when nucleophilic DNA bases react with methylating agent methyl methanesulfonate (MMS),… (more)

Subjects/Keywords: DNA methylation; Synthesis of 7Me-Deaza-deoxyguanosine; DNMT; DNMT inhibitors; Oligonucleotides; Polymerase bypass; Chemistry

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Rana, J. (2015). Synthetic approaches to the understanding of DNA nucleobase methylation. (Doctoral Dissertation). New Jersey Institute of Technology. Retrieved from https://digitalcommons.njit.edu/dissertations/107

Chicago Manual of Style (16^th Edition):

Rana, Jagruti. “Synthetic approaches to the understanding of DNA nucleobase methylation.” 2015. Doctoral Dissertation, New Jersey Institute of Technology. Accessed January 16, 2021. https://digitalcommons.njit.edu/dissertations/107.

MLA Handbook (7^th Edition):

Rana, Jagruti. “Synthetic approaches to the understanding of DNA nucleobase methylation.” 2015. Web. 16 Jan 2021.

Vancouver:

Rana J. Synthetic approaches to the understanding of DNA nucleobase methylation. [Internet] [Doctoral dissertation]. New Jersey Institute of Technology; 2015. [cited 2021 Jan 16]. Available from: https://digitalcommons.njit.edu/dissertations/107.

Council of Science Editors:

Rana J. Synthetic approaches to the understanding of DNA nucleobase methylation. [Doctoral Dissertation]. New Jersey Institute of Technology; 2015. Available from: https://digitalcommons.njit.edu/dissertations/107

5. Viziteu, Elena. RECQ1 Helicase Involvement in the Resistance to Replication Stress and Chemotherapy in Multiple Myeloma Myélome Multiple : Implication de l'hélicase RECQ1 dans la resistance au stress réplicatif et à la chimiothérapie dans le myélome multiple.

Degree: Docteur es, Biologie Santé, 2015, Montpellier

URL: http://www.theses.fr/2015MONTT008

► Le myélome multiple (MM) est une néoplasie B caractérisée par l’accumulation d’un clone plasmocytaire dans la moelle osseuse. Des études ont démontré que les modifications… (more)

▼ Le myélome multiple (MM) est une néoplasie B caractérisée par l’accumulation d’un clone plasmocytaire dans la moelle osseuse. Des études ont démontré que les modifications épigénétiques comme la méthylation de l’ADN jouent un rôle dans la régulation d’expression de différents gènes associés au cancer. Dans une étude récente, nous avons pu décrire un score génique de méthylation de l’ADN permettant de prédire la sensibilité des cellules de MM aux inhibiteurs de DNMT (DNA methyltranfexrase) (Moreaux, et al 2012). Parmi les gènes dont l’expression est inhibée par les inhibiteurs de DNMT et associés avec un pronostic péjoratif chez les patients atteints de MM, nous avons identifié RECQ1. RECQ1 est une hélicase de la famille RECQ qui s’associe aux origines de réplication durant la phase S du cycle cellulaire et joue un rôle important dans l’élongation des fourches de réplication. RECQ1 est fortement exprimé dans différents types de tumeurs solides et l’inhibition de RECQ1 conduit à la catastrophe mitotique et inhibe la croissance de tumeurs solides. Le but de notre projet a été de caractériser la fonction de RECQ1 dans la physiopathologie du MM et les mécanismes de résistance aux traitements. Afin d’étudier le rôle biologique de RECQ1 dans les plasmocytes tumoraux, nous avons utilisé des vecteurs lentiviraux pour induire de façon inductible la surexpression ou l'inhibition de RECQ1. La déplétion de RECQ1 dans les cellules de MM entraîne une inhibition de la croissance, une induction significative d’apoptose et la formation de foyers 53BP1 indiquant la présence de cassures d’ADN double brin. Une forte expression de RECQ1 étant associée à un mauvais pronostic et la déplétion de RECQ1 conduisant à une induction de cassures d’ADN double brin, nous nous sommes demandé si l’inhibition de l’expression de RECQ1 pourrait sensibiliser les cellules de MM aux agents génotoxiques utilisés dans le traitement du MM. La déplétion de RECQ1 sensibilise, de façon significative, les cellules de MM au melphalan suggérant que l’association d’un inhibiteur de DNMT pour cibler RECQ1 et du melphalan pourrait avoir un effet synergique chez les patients RECQ1++. La surexpression de RECQ1 protège les lignées cellulaires de myélome contra l'apoptose induite par melphalan et bortézomib. De plus, l'épuisement RECQ1 sensibilise les cellules de myélome de traitement est démontré que RECQ1 interagit avec des protéines impliquées dans différentes voies de réparation des dommages de l’ADN : PARP1 (NHEJ/BER), RAD51 (HR), MSH2 et MSH6 (Mismatch repair). RECQ1 interagit avec PARP1 dans la fraction chromatinienne des cellules de MM mais pas avec RAD51 ni MSH2. Cette interaction est significativement induite en présence de melphalan. Des inhibiteurs de PARP sont actuellement en développement préclinique ou en essai clinique. De façon intéressante, la déplétion de RECQ1 sensibilise significativement les cellules de MM à un inhibiteur de PARP in vitro suggérant que l’association d’un inhibiteur de DNMT pour cibler RECQ1 et d’un inhibiteur de PARP pourrait avoir un… Advisors/Committee Members: Moreaux, Jérôme (thesis director).

Subjects/Keywords: Myélome multiple; Dnmt; Hélicase RECQ1; Genes; Pronostic; Traitement; Multiple Myeloma; Dnmt; Recq1; Genes; Prognosis; Treatment

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Viziteu, E. (2015). RECQ1 Helicase Involvement in the Resistance to Replication Stress and Chemotherapy in Multiple Myeloma Myélome Multiple : Implication de l'hélicase RECQ1 dans la resistance au stress réplicatif et à la chimiothérapie dans le myélome multiple. (Doctoral Dissertation). Montpellier. Retrieved from http://www.theses.fr/2015MONTT008

Chicago Manual of Style (16^th Edition):

Viziteu, Elena. “RECQ1 Helicase Involvement in the Resistance to Replication Stress and Chemotherapy in Multiple Myeloma Myélome Multiple : Implication de l'hélicase RECQ1 dans la resistance au stress réplicatif et à la chimiothérapie dans le myélome multiple.” 2015. Doctoral Dissertation, Montpellier. Accessed January 16, 2021. http://www.theses.fr/2015MONTT008.

MLA Handbook (7^th Edition):

Viziteu, Elena. “RECQ1 Helicase Involvement in the Resistance to Replication Stress and Chemotherapy in Multiple Myeloma Myélome Multiple : Implication de l'hélicase RECQ1 dans la resistance au stress réplicatif et à la chimiothérapie dans le myélome multiple.” 2015. Web. 16 Jan 2021.

Vancouver:

Viziteu E. RECQ1 Helicase Involvement in the Resistance to Replication Stress and Chemotherapy in Multiple Myeloma Myélome Multiple : Implication de l'hélicase RECQ1 dans la resistance au stress réplicatif et à la chimiothérapie dans le myélome multiple. [Internet] [Doctoral dissertation]. Montpellier; 2015. [cited 2021 Jan 16]. Available from: http://www.theses.fr/2015MONTT008.

Council of Science Editors:

Viziteu E. RECQ1 Helicase Involvement in the Resistance to Replication Stress and Chemotherapy in Multiple Myeloma Myélome Multiple : Implication de l'hélicase RECQ1 dans la resistance au stress réplicatif et à la chimiothérapie dans le myélome multiple. [Doctoral Dissertation]. Montpellier; 2015. Available from: http://www.theses.fr/2015MONTT008

6. Bagacean, Cristina. Epigenetics in leukemia : Epigénétique dans les leucémies.

Degree: Docteur es, Immunologie, 2018, Brest

URL: http://www.theses.fr/2018BRES0012

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Les dérivés de la cytosine sont d’importantes modifications épigénétiques dont le rôle dans l’évolution de la leucémie lymphoïde chronique (LLC) n’est pas totalement exploré. Dans… (more)

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Les dérivés de la cytosine sont d’importantes modifications épigénétiques dont le rôle dans l’évolution de la leucémie lymphoïde chronique (LLC) n’est pas totalement exploré. Dans ce contexte, notre première étude vise à examiner le niveau global de la 5-methylcytosine (5-mCyt), 5-hydroxymethylcytosine (5-hmCyt), 5-carboxylcytosine (5-CaCyt) et 5-hydroxymethyluridine (5-hmU) dans des lymphocytes B purifiés de patients LLC (n=56) et d’individus sains (n=17). Les principaux acteurs de la régulation épigénétique (DNMT1/3A/3B, MBD2/4, TET1/2/3, SAT1) ont été évalués par PCR quantitative en temps réel. L’analyse a permis de mettre en exergue trois groupes de patients. En premier lieu, un groupe de patients stables (délai médian de progression [PFS] et délai au premier traitement [TFT] >120 mois), avec un profil épigénétique similaire au groupe contrôle. Deuxièmement, un groupe intermédiaire (PFS=84; TFT=120 mois) qui présente une augmentation de la déméthylation de l’ADN expliquée par l'induction SAT1 / TET2 pendant la progression de la maladie. Troisièmement, un groupe de patients avec une forme active de la maladie (PFS=52; TFT=112 mois) qui présentent une hyperlymphocytose, une réduction du temps de doublement des lymphocytes et des modifications épigénétiques majeures. Au sein de ce groupe, une réduction est observée pour la 5-mCyt, 5-hmCyt, 5-CaCyt et serait associée à une diminution des DNMTs, TETs et MBDs au cours de la progression de la maladie. Les profils épigénétiques mis en évidence sont indépendants du statut mutationnel IGHV mais sont associés avec les anomalies cytogénétiques. Nous nous sommes également intéressés à cette association et nous avons montré dans la deuxième étude que les modifications des dérivées de la cytosine peuvent affiner le pouvoir pronostic des anomalies cytogénétiques. En conclusion, nos résultats suggèrent que les variations de la méthylation ainsi que des intermédiaires de la déméthylation de l’ADN sont impliqués dans la progression de la LLC.

Cytosine derivatives are important epigenetic modifications whose role in the pathogenesis and evolution of chronic lymphocytic leukemia (CLL) is not fully explored. In this context, our first study aims to examine the global DNA level of 5-methylcytosine (5-mCyt), 5-hydroxymethylcytosine (5-hmCyt), 5-carboxylcytosine (5-CaCyt) and 5-hydroxymethyluridine (5-hmU) in purified B lymphocytes of CLL patients (n = 56) and healthy individuals (n = 17). The main actors in epigenetic regulation (DNMT1 / 3A / 3B, MBD2 / 4, TET1 / 2/3, SAT1) were evaluated by quantitative real time PCR. The analysis highlighted three groups of patients. First, a group of patients with stable disease (median time to progression [PFS] and time to first treatment [TFT]> 120 months), with an epigenetic profile similar to the control group. Secondly, an intermediate group (PFS = 84, TFT = 120 months) which shows an increase in DNA demethylation explained by SAT1 / TET2 induction during disease progression. Third, a group of patients with an active form of the disease (PFS…

Advisors/Committee Members: Renaudineau, Yves (thesis director), Cristea, Victor (thesis director).

Subjects/Keywords: Leucémie lymphoïde chronique; Méthylation de l'ADN; Hydroxyméthylation de l'ADN; TET; DNMT; Chronic lymphocytic leukemia; DNA methylation; DNA hydroxymethylation; TET; DNMT

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Bagacean, C. (2018). Epigenetics in leukemia : Epigénétique dans les leucémies. (Doctoral Dissertation). Brest. Retrieved from http://www.theses.fr/2018BRES0012

Chicago Manual of Style (16^th Edition):

Bagacean, Cristina. “Epigenetics in leukemia : Epigénétique dans les leucémies.” 2018. Doctoral Dissertation, Brest. Accessed January 16, 2021. http://www.theses.fr/2018BRES0012.

MLA Handbook (7^th Edition):

Bagacean, Cristina. “Epigenetics in leukemia : Epigénétique dans les leucémies.” 2018. Web. 16 Jan 2021.

Vancouver:

Bagacean C. Epigenetics in leukemia : Epigénétique dans les leucémies. [Internet] [Doctoral dissertation]. Brest; 2018. [cited 2021 Jan 16]. Available from: http://www.theses.fr/2018BRES0012.

Council of Science Editors:

Bagacean C. Epigenetics in leukemia : Epigénétique dans les leucémies. [Doctoral Dissertation]. Brest; 2018. Available from: http://www.theses.fr/2018BRES0012

7. Sabou, Alina Marcela. Identification d'une protéine parasitaire interagissant avec le facteur de transcription UHRF1 dans les cellules infectées par Toxoplasma gondii : Toxoplasma gondii ROP16 kinase silences the cyclin B1 gene promoter by hijacking host cell UHRF1-dependent epigenetic pathways.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2018, Université de Strasbourg

URL: http://www.theses.fr/2018STRAJ050

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La toxoplasmose, déterminée par le parasite Toxoplasma gondii, est l'une des infections les plus répandues au monde, en raison de la persistance à vie sous… (more)

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La toxoplasmose, déterminée par le parasite Toxoplasma gondii, est l'une des infections les plus répandues au monde, en raison de la persistance à vie sous forme latente de ce parasite au sein de ces hôtes. Ce parasite fait partie des Apicomplexa et détourne les voies de signalisation de l'hôte par des mécanismes épigénétiques qui convergent vers des protéines nucléaires clés. Nous rapportons ici une nouvelle stratégie de persistance parasitaire impliquant la protéine de rhoptries ROP16 de T. gondii, sécrétée précocement lors de l'invasion, qui cible le facteur de transcription UHRF1 (Ubiquitin-like containing PHD and RING fingers domain 1) et induit un arrêt du cycle de la cellule-hôte. Ceci est induit par l'activité de la DNMT et le remodelage de la chromatine au niveau du promoteur du gène de la cycline B1 par le recrutement d’UHRF1 phosphorylé associé à un complexe protéique multienzymatique répressif. Cela conduit à la désacétylation et à la méthylation de l'histone H3 entourant le promoteur de la cycline B1 pour réduire de manière épigénétique son activité transcriptionnelle. De plus, l'infection par T. gondii provoque une hyper-méthylation de l'ADN dans la cellule hôte par la régulation positive des DNMTs. ROP16 est déjà connue pour activer et phosphoryler des facteurs de transcription de l'immunité protectrice tels que STAT 3/6/5 et le suppresseur tumoral p53 impliqué dans la progression du cycle cellulaire. De plus, ROP16 module ces voies de signalisation de l'hôte de manière souche-dépendante. Comme dans le cas de STAT3, les effets de ROP16 sur UHRF1 dépendent du polymorphisme d'un seul acide aminé du domaine kinase de ROP16. Ce travail montre que Toxoplasma module un nouvel initiateur épigénétique, UHRF1, via un événement précoce initié par la kinase parasitaire ROP16.

Toxoplasmosis, caused by the apicomplexan parasite Toxoplasma gondii, is one of the most common infections in the world due to the lifelong persistence of this parasite in a latent stage in its hosts. T. gondii hijacks host signaling pathways through epigenetic mechanisms which converge on key nuclear proteins. Here we report a new parasite persistence strategy involving Toxoplasma rhoptry protein ROP16 secreted early during invasion, which targets the transcription factor UHRF1 (Ubiquitin-like containing PHD and RING fingers domain 1), and leads to host cell cycle arrest. This is mediated by DNMT activity and chromatin remodeling at the cyclin B1 gene promoter through recruitment of phosphorylated UHRF1 associated with a repressive multienzymatic protein complex. This leads to deacetylation and methylation of histone H3 surrounding the cyclin B1 gene promoter to epigenetically silence its transcriptional activity. Moreover, T. gondii infection causes DNA hypermethylation in its host cell, by upregulation of DNMTs. ROP16 is already known to activate and phosphorylate protective immunity transcription factors such as STAT 3/6/5 and the tumor suppressor p53 involved in cell cycle progression. Moreover, ROP16 modulates host signaling…

Advisors/Committee Members: Pfaff, Alexander (thesis director).

Subjects/Keywords: Toxoplasma gondii; UHFR1; Cycline B1; DNMT; Régulation épigenetique; ROP16; Toxoplasma gondii; UHFR1; ROP16; Cyclin B1; DNMT; Epigenetic regulation; 572.6; 572.8

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sabou, A. M. (2018). Identification d'une protéine parasitaire interagissant avec le facteur de transcription UHRF1 dans les cellules infectées par Toxoplasma gondii : Toxoplasma gondii ROP16 kinase silences the cyclin B1 gene promoter by hijacking host cell UHRF1-dependent epigenetic pathways. (Doctoral Dissertation). Université de Strasbourg. Retrieved from http://www.theses.fr/2018STRAJ050

Chicago Manual of Style (16^th Edition):

Sabou, Alina Marcela. “Identification d'une protéine parasitaire interagissant avec le facteur de transcription UHRF1 dans les cellules infectées par Toxoplasma gondii : Toxoplasma gondii ROP16 kinase silences the cyclin B1 gene promoter by hijacking host cell UHRF1-dependent epigenetic pathways.” 2018. Doctoral Dissertation, Université de Strasbourg. Accessed January 16, 2021. http://www.theses.fr/2018STRAJ050.

MLA Handbook (7^th Edition):

Sabou, Alina Marcela. “Identification d'une protéine parasitaire interagissant avec le facteur de transcription UHRF1 dans les cellules infectées par Toxoplasma gondii : Toxoplasma gondii ROP16 kinase silences the cyclin B1 gene promoter by hijacking host cell UHRF1-dependent epigenetic pathways.” 2018. Web. 16 Jan 2021.

Vancouver:

Sabou AM. Identification d'une protéine parasitaire interagissant avec le facteur de transcription UHRF1 dans les cellules infectées par Toxoplasma gondii : Toxoplasma gondii ROP16 kinase silences the cyclin B1 gene promoter by hijacking host cell UHRF1-dependent epigenetic pathways. [Internet] [Doctoral dissertation]. Université de Strasbourg; 2018. [cited 2021 Jan 16]. Available from: http://www.theses.fr/2018STRAJ050.

Council of Science Editors:

Sabou AM. Identification d'une protéine parasitaire interagissant avec le facteur de transcription UHRF1 dans les cellules infectées par Toxoplasma gondii : Toxoplasma gondii ROP16 kinase silences the cyclin B1 gene promoter by hijacking host cell UHRF1-dependent epigenetic pathways. [Doctoral Dissertation]. Université de Strasbourg; 2018. Available from: http://www.theses.fr/2018STRAJ050

University of Debrecen

8. Alsubhi, Abdulrahman. Epigenetic Therapy in Cancer .

Degree: DE – Általános Orvostudományi Kar, University of Debrecen

URL: http://hdl.handle.net/2437/233528

► The epigenetic modifications can change the state of selective part in the DNA by different enzymes such DNA methyltransferases and the histone deacetylases. Dysregulation of… (more)

Subjects/Keywords: Epigenetic DNMT HDAC Therapy Cancer

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Alsubhi, A. (n.d.). Epigenetic Therapy in Cancer . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/233528

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Alsubhi, Abdulrahman. “Epigenetic Therapy in Cancer .” Thesis, University of Debrecen. Accessed January 16, 2021. http://hdl.handle.net/2437/233528.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Alsubhi, Abdulrahman. “Epigenetic Therapy in Cancer .” Web. 16 Jan 2021.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

Alsubhi A. Epigenetic Therapy in Cancer . [Internet] [Thesis]. University of Debrecen; [cited 2021 Jan 16]. Available from: http://hdl.handle.net/2437/233528.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

Alsubhi A. Epigenetic Therapy in Cancer . [Thesis]. University of Debrecen; Available from: http://hdl.handle.net/2437/233528

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

9. Azadi, Sahar. Alternativ splicing : Mutationer i BRCA1 och BRCA2 orsakar bröstcancer.

Degree: The Institute of Technology, 2012, Linköping UniversityLinköping University

URL: http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-106377

► During the past decade it has been shown that alternative splicing is a important mechanism for the proteome diversity. AS is a mechanism that… (more)

Subjects/Keywords: Alternativ splicing; BRCA1; BRCA2; Breast Cancer; Splicing; DNMT; PARP

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APA (6^th Edition):

Azadi, S. (2012). Alternativ splicing : Mutationer i BRCA1 och BRCA2 orsakar bröstcancer. (Thesis). Linköping UniversityLinköping University. Retrieved from http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-106377

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Azadi, Sahar. “Alternativ splicing : Mutationer i BRCA1 och BRCA2 orsakar bröstcancer.” 2012. Thesis, Linköping UniversityLinköping University. Accessed January 16, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-106377.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Azadi, Sahar. “Alternativ splicing : Mutationer i BRCA1 och BRCA2 orsakar bröstcancer.” 2012. Web. 16 Jan 2021.

Vancouver:

Azadi S. Alternativ splicing : Mutationer i BRCA1 och BRCA2 orsakar bröstcancer. [Internet] [Thesis]. Linköping UniversityLinköping University; 2012. [cited 2021 Jan 16]. Available from: http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-106377.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Azadi S. Alternativ splicing : Mutationer i BRCA1 och BRCA2 orsakar bröstcancer. [Thesis]. Linköping UniversityLinköping University; 2012. Available from: http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-106377

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Louisville

10. Li, Yihong. Sulforaphane protects against ethanol-induced apoptosis and teratogenesis through epigenetic modulation of anti-apoptotic genes.

Degree: PhD, 2020, University of Louisville

URL: https://ir.library.louisville.edu/etd/3417

► Background. Ethanol-induced excessive apoptosis in neural crest cells (NCCs), a multipotent progenitor cell population, is one of the major mechanisms underlying the pathogenesis of… (more)

▼ Background. Ethanol-induced excessive apoptosis in neural crest cells (NCCs), a multipotent progenitor cell population, is one of the major mechanisms underlying the pathogenesis of Fetal Alcohol Spectrum Disorders (FASD). However, the molecular mechanisms underlying FASD that results from maternal alcohol exposure during pregnancy are poorly understood. The overall goals of this study are to examine the mechanisms by which ethanol induces apoptosis and malformations in vitro and in vivo, and to develop a nutritional-based approach by using SFN and SFN-rich BSE to prevent FASD through epigenetic modulation. Results. This study demonstrates that ethanol exposure resulted in a significant increase in the DNMT activity and the expression of DNMT3a in human neural crest cells. SFN can significantly diminish ethanol-induced increases in DNMT activity and the expression of DNMT3a. We have also found that ethanol-induced up-regulation of DNMT3a and an increase in DNMT activity resulted in hypermethylation at the promoters of the selected anti-apoptotic genes and that SFN can diminish ethanol-induced hypermethylation at the promoters of the anti-apoptotic genes by preventing ethanol-induced up-regulation of DNMT3a and increase in DNMT activity. In addition, the knockdown of DNMT3a or treatment with SFN significantly diminished ethanol-induced decreases in the mRNA and protein expression of NAIP and XIAP and prevented ethanol-induced apoptosis in human neural crest cells. The knockdown of DNMT3a also enhanced the effects of SFN on the mRNA and protein expression of NAIP and XIAP and the protective effects of SFN on ethanol-induced apoptosis. This study also shows that ethanol exposure can increase HDAC activity and the expression of HDAC2 in human neural crest cells. SFN treatment significantly diminished ethanol-induced increase in HDAC activity and the up-regulation of HDAC2. We have also found that ethanol-induced increase in HDAC activity and up-regulation of HDAC2 resulted in the reduction of H3 acetylation at the promoters of AKT1, BIRC6 and XIAP and that SFN diminished ethanol-induced reduction of H3 acetylation at the promoters of anti-apoptotic genes by inhibiting HDAC activity and reducing ethanol-induced up-regulation of HDAC2. In addition, SFN treatment or knockdown of HDAC2 significantly diminished ethanol-induced decreases in the mRNA and protein expression of AKT1, BIRC6 and XIAP and prevented ethanol-induced apoptosis in human neural crest cells. The knockdown of HDAC2 also enhanced the effects of SFN on the mRNA and protein expression of AKT1, BIRC6 and XIAP and the protection against ethanol-induced apoptosis. In addition, our studies have shown that ethanol exposure can inhibit EMT through the down-regulation of Snail1 by decreasing H3K4me3 enrichment at the promoter regions of Snail1 and increase apoptosis in neural crest cells. SFN treatment can reverse the ethanol-induced reduction of the H3K4me3 enrichment at the promoter regions of Snail1, restore… Advisors/Committee Members: Chen, Shao-yu, Watson, Walter, Cai, Lu, Wise Sr., John, Zhang, Quenwei.

Subjects/Keywords: FASD; epigenetics; apoptosis; DNMT; HDAC; KDM; Other Pharmacy and Pharmaceutical Sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Li, Y. (2020). Sulforaphane protects against ethanol-induced apoptosis and teratogenesis through epigenetic modulation of anti-apoptotic genes. (Doctoral Dissertation). University of Louisville. Retrieved from https://ir.library.louisville.edu/etd/3417

Chicago Manual of Style (16^th Edition):

Li, Yihong. “Sulforaphane protects against ethanol-induced apoptosis and teratogenesis through epigenetic modulation of anti-apoptotic genes.” 2020. Doctoral Dissertation, University of Louisville. Accessed January 16, 2021. https://ir.library.louisville.edu/etd/3417.

MLA Handbook (7^th Edition):

Li, Yihong. “Sulforaphane protects against ethanol-induced apoptosis and teratogenesis through epigenetic modulation of anti-apoptotic genes.” 2020. Web. 16 Jan 2021.

Vancouver:

Li Y. Sulforaphane protects against ethanol-induced apoptosis and teratogenesis through epigenetic modulation of anti-apoptotic genes. [Internet] [Doctoral dissertation]. University of Louisville; 2020. [cited 2021 Jan 16]. Available from: https://ir.library.louisville.edu/etd/3417.

Council of Science Editors:

Li Y. Sulforaphane protects against ethanol-induced apoptosis and teratogenesis through epigenetic modulation of anti-apoptotic genes. [Doctoral Dissertation]. University of Louisville; 2020. Available from: https://ir.library.louisville.edu/etd/3417

The Ohio State University

11. Shaw, Yeng-Jeng. Small molecule-based drug design of anticancer agents that target protein kinase B/ AKT, Bcl-xL and DNA methyltransferases for the treatment of prostate cancer.

Degree: PhD, Pharmacy, 2005, The Ohio State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1128693982

► Prostate cancer is the most common form of cancer in men and the second leading cause of cancer-related deaths in the United States. So far,… (more)

▼ Prostate cancer is the most common form of cancer in men and the second leading cause of cancer-related deaths in the United States. So far, several mechanisms have been identified by which androgen-independent prostate cancer can develop, including constitutively active AKT pathway, overexpression of Bcl-xL and hypermethylation of tumor suppressor and caretaker genes, such as RASSF1A and GSTP1. In this dissertation research, we have developed three classes of anticancer agents that target the AKT signaling pathway, Bcl-xL, and DNA methyltransferases based on small molecules as our molecular templates.In terms of targeting the AKT pathway, we examined the antiproliferative effect of our lead compound doxazosin, our pharmacological study revealed that doxazosin’s apoptotic effect was mediated, in part, through the down-regulation of phospho-AKT. Therefore, a systematic modification of doxazosin was carried out yielding the optimal compounds 33 and 44 which exhibited an order of magnitude improvement in antiproliferative potency. Development of the Bcl-xL inhibitor arose from our attempt to develop non-nucleoside DNA hypomethylating agents based on procainamide and procaine as molecular templates. However, the antiproliferative effects of these procainamide derivatives in PC-3 cells could not be attributed to the alteration of DNA methylation status. A search for a molecular target of these agents attributed their antiproliferative effect in PC-3 cells to the inhibition of Bcl-xL function. Among these derivatives, compound 27 exhibited the greatest inhibitory effect against Bcl-xL activity. Exposure of PC-3 cells to 27 resulted in the release of cytochrome c from mitochondria, followed by the activation of caspase-9 and PARP cleavage. To continue our research on the development of non-nucleoside DNA hypomethylating agents, (-)-epicatechin gallate (ECG) was selected as our molecular template based on the literature describing its ability to inhibit DNA methyltransferase (DNMT) activity. Screening of some candidates by methylation-specific PCR (MSP) in three cancer cell lines indicated that RASSF1A gene could be consistently demethylated by compound 6A. Altogether, through this dissertation research, we have successfully developed three classes of anticancer agents that modulate different molecular targets. These findings suggest that small molecule-based drug design can be a powerful tool to develop more structurally diversified anticancer agents. Advisors/Committee Members: Chen, Ching-Shih (Advisor).

Subjects/Keywords: Akt; Bcl-xL; DNMT

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Shaw, Y. (2005). Small molecule-based drug design of anticancer agents that target protein kinase B/ AKT, Bcl-xL and DNA methyltransferases for the treatment of prostate cancer. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1128693982

Chicago Manual of Style (16^th Edition):

Shaw, Yeng-Jeng. “Small molecule-based drug design of anticancer agents that target protein kinase B/ AKT, Bcl-xL and DNA methyltransferases for the treatment of prostate cancer.” 2005. Doctoral Dissertation, The Ohio State University. Accessed January 16, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=osu1128693982.

MLA Handbook (7^th Edition):

Shaw, Yeng-Jeng. “Small molecule-based drug design of anticancer agents that target protein kinase B/ AKT, Bcl-xL and DNA methyltransferases for the treatment of prostate cancer.” 2005. Web. 16 Jan 2021.

Vancouver:

Shaw Y. Small molecule-based drug design of anticancer agents that target protein kinase B/ AKT, Bcl-xL and DNA methyltransferases for the treatment of prostate cancer. [Internet] [Doctoral dissertation]. The Ohio State University; 2005. [cited 2021 Jan 16]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1128693982.

Council of Science Editors:

Shaw Y. Small molecule-based drug design of anticancer agents that target protein kinase B/ AKT, Bcl-xL and DNA methyltransferases for the treatment of prostate cancer. [Doctoral Dissertation]. The Ohio State University; 2005. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1128693982

12. Erdmann, Alexandre. Conception, synthèse et caractérisation de nouveaux inhibiteurs de méthyltranférases d'ADN à visée anticancéreuse : Conception, sy,thesis and characterization of new DNA methyltransferase inhibitors as anticancer drug.

Degree: Docteur es, Chimie médicinale, 2015, Université Toulouse III – Paul Sabatier

URL: http://www.theses.fr/2015TOU30270

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Le domaine de l'épigénétique couvre l'ensemble des phénomènes héritables et transmissibles qui interviennent dans l'expression du génome sans modifier la séquence nucléotidique. L'information épigénétique est… (more)

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Le domaine de l'épigénétique couvre l'ensemble des phénomènes héritables et transmissibles qui interviennent dans l'expression du génome sans modifier la séquence nucléotidique. L'information épigénétique est régulée par les modifications de la chromatine impliquant les histones et l'ADN. La méthylation de l'ADN est un phénomène réversible jouant un rôle crucial dans l'expression des gènes puisque la méthylation des promoteurs de gènes empêche leur transcription. La modulation aberrante de cette marque épigénétique est associée à diverses pathologies telles que le cancer. Cette méthylation étant réversible, elle peut être ciblée afin de reprogrammer la cellule cancéreuse. Les méthyltransferases d'ADN (DNMT), étant les enzymes responsables de la méthylation, représentent la cible principale de notre stratégie de recherche. Leur inhibition par des petites molécules est au centre de nos recherches de thérapies anticancéreuses dont les bases sont représentées par deux catégories d'inhibiteurs de DNMT existant. Les premiers sont des analogues de cytosine qui est la cible de la méthylation. Ils sont connus pour s'intégrer dans l'ADN et former un complexe covalent irréversible avec l’enzyme (complexe suicide) mais ils souffrent d'un manque de stabilité et de certains effets indésirables dus à leur incorporation dans l’ADN. Les seconds sont les inhibiteurs non nucléosidiques qui sont divers et parfois connus pour cibler d’autres enzymes. Ils ont l’avantage de pouvoir être utilisés comme sondes pour comprendre plus précisément le mécanisme d'inhibition mais ils manquent de spécificité et de sélectivité. Au cours de cette thèse, une banque de molécules a été criblée à partir de la combinaison d'un test enzymatique et d'un test cellulaire visant à inhiber ces enzymes. Les synthèses de trois familles de molécules potentiellement inhibitrices de DNMT issus de ce criblage sont décrites en expliquant le chemin de drug design emprunté pour obtenir des informations mécanistiques d’inhibition de la méthylation d’ADN, notamment de réactivité avec la cible. Les découvertes ont été inspirées par des études de modélisation permettant de mettre en évidence une sélectivité de certains inhibiteurs. La synthèse chimique a également abouti à une nouvelle voie de synthèse d’accès aux diaminopyrimidines dont l’impact permet de faciliter les études chimiques de dérivés quinazolines comme inhibiteur non nucléosidiques utiles pour les thérapies anticancéreuses.

Epigenetic is defined as the study of heritable changes in the genes expression without altering the DNA sequence. Two main processes are implicated in this field, the histones modifications and the DNA methylation. By introducing an acetyl or a methyl group on the histone tails or by methylation of DNA, the chromatin state is modified and the gene expression is controlled. Aberrant epigenetic modifications are associated with several diseases, in particular with cancer. In cancer cells, the whole DNA is hypomethylated, thus promoting genome instability, while the promoter region is…

Advisors/Committee Members: Arimondo, Paola Barbara (thesis director), Massiot, Georges (thesis director).

Subjects/Keywords: Méthylation de l’ADN; Méthyltransférases d’ADN; Inhibiteur de DNMT; Drug design; Iaminopyrimidines; Inhibiteurs sélectifs; Inhibiteurs covalents; Cancer; DNA methylation; DNA methyltransferases; DNMT inhibitors; Drug design; Diaminopyrimidines; Selective inhibitor; Covalent inhibitor; Cancer

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Erdmann, A. (2015). Conception, synthèse et caractérisation de nouveaux inhibiteurs de méthyltranférases d'ADN à visée anticancéreuse : Conception, sy,thesis and characterization of new DNA methyltransferase inhibitors as anticancer drug. (Doctoral Dissertation). Université Toulouse III – Paul Sabatier. Retrieved from http://www.theses.fr/2015TOU30270

Chicago Manual of Style (16^th Edition):

Erdmann, Alexandre. “Conception, synthèse et caractérisation de nouveaux inhibiteurs de méthyltranférases d'ADN à visée anticancéreuse : Conception, sy,thesis and characterization of new DNA methyltransferase inhibitors as anticancer drug.” 2015. Doctoral Dissertation, Université Toulouse III – Paul Sabatier. Accessed January 16, 2021. http://www.theses.fr/2015TOU30270.

MLA Handbook (7^th Edition):

Erdmann, Alexandre. “Conception, synthèse et caractérisation de nouveaux inhibiteurs de méthyltranférases d'ADN à visée anticancéreuse : Conception, sy,thesis and characterization of new DNA methyltransferase inhibitors as anticancer drug.” 2015. Web. 16 Jan 2021.

Vancouver:

Erdmann A. Conception, synthèse et caractérisation de nouveaux inhibiteurs de méthyltranférases d'ADN à visée anticancéreuse : Conception, sy,thesis and characterization of new DNA methyltransferase inhibitors as anticancer drug. [Internet] [Doctoral dissertation]. Université Toulouse III – Paul Sabatier; 2015. [cited 2021 Jan 16]. Available from: http://www.theses.fr/2015TOU30270.

Council of Science Editors:

Erdmann A. Conception, synthèse et caractérisation de nouveaux inhibiteurs de méthyltranférases d'ADN à visée anticancéreuse : Conception, sy,thesis and characterization of new DNA methyltransferase inhibitors as anticancer drug. [Doctoral Dissertation]. Université Toulouse III – Paul Sabatier; 2015. Available from: http://www.theses.fr/2015TOU30270

13. Chappuit, Lucrezia. Design, synthèse et évaluation biochimique d’inhibiteurs des ADN Méthyltransférases : Design, synthesis and biochemical evaluation of DNA Methyltransferases inhibitors.

Degree: Docteur es, Chimie moléculaire, 2018, Sorbonne université

URL: http://www.theses.fr/2018SORUS372

►

Ce manuscrit présente le développement de nouveaux inhibiteurs de la DNMT1 (DNA Methyl- transferase), enzyme impliquée dans les modifications épigénétiques de l’ADN et dont la… (more)

Subjects/Keywords: Cancer épigénétique; DNMT; Méthylation ADN; Modélisation moléculaire; Prolino-homo-tryptophanes, pyrazoles; Test d’inhibition; Pyrazoles; Epigenetic cancer; DNMT; DNA methylation; Molecular modeling; Prolino-homo-tryptophan; Inhibition test; Pyrazole; 572; 614.5999

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chappuit, L. (2018). Design, synthèse et évaluation biochimique d’inhibiteurs des ADN Méthyltransférases : Design, synthesis and biochemical evaluation of DNA Methyltransferases inhibitors. (Doctoral Dissertation). Sorbonne université. Retrieved from http://www.theses.fr/2018SORUS372

Chicago Manual of Style (16^th Edition):

Chappuit, Lucrezia. “Design, synthèse et évaluation biochimique d’inhibiteurs des ADN Méthyltransférases : Design, synthesis and biochemical evaluation of DNA Methyltransferases inhibitors.” 2018. Doctoral Dissertation, Sorbonne université. Accessed January 16, 2021. http://www.theses.fr/2018SORUS372.

MLA Handbook (7^th Edition):

Chappuit, Lucrezia. “Design, synthèse et évaluation biochimique d’inhibiteurs des ADN Méthyltransférases : Design, synthesis and biochemical evaluation of DNA Methyltransferases inhibitors.” 2018. Web. 16 Jan 2021.

Vancouver:

Chappuit L. Design, synthèse et évaluation biochimique d’inhibiteurs des ADN Méthyltransférases : Design, synthesis and biochemical evaluation of DNA Methyltransferases inhibitors. [Internet] [Doctoral dissertation]. Sorbonne université; 2018. [cited 2021 Jan 16]. Available from: http://www.theses.fr/2018SORUS372.

Council of Science Editors:

Chappuit L. Design, synthèse et évaluation biochimique d’inhibiteurs des ADN Méthyltransférases : Design, synthesis and biochemical evaluation of DNA Methyltransferases inhibitors. [Doctoral Dissertation]. Sorbonne université; 2018. Available from: http://www.theses.fr/2018SORUS372

University of Guelph

14. Mitchnick, Krista. The Dissociable Involvement of Epigenetic Mechanisms in Hippocampus- and Perirhinal Cortex-mediated Object Memory in Male Rats.

Degree: PhD, Department of Psychology, 2018, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/13096

► This thesis investigated the involvement of several epigenetic proteins in hippocampus (HPC)- and perirhinal cortex (PRh)-mediated object recognition. Previous literature has demonstrated the requirement for… (more)

▼ This thesis investigated the involvement of several epigenetic proteins in hippocampus (HPC)- and perirhinal cortex (PRh)-mediated object recognition. Previous literature has demonstrated the requirement for both DNA methylation and histone acetylation, two prominent epigenetic mechanisms, in HPC-dependent memory, including object recognition, but at the outset of these experiments no one had studied these mechanisms within the PRh, another structure necessary for object recognition. Specifically, we determined the involvement of the DNA methyltransferases DNMT1, DNMT3a, and DNMT3b, which are required for DNA methylation; the GADD45 isoforms GADD45a, GADD45b, and GADD45g, which are involved in DNA demethylation; and three prominent histone acetyltransferases, CBP, p300, and PCAF, which are involved in histone acetylation, in both the HPC and PRh for object-in-place (OiP) memory. The use of the OiP task enabled us to compare the involvement of these mechanisms within these two regions, as successful performance in this paradigm requires the HPC and PRh for processing of object location and object identity, respectively. The role of these factors in short-term (20min) and long-term (24h) OiP memory was assessed using intra-HPC and PRh administration of various compounds that selectively inhibit or activate these proteins. Furthermore, quantitative polymerase chain reaction (qPCR) was used to measure mRNA expression of these factors. Similarly, chromatin immunoprecipitation and methylated DNA immunoprecipitation, followed by qPCR, were used to measure protein and 5mC occupancy, respectively, on specific genomic loci. Our results demonstrate that epigenetic mechanisms are necessary for PRh-mediated memory, but additionally illustrate differential involvement of these epigenetic factors in the HPC and PRh for successful OiP memory. Notably, we determined that DNMT1 and GADD45a, neither of which have been implicated in mnemonic processes, are both necessary in PRh, but not the HPC, for long-term OiP memory. Moreover, our results suggest that GADD45a modulates DNMT1-mediated methylation on two intergenic loci, following learning. Additionally, we have shown that PCAF functionally interacts with ERalpha to support short-term memory in the HPC, but not PRh. These regional dissociations are likely due to the differences in information processing, highlighting the importance of comparing the involvement of epigenetic mechanisms between mnemonic structures. Advisors/Committee Members: Winters, Boyer (advisor), Winters, Boyer (advisor).

Subjects/Keywords: DNA methylation; DNA demethylation; histone acetylation; DNMT; GADD45; PCAF; CBP; p300; estrogen receptor alpha

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mitchnick, K. (2018). The Dissociable Involvement of Epigenetic Mechanisms in Hippocampus- and Perirhinal Cortex-mediated Object Memory in Male Rats. (Doctoral Dissertation). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/13096

Chicago Manual of Style (16^th Edition):

Mitchnick, Krista. “The Dissociable Involvement of Epigenetic Mechanisms in Hippocampus- and Perirhinal Cortex-mediated Object Memory in Male Rats.” 2018. Doctoral Dissertation, University of Guelph. Accessed January 16, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/13096.

MLA Handbook (7^th Edition):

Mitchnick, Krista. “The Dissociable Involvement of Epigenetic Mechanisms in Hippocampus- and Perirhinal Cortex-mediated Object Memory in Male Rats.” 2018. Web. 16 Jan 2021.

Vancouver:

Mitchnick K. The Dissociable Involvement of Epigenetic Mechanisms in Hippocampus- and Perirhinal Cortex-mediated Object Memory in Male Rats. [Internet] [Doctoral dissertation]. University of Guelph; 2018. [cited 2021 Jan 16]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/13096.

Council of Science Editors:

Mitchnick K. The Dissociable Involvement of Epigenetic Mechanisms in Hippocampus- and Perirhinal Cortex-mediated Object Memory in Male Rats. [Doctoral Dissertation]. University of Guelph; 2018. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/13096

Freie Universität Berlin

15. Höche, Alexander. Expression analysis of the DNA methyltransferases DNMT1 and DNMT3b in childhood acute leukemias.

Degree: 2012, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-6415

► INTRODUCTION AND AIM OF STUDY: The DNA methyltransferases DNMT1, DNMT3a, and DNMT3b catalyze DNA methylation. This leads to compression and inactivation of the methylated DNA… (more)

▼ INTRODUCTION AND AIM OF STUDY: The DNA methyltransferases DNMT1, DNMT3a, and DNMT3b catalyze DNA methylation. This leads to compression and inactivation of the methylated DNA region via complex epigenetic mechanisms. Under physiological conditions, the genome is globally hypermethylated, whereas gene promoters tend to be hypomethylated. In tumorigenesis these promoters, especially those of tumor-suppressor-genes, often undergo methylation and consecutive inactivation, while the rest of the genome is aberrantly hypomethylated. Promoter hypermethylation is shown to correlate with increased DNMT expression in some tumors. Promoter hypermethylation could be partially reversed by DNMT inhibitors in Phase I - III studies. DNMT expression has not yet been analyzed in pediatric AML and relapse of ALL. In this study, the expression of DNMT1 and DNMT3b (the DNMTs which are considered to be mainly responsible for aberrant methylation in tumor cells) and the expression of selected isoforms was analyzed in newly diagnosed pediatric AML and relapse of pediatric ALL. The expression was compared to that in healthy subjects. Furthermore, the prognostic role of DNMT expression was examined. MATERIAL AND METHODS: The DNMT expression in tumor cells of 26 patients with first relapse of pediatric ALL (7patients in CCR and 19 patients with subsequent event) and 47 patients with newly diagnosed pediatric AML (34 patients in CCR and 13 patients with subsequent event) was examined and compared to the expression in leukocytes of 22 healthy subjects. After cell filtration RNA was isolated and reversely transcribed into cDNA, which was quantified by Real-Time-PCR after establishment of standard curves and normalized with 2 reference genes (RpL13a served as a stably expressed gene and PCNA as a proliferation marker). RESULTS: Expression of DNMT1 is not altered in leukemic cells compared to the control group if normalized with RpL13a, whereas it is decreased if normalized with PCNA. Expression of DNMT3b is increased in ALL if normalized with RpL13a but not altered if normalized with PCNA. In AML cells, DNMT3b expression is increased after normalization with both reference genes. The isoform DNMT1’ accounts for 90% of the entire DNMT1 expression in all groups. All other isoforms were not included into the statistical analysis since they were not detectable in all of the samples. DNMT3b4 was detected in 70% of the samples of the ALL- and AML-group, respectively, whereas it was not detected in the control group. No differences were found between the subgroups with different outcome. DISCUSSION: Expression of DNMT1 is not altered in the examined leukemic cells compared to the control group despite the elevated level of proliferation. This relatively low level of expression in leukemic cells might contribute to the hypomethylation of newly synthesized DNA. DNMT3b expression is elevated in AML-cells after normalization with both reference genes. This might lead to aberrant hypermethylation of promoter regions as well as to hypomethylation by DNMT3b4 via… Advisors/Committee Members: m (gender), Prof. Dr. med. Dr. rer. nat. K. Seeger (firstReferee), Priv.-Doz. Dr. med. Chr. Scholz (furtherReferee), Priv.-Doz. Dr. med. A. Claviez (furtherReferee).

Subjects/Keywords: DNMT expression; pediatric AML; pediatric ALL; DNA methylation; Real-Time-PCR; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

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APA (6^th Edition):

Höche, A. (2012). Expression analysis of the DNA methyltransferases DNMT1 and DNMT3b in childhood acute leukemias. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-6415

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Höche, Alexander. “Expression analysis of the DNA methyltransferases DNMT1 and DNMT3b in childhood acute leukemias.” 2012. Thesis, Freie Universität Berlin. Accessed January 16, 2021. http://dx.doi.org/10.17169/refubium-6415.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Höche, Alexander. “Expression analysis of the DNA methyltransferases DNMT1 and DNMT3b in childhood acute leukemias.” 2012. Web. 16 Jan 2021.

Vancouver:

Höche A. Expression analysis of the DNA methyltransferases DNMT1 and DNMT3b in childhood acute leukemias. [Internet] [Thesis]. Freie Universität Berlin; 2012. [cited 2021 Jan 16]. Available from: http://dx.doi.org/10.17169/refubium-6415.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Höche A. Expression analysis of the DNA methyltransferases DNMT1 and DNMT3b in childhood acute leukemias. [Thesis]. Freie Universität Berlin; 2012. Available from: http://dx.doi.org/10.17169/refubium-6415

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Loughborough University

16. Hunter, David. The impact of exercise interventions and omega-3 polyunsaturated fatty acid supplementation on DNA methylation and gene expression.

Degree: PhD, 2019, Loughborough University

URL: https://doi.org/10.26174/thesis.lboro.8268551.v1 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.785284

► Epigenetics is a rapidly developing field of study which investigates chemical modifications to the genome, independent of the DNA sequence, which regulate gene expression profiles.… (more)

▼ Epigenetics is a rapidly developing field of study which investigates chemical modifications to the genome, independent of the DNA sequence, which regulate gene expression profiles. The most commonly studied epigenetic modification, DNA methylation, has been demonstrated to be influenced by lifestyle factors including diet and exercise. The modulation of DNA methylation by lifestyle factors is one potential mechanism for the reduction in disease risk induced by a healthy lifestyle. This thesis aimed to identify the impact of exercise on DNA methylation and mRNA expression and determine whether fatty acid supplementation may modulate this response. Custom assays were developed and validated (Chapter 4) to assess the DNA methylation of peroxisome proliferative activated receptor gamma coactivator 1 alpha (PPARGC1A), interleukin 6 (IL6) and tumor necrosis factor alpha (TNF) at specific cytosine bases in genomic locations previously identified to be biologically relevant. Assays to investigate the mRNA expression of PPARGC1A, IL6, TNF and the DNA methyltransferases (DNMT) were validated to ensure accurate results. In Chapter 5, DNMT mRNA expression decreased following an acute bout of exercise to volitional fatigue; whereas, no changes in DNA methylation were identified as a result of exercise or supplementation of omega-3 polyunsaturated fatty acids (n-3 PUFAs). However, an interaction was determined between exercise and n-3 PUFA supplementation for the DNA methylation of a single IL6 CpG site. Following exercise, decreased DNA methylation and increased mRNA expression of IL6 was detected after n-3 PUFA supplementation compared to the trial before supplementation. IL6 methylation was correlated to the n-3 PUFA content in whole blood following supplementation suggesting increased n-3 PUFA content following supplementation may prime the cells for future exercise stimuli. Chapter 6 sought to investigate whether acute exercise of an increased duration would modulate DNA methylation profiles and adopted a double-blind randomised repeated measures design to try and confirm the interaction between exercise and n-3 PUFA supplementation. Following a one-hour cycling bout, consisting of 45 mins cycling at 70% of V̇O2 followed by a 15 min time trial, we determined global hypomethylation, a reduction in PPARGC1A DNA methylation and increased mRNA expression of PPARGC1A. These methylation changes were associated with a similar reduction in DNMT expression as reported in Chapter 5. In line with the positive correlations between whole blood n-3 PUFA content in the previous chapter, an increase in IL6 methylation was determined following n-3 PUFA supplementation compared to the impact of supplementation with extra virgin olive oil; however, this relationship was not further modulated by exercise. The focus of Chapter 7 was the impact of acute resistance exercise on DNA methylation profiles and whether resistance training and fatty acid supplementation could modulate the epigenetic response. Acute resistance exercise was sufficient to…

Subjects/Keywords: Medical and Health Sciences not elsewhere classified; DNA methylation; Epigenetics; Epigenetic; PPARGC1A; IL6; TNF; n-3 PUFA; Exercise; DNMT

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hunter, D. (2019). The impact of exercise interventions and omega-3 polyunsaturated fatty acid supplementation on DNA methylation and gene expression. (Doctoral Dissertation). Loughborough University. Retrieved from https://doi.org/10.26174/thesis.lboro.8268551.v1 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.785284

Chicago Manual of Style (16^th Edition):

Hunter, David. “The impact of exercise interventions and omega-3 polyunsaturated fatty acid supplementation on DNA methylation and gene expression.” 2019. Doctoral Dissertation, Loughborough University. Accessed January 16, 2021. https://doi.org/10.26174/thesis.lboro.8268551.v1 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.785284.

MLA Handbook (7^th Edition):

Hunter, David. “The impact of exercise interventions and omega-3 polyunsaturated fatty acid supplementation on DNA methylation and gene expression.” 2019. Web. 16 Jan 2021.

Vancouver:

Hunter D. The impact of exercise interventions and omega-3 polyunsaturated fatty acid supplementation on DNA methylation and gene expression. [Internet] [Doctoral dissertation]. Loughborough University; 2019. [cited 2021 Jan 16]. Available from: https://doi.org/10.26174/thesis.lboro.8268551.v1 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.785284.

Council of Science Editors:

Hunter D. The impact of exercise interventions and omega-3 polyunsaturated fatty acid supplementation on DNA methylation and gene expression. [Doctoral Dissertation]. Loughborough University; 2019. Available from: https://doi.org/10.26174/thesis.lboro.8268551.v1 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.785284

Johannes Gutenberg Universität Mainz

17. Weyrich, Alexandra. DNA methylation, histone modification and the transcription factor dE2F1 in Drosophila.

Degree: 2007, Johannes Gutenberg Universität Mainz

URL: http://ubm.opus.hbz-nrw.de/volltexte/2007/1317/

►

Drosophila melanogaster enthält eine geringe Menge an 5-methyl-Cytosin. Die von mir untersuchte männliche Keimbahn von Drosophila weist jedoch keine nachweisbaren Mengen an DNA-Methylierung auf. Eine… (more)

▼

Drosophila melanogaster enthält eine geringe Menge an 5-methyl-Cytosin. Die von mir untersuchte männliche Keimbahn von Drosophila weist jedoch keine nachweisbaren Mengen an DNA-Methylierung auf. Eine künstliche Expression der murinen de novo Methyltransferasen, DNMT3A und DNMT3B1, in den Fliegenhoden, führte nicht zu der erwarteten Methylierungszunahme und hatte keinen Effekt auf die Fruchtbarkeit der Männchen. Auch die gewebespezifische Expression unter der Verwendung des UAS/GAL4-Systems zeigte keine phenotypischen Veränderungen. Hingegen fanden wir auf Protein-Ebene des Chromatins von D. melanogaster und D. hydei spezifische Modifikationsmuster der Histone H3 und H4 in der Keimbahn, wie auch in den somatischen Zellen des Hodenschlauches. Die Modifikationsmuster der beiden Zelltypen unterscheiden sich grundlegend und weichen zudem von dem für Eu- und Heterochromatin erwarteten ab, was auf eine größere Komplexität des „Histon-Codes“ als angenommen hindeutet. Folglich liegt die epigenetische Information in Drosophila wahrscheinlich anstatt auf DNA- auf Protein-Ebene, wodurch Genexpression über die Chromatinstruktur reguliert wird. Es wurde gezeigt, dass der Transkriptionsfaktor E2F, der eine Schlüsselfunktion im Zellzyklus hat, durch unterschiedliche Transkripte offenbar quantitativ reguliert wird. Unsere Nachforschungen ergaben, dass die drei E2F1 Genprodukte in Drosophila neben ihrer Zellspezifität auch in unterschiedlichen Expressionsniveaus auftreten, was die Annahme einer quantitativen Expression unterstützt. Die verschiedenen Funktionen der multiplen Gene in Säugern, könnten so funktionell kompensiert werden. Die durch die Expression dreier dE2F1-Transkripte vermutete Synthese verschiedener Proteine konnte nicht bewiesen werden.

Drosophila melanogaster includes a low amount of 5-methylcytosine. My investigations of the male germ line of Drosophila displayed no detectable amounts of DNA-methylation. The two artificially expressed murine de novo methyltransferases, DNMT3A and DNMT3B1, in the flies` testis, did not increase the methylation level, neither had an effect on the male’s fertility. A tissue-specific expression by the usage of the UAS/GAL4-system did not show any phenotypic changes. On the chromatin level of D. melanogaster and D. hydei we found specific modification patterns of histone H3 and H4 in the male germ line as well as in somatic cells. The patterns of modification of both cell types differ from each other and deviate from the one expected for eu- and heterochromatin, indicating a higher complexity of the “histone-code” as assumed. Hence the epigenetic information in Drosophila may be based on the protein, instead of the DNA level. It was shown that the transcription factor E2F, known to play a key function in cell cycle, might be regulated by different transcripts quantitatively. Our studies demonstrated that the three gene products of E2F1 in Drosophila are besides their cell specificity, present in different expression levels, supporting the presumption of a quantitative regulation.…

Subjects/Keywords: Drosophila, Spermatogenese, Epigenetik, DNA-Methylierung, Histon-Modifikationen, Dnmt, E2F, Trankriptionsfaktor; Drosophila, Spermatogenesis, Epigenetic, DNA methylation, histone modifications, Dnmt, E2F, transcriptionfactor; Life sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Weyrich, A. (2007). DNA methylation, histone modification and the transcription factor dE2F1 in Drosophila. (Doctoral Dissertation). Johannes Gutenberg Universität Mainz. Retrieved from http://ubm.opus.hbz-nrw.de/volltexte/2007/1317/

Chicago Manual of Style (16^th Edition):

Weyrich, Alexandra. “DNA methylation, histone modification and the transcription factor dE2F1 in Drosophila.” 2007. Doctoral Dissertation, Johannes Gutenberg Universität Mainz. Accessed January 16, 2021. http://ubm.opus.hbz-nrw.de/volltexte/2007/1317/.

MLA Handbook (7^th Edition):

Weyrich, Alexandra. “DNA methylation, histone modification and the transcription factor dE2F1 in Drosophila.” 2007. Web. 16 Jan 2021.

Vancouver:

Weyrich A. DNA methylation, histone modification and the transcription factor dE2F1 in Drosophila. [Internet] [Doctoral dissertation]. Johannes Gutenberg Universität Mainz; 2007. [cited 2021 Jan 16]. Available from: http://ubm.opus.hbz-nrw.de/volltexte/2007/1317/.

Council of Science Editors:

Weyrich A. DNA methylation, histone modification and the transcription factor dE2F1 in Drosophila. [Doctoral Dissertation]. Johannes Gutenberg Universität Mainz; 2007. Available from: http://ubm.opus.hbz-nrw.de/volltexte/2007/1317/

University of Vienna

18. Habenschuss, Thomas. Epigenetics.

Degree: 2009, University of Vienna

URL: http://othes.univie.ac.at/4003/

►

Eine der am meisten erforschten epigenetischen Mechanismen ist die Methylierung von DNA. Diese Arbeit beschränkt sich auf die Cytosin-Methylierung, von der eine Vielfalt an Organismen… (more)

▼

Eine der am meisten erforschten epigenetischen Mechanismen ist die Methylierung von DNA. Diese Arbeit beschränkt sich auf die Cytosin-Methylierung, von der eine Vielfalt an Organismen betroffen ist. Das hauptsächliche Vorkommen von 5-Methyl-Cytosin (5mC) besteht in Anhäufungen von Cytosin und Guanin, sogenannten CpG-Inseln. In Pflanzen findet man auch CpNpG-Inseln vor, wobei N für ein beliebiges Nukleotid steht. CpG-Inseln können mosaikartig verteilt oder über das gesamte Genom verstreut sein. Die Methylierung von Cytosin wird gemeinhin mit der Funktionsstille eines Gens in Verbindung gebracht. 5mC kommt nicht als Baustein für die DNA vor. Stattdessen katalysiert eine Vielzahl an Enzymen den Transfer einer Methylgruppe vom gemeinsamen Coenzym S-Adenosyl-L-Methionin (SAM) auf das jeweilige Ziel-Cytosin innerhalb des Genoms. Diese Enzyme werden grundsätzlich in drei Klassen eingeteilt, welche DNMT1, DNMT2, sowie DNMT3 genannt werden. Pflanzen enthalten eine zusätzliche Klasse, die sogenannten Chromomethylasen (CMTs). Die Entfernung des Methylierungsstatus erfolgt mittels Ausschnitt des ganzen Nukleotids. Unterschiedliche Nährstoffe liefern die notwendige Methylgruppe. Einer davon ist Methionin direkt, als Bestandteil von SAM. Andere sind Folsäure, Cobalamin und Cholin. Epigenetische Vorgänge, die auf Cytosin-Methylierung beruhen, sind genomisches ‚imprinting’ und die Formierung von metastabilen Epiallelen. ‚Imprint’-Markierungen werden im Zuge der Genese von Keimzellen und im früh-embryonalen Stadium reguliert. Dabei ist ein Allel eines bestimmten Gens deaktiviert, während das andere normal exprimiert wird. Welches Allel exprimiert wird, ist abhängig von dessen elterlicher Herkunft. Metastabile Epiallele bilden sich während der Embryonal- und Fötalentwicklung. Ihre Bildung ist von der Nährstoffzusammensetzung durch den Mutterorganismus abhängig. Allgemein sind Gene mit einer Insertion betroffen. Ein hoher Methylierungsgrad dieser Insertion kann beträchtliche phänotypische und physiologische Änderungen bewirken. Unter den Zivilisationskrankheiten wird der Krebs momentan vorrangig im Zusammenhang mit epigenetischen Mechanismen untersucht. Mehrere Biomarker und damit in Beziehung stehende Gene sind identifiziert worden und die Entwicklung und klinische Erprobung von Medikamenten schreitet voran. Allerdings bestehen in jedem Fall Bedenken bezüglich der Abfolge von sich verändernden epigenetischen Erscheinungen und der Entstehung eines Tumors. Es gibt einige Ansätze, die dafür sprechen, dass epigenetische Veränderungen nur die Folge sind, nachdem sich eine somatische Zelle zu einer Krebszelle entwickelt hat. Das letzte Kapitel der vorliegenden Arbeit gibt einen Überblick über die aktuelle Methodik bezüglich der DNA-Methylierungsforschung.

One of the most investigated epigenetic mechanisms is the methylation of DNA. This survey is concentrated on cytosine methylation which concerns a variety of organisms. 5-methyl-cytosine (5mC) mainly occurs in clusters of cytosine and guanine, so-called CpG islands. In plants CpNpG…

Subjects/Keywords: 42.20 Genetik; 42.13 Molekularbiologie; Epigenetik / DNA-Methylierung / Cytosin-Methylierung / DNMT / Methylgruppen-Donatoren / genomisches imprinting / metastabile Epiallele; epigenetics / DNA methylation / cytosine methylation / DNMT / methyl group donators / genomic imprinting / metastable epialleles

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Habenschuss, T. (2009). Epigenetics. (Thesis). University of Vienna. Retrieved from http://othes.univie.ac.at/4003/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Habenschuss, Thomas. “Epigenetics.” 2009. Thesis, University of Vienna. Accessed January 16, 2021. http://othes.univie.ac.at/4003/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Habenschuss, Thomas. “Epigenetics.” 2009. Web. 16 Jan 2021.

Vancouver:

Habenschuss T. Epigenetics. [Internet] [Thesis]. University of Vienna; 2009. [cited 2021 Jan 16]. Available from: http://othes.univie.ac.at/4003/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Habenschuss T. Epigenetics. [Thesis]. University of Vienna; 2009. Available from: http://othes.univie.ac.at/4003/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

19. Farias, Nathan. The role of folic acid in maintaining colorectal cancer cell DNA methylation patterns, and cancer stem cell phenotype in vitro.

Degree: MS, Department of Biomedical Sciences, 2014, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7734

► Folic acid is a B vitamin involved in DNA CpG methylation. Mandated dietary fortification has led to a subsequent increase in blood folate concentration which… (more)

Subjects/Keywords: Folate; Folic Acid; DNMT; Cancer Stem Cell; Colorectal Cancer; DNA Methylation; HCT116; SW480

…54 Figure 15. DNMT protein expression in 10 day old SW480 and HCT116 colonospheres ....55… …viii LIST OF ABBREVIATIONS APC APS BMP BSA CIMP CpG CRC CSC DAPI DHFR DMEM DNA DNMT EGF FBS… …reestablished in the 18 embryo by a group of de novo DNA methyltransferases (DNMT)… …deoxycytidine disrupted DNMT protein interactions and sensitized cancer cells to 22…

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APA (6^th Edition):

Farias, N. (2014). The role of folic acid in maintaining colorectal cancer cell DNA methylation patterns, and cancer stem cell phenotype in vitro. (Masters Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7734

Chicago Manual of Style (16^th Edition):

Farias, Nathan. “The role of folic acid in maintaining colorectal cancer cell DNA methylation patterns, and cancer stem cell phenotype in vitro.” 2014. Masters Thesis, University of Guelph. Accessed January 16, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7734.

MLA Handbook (7^th Edition):

Farias, Nathan. “The role of folic acid in maintaining colorectal cancer cell DNA methylation patterns, and cancer stem cell phenotype in vitro.” 2014. Web. 16 Jan 2021.

Vancouver:

Farias N. The role of folic acid in maintaining colorectal cancer cell DNA methylation patterns, and cancer stem cell phenotype in vitro. [Internet] [Masters thesis]. University of Guelph; 2014. [cited 2021 Jan 16]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7734.

Council of Science Editors:

Farias N. The role of folic acid in maintaining colorectal cancer cell DNA methylation patterns, and cancer stem cell phenotype in vitro. [Masters Thesis]. University of Guelph; 2014. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7734

Freie Universität Berlin

20. Schäffer, Susanne. Investigations about the function of the cGMP-dependent kinase I alpha during the development of the nervous system.

Degree: 2006, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-13474

► To broaden our knowledge about the role of cGKIa in the nervous system, especially in sensory neuron axonal growth, this thesis focussed on the following… (more)

▼ To broaden our knowledge about the role of cGKIa in the nervous system, especially in sensory neuron axonal growth, this thesis focussed on the following issues: a) Using an isoform specific antibody the expression of cGKIa was investigated in wholemounts, brain sections, and western blots during embryonic and early postnatal development of the mouse nervous system. The observed spatiotemporal expression pattern of cGKIa suggests a functional role for the kinase in regulating axonal growth, migration, and differentiation of several neuronal populations. b) Cells known to express cGKIa in the wildtype were analysed for potential pathfinding errors or migration deficits in mice deficient for cGKI. For this purpose immunohistochemical studies employing several antibodies and Silver /Nissl-Stainings were carried out. However, none of the structures examined varied from those of wildtype littermates with respect to pathfinding errors or other malformations. c) cGMP-activated cGKI phosphorylates several intracellular target proteins. Three of those proteins (VASP, CRP2 and myosin phosphatase/myosin IIB) were chosen for further investigations due to their ability to regulate cytoskelatal dynamics. Phosphorylation studies using isolated dorsal root ganglia (DRGs) from cGKI-deficient and wildtyp mice allowed the clear identification of VASP as a phosphorylation target of cGKI in sensory neurons. Furthermore, using a panel of antibodies several developmental stages of the corresponding knockout mice were immunohistochemically tested for pathfinding errors with respect to those found in the cGKI-knockout mouse. However, in none of these knockout mice pathfinding of DRG axons was disturbed, suggesting that - disregard of potential compensatory effects - none of these proteins is involved in the pathfinding errors, detected in cGKI deficient mice. d) Assuming that none of the cGKI targets investigated so far is essential for pathfinding of sensory axons, it was necessary to pursuit alternative approaches to identify potential targets and binding partners of cGKI or cGKIa in the nervous system, possibly playing a role in DRGs too. In an approach to find potential substrates of cGKI, tissue lysates from cGKI deficient or wildtype cerebellum after stimulation by the cGKI activator 8-pCPT-cGMP were separated by two-dimensional gelelectrophoresis and compared for differences in the pattern of protein expression or phosphorylation, respectively. Comparative studies of changes in protein expression due to the lack of cGKI revealed both downregulated and upregulated proteins, which were identified by mass spectrometry. Although some differences in the phosphorylaton pattern of wildtype and cGKI-deficient mice were observed also, identification of those proteins requires further investigations due to methodological problems. In a second approach the yeast two-hybrid system was used to screen an E17 mouse library for intracellular interaction partners of cGKIa. Two potential interaction partners for cGKIa have been found: the… Advisors/Committee Members: n (gender), Prof. Dr. Fritz G. Rathjen (firstReferee), Prof. Dr. Gary R. Lewin (furtherReferee).

Subjects/Keywords: cGKIalpha; cGMP; VASP; Dnmt; nervous system; 500 Naturwissenschaften und Mathematik::570 Biowissenschaften; Biologie::570 Biowissenschaften; Biologie

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APA (6^th Edition):

Schäffer, S. (2006). Investigations about the function of the cGMP-dependent kinase I alpha during the development of the nervous system. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-13474

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Schäffer, Susanne. “Investigations about the function of the cGMP-dependent kinase I alpha during the development of the nervous system.” 2006. Thesis, Freie Universität Berlin. Accessed January 16, 2021. http://dx.doi.org/10.17169/refubium-13474.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Schäffer, Susanne. “Investigations about the function of the cGMP-dependent kinase I alpha during the development of the nervous system.” 2006. Web. 16 Jan 2021.

Vancouver:

Schäffer S. Investigations about the function of the cGMP-dependent kinase I alpha during the development of the nervous system. [Internet] [Thesis]. Freie Universität Berlin; 2006. [cited 2021 Jan 16]. Available from: http://dx.doi.org/10.17169/refubium-13474.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Schäffer S. Investigations about the function of the cGMP-dependent kinase I alpha during the development of the nervous system. [Thesis]. Freie Universität Berlin; 2006. Available from: http://dx.doi.org/10.17169/refubium-13474

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

21. Dunn, Jessilyn. Genome-scale DNA methylation changes in endothelial cells by disturbed flow and its role in atherosclerosis.

Degree: PhD, Biomedical Engineering (Joint GT/Emory Department), 2015, Georgia Tech

URL: http://hdl.handle.net/1853/53536

► Atherosclerosis is an inflammatory disease of the arterial walls and is the major cause of heart attack and stroke. Atherosclerosis is localized to curves or… (more)

Subjects/Keywords: DNMT; Transcriptome; Shear stress; Disturbed flow; Atherosclerosis; HoxA5; Klf3; Endothelial cells; DNA methylome; Gene expression

…Global DNA Methylation Status In Vitro 30! DNMT Activity Assay 31! Monocyte adhesion assay… …siRNA Inhibits D-flow-induced Inflammation In Vitro 38! DNMT Inhibition by 5-Aza-2… …Figure 3.12: DNMT inhibition blocks OS-induced endothelial inflammation. 40! Figure 3.13… …Treatment with the DNMT inhibitor 5Aza inhibits atherosclerosis. 42! Figure 3.14: 5Aza treatment… …Disturbed flow DMR Differentially methylated region DNMT DNA (cytosine-5-)…

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APA (6^th Edition):

Dunn, J. (2015). Genome-scale DNA methylation changes in endothelial cells by disturbed flow and its role in atherosclerosis. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/53536

Chicago Manual of Style (16^th Edition):

Dunn, Jessilyn. “Genome-scale DNA methylation changes in endothelial cells by disturbed flow and its role in atherosclerosis.” 2015. Doctoral Dissertation, Georgia Tech. Accessed January 16, 2021. http://hdl.handle.net/1853/53536.

MLA Handbook (7^th Edition):

Dunn, Jessilyn. “Genome-scale DNA methylation changes in endothelial cells by disturbed flow and its role in atherosclerosis.” 2015. Web. 16 Jan 2021.

Vancouver:

Dunn J. Genome-scale DNA methylation changes in endothelial cells by disturbed flow and its role in atherosclerosis. [Internet] [Doctoral dissertation]. Georgia Tech; 2015. [cited 2021 Jan 16]. Available from: http://hdl.handle.net/1853/53536.

Council of Science Editors:

Dunn J. Genome-scale DNA methylation changes in endothelial cells by disturbed flow and its role in atherosclerosis. [Doctoral Dissertation]. Georgia Tech; 2015. Available from: http://hdl.handle.net/1853/53536

22. Skiles, William Mark. Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals.

Degree: PhD, Biomedical Sciences, 2017, Texas A&M University

URL: http://hdl.handle.net/1969.1/173200

► In recent years, there has been increased interest into better understanding how environmental In recent years, there has been increased interest into better understanding how… (more)

▼ In recent years, there has been increased interest into better understanding how environmental In recent years, there has been increased interest into better understanding how environmental exposures influence the long-term health of an organism. Chemical pollutants, dietary deficiencies, embryonic stress and multiple other external factors have all demonstrated long-lasting effects upon development, metabolism, and health even after transient exposures. The mechanisms by which these exposures can impact development far beyond the period of exposure remain largely unknown. To gain better insight into the developmental origins of both birth defects and disease, we must better understand how environmental exposures alter development. In this work, we will examine the capacity of the environment to impact chromatin states, and then determine whether these changes are heritable; and are thus potentially causal in the development of disease. This is an important question due to the recent recognition that aberrant chromatin states can lead to pathological patterns of gene expression, a circumstance commonly referred to as “epimutations”. Dysregulation of gene expression patterns during development have been shown to cause a multitude of irregular phenotypes in offspring and lifelong disorders in mature organisms. This altered chromatin state, coined an epimutation by Dr. Emma Whitelaw, is important due to the mutation not being in the genetic code itself, but in the way DNA regulatory regions are packaged within the chromatin template, and thus accessed by the protein factors directing gene transcription. The body of work presented here will examine the ability of common environmental exposures to modulate chromatin structure. We will examine these changes over time in an effort to better understand the inheritance of epigenetic change. Secondly, we will measure whether environmentally induced alterations in chromatin structure within the germline persist, and are heritable. These questions are all relevant to better understanding the developmental origins of disease. Advisors/Committee Members: Golding, Michael C (advisor), Long, Charles R (advisor), Seabury, Christopher M (committee member), Johnson, Natalie M (committee member).

Subjects/Keywords: oxidative stress; assisted reproductive technologies; genomic imprinting; histone demethylase; TET; DNMT; DNA methylation; epigenetics; developmental programming; DOHAD; birth defect; epigenetics; preconception; sperm

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APA (6^th Edition):

Skiles, W. M. (2017). Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/173200

Chicago Manual of Style (16^th Edition):

Skiles, William Mark. “Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals.” 2017. Doctoral Dissertation, Texas A&M University. Accessed January 16, 2021. http://hdl.handle.net/1969.1/173200.

MLA Handbook (7^th Edition):

Skiles, William Mark. “Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals.” 2017. Web. 16 Jan 2021.

Vancouver:

Skiles WM. Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals. [Internet] [Doctoral dissertation]. Texas A&M University; 2017. [cited 2021 Jan 16]. Available from: http://hdl.handle.net/1969.1/173200.

Council of Science Editors:

Skiles WM. Environmentally Induced Epimutations, Their Persistence, and Potential Causality in the Development of Disease in the Offspring of Exposed Individuals. [Doctoral Dissertation]. Texas A&M University; 2017. Available from: http://hdl.handle.net/1969.1/173200

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Open Access Theses and Dissertations