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Dissertations / Theses on the topic 'Dot1x'

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1

Engfors, Emil, and Jens Markstedt. "Packetfence och Cisco ISE : En jämförelse av NAC." Thesis, Luleå tekniska universitet, Institutionen för system- och rymdteknik, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:ltu:diva-65035.

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Syftet med detta arbete var att jämföra de två mjukvarorna Packetfence och Cisco Identity Services Engine. Målet är att bilda en förståelse kring hur den här typen av mjukvaror kan implementeras i ett nätverk av olika storlekar och även en insikt över hur detta kan minska den administrativa belastningen. Den här typen av system kan även användas för att centralt styra åtkomst till ett företags resurser och kan säkra upp olika typ av enheter och program. Det genomfördes en installation för att upptäcka skillnader mellan systemen, därefter konfigurerades de så likt varandra som möjligt för att
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2

Manfredsson, Alexander. "Spårbarhet i ett nätverk : En jämförelse mellan IPsec och 802.1x." Thesis, Linnéuniversitetet, Institutionen för datavetenskap, fysik och matematik, DFM, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-23777.

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På ett företag eller universitet finns det oftast regler/policys som förklarar hur manfår använda deras nätverk. Om någon bryter mot reglerna vill man kunna identifierapersonen. Denna rapport inriktar sig på att identifiera en användare i ett nätverk. För att kunna identifiera en användare behöver man uppnå spårbarhet. En jämförelsemellan två teknologier (IPsec och dot1x) utfördes, två testmiljöer för detta sattes uppen för vardera teknologi. PfSense (routern) ansluter användarna från det internanätverket till det externa. I routern kan man sedan med hjälp av Packet Capture sevad användaren gö
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3

Gray, de Cristoforis Angelica [Verfasser], and Tanja [Akademischer Betreuer] Vogel. "Role of DOT1L in spinal cord formation." Freiburg : Universität, 2021. http://d-nb.info/1238016545/34.

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4

Godfrey, Laura. "The role of DOT1L in MLL-AF4 leukaemia." Thesis, University of Oxford, 2018. https://ora.ox.ac.uk/objects/uuid:9a1ad020-202a-4413-b9be-cdef28b2d124.

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DOT1L is a methyltransferase which has been shown to methylate H3K79 (Ng et al. 2002; Feng et al. 2002; Lacoste et al. 2002). DOT1L and H3K79me have been shown to be involved in active transcription and in particular has been shown to be important for MLL-AF4 leukaemia, where high levels of H3K79me are found at MLL-AF4 gene targets (Krivtsov et al. 2008; Bernt et al 2011). The exact mechanism of how DOT1L is recruited to MLL-AF4 gene targets leading to high levels of H3K79me is currently unknown, especially as it has been demonstrated that AF4 and DOT1L exist in mutually exclusive complexes (L
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5

Zhovmer, Alexander. "Nouveaux acteurs à l'interface de la transcription et de la réparation." Phd thesis, Université de Strasbourg, 2012. http://tel.archives-ouvertes.fr/tel-00755451.

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Les résultats du criblage siRNA destiné à identifier de nouveaux acteurs de la NER, sont en court d'exploitation mais nous mettons déjà en évidence le rôle de certains gènes impliqués dans la biochimie des ARNm comme ceux empêchant la formation des hybrides ARN/ADN dans l'efficacité de réparation des lésions UV. En étudiant le rôle de la methyltransférase DOT1L, nous avons montré que son absence dans des fibroblastes embryonnaires de souris (MEFDOT1L) conduit à une sensibilité de ces cellules aux irradiations UV alors que la réparation des lésions produites par cette irradiation est intacte. L
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6

Sabra, Mirna. "Caractérisation de la réponse à l’instabilité des centromères (iCDR) déclenchée par la protéine ICP0 du Virus Herpès Simplex de type 1 (HSV-1)." Thesis, Lyon 1, 2010. http://www.theses.fr/2010LYO10022.

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L’infection par le virus de l’herpès simplex de type 1 (HSV-1), un virus pathogène humain majeur, engendre la déstabilisation des centromères. Cette déstabilisation est induite par la protéine virale ICP0, et entraîne la dégradation par ICP0, via le protéasome, des protéines CENP-A, -B et CENP-C. Des résultats obtenus au laboratoire ont mis en évidence le phénomène iCDR (pour interphase Centromere Damage Response) qui implique la redistribution de la coïline, fibrillarine et SMN dans ces structures centromériques déstabilisées par ICP0 mais également par des drogues ou des siRNAs dirigés contr
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7

Ferrari, Francesco [Verfasser], and Thomas [Akademischer Betreuer] Manke. "Computational analysis of global and DOT1L-dependent epigenetic dynamics during in-vitro neuronal differentiation." Freiburg : Universität, 2020. http://d-nb.info/1219851280/34.

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8

Chen, Liying Michelle. "Targeting the Epigenetic Lesion in MLL-Rearranged Leukemia." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10663.

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It has become increasingly apparent that the misregulation of histone modification actively contributes to cancer. The histone H3 lysine 79 (H3K79) methyltransferase Dot1l has been implicated in the development of leukemias bearing translocations of the Mixed Lineage Leukemia (MLL) gene. We studied the global epigenetic profile for H3K79 dimethylation and found abnormal H3K79 dimethylation profiles exist not only in leukemias driven by MLL-fusion proteins with nuclear partners like AF9, but also in leukemia with MLL-fusions containing cytoplasmic partners like AF6. Genetic inactivation of Dot1
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9

Castillo, Aguilera Omar. "Conception, synthèse et évaluation pharmacologique d’inhibiteurs potentiels de DOT1L impliqués dans la régulation épigénétique du cancer." Thesis, Lille 2, 2017. http://www.theses.fr/2017LIL2S053/document.

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Le cancer, principale cause de mortalité dans le monde, est un problème majeur de santé publique. Malgré les nombreux traitements disponibles, il est nécessaire de développer de nouvelles thérapies plus efficaces et moins envahissantes. Aujourd’hui la connaissance du génome humain a dirigé la recherche vers de nouvelles approches: il est possible de moduler la réponse biologique en contrôlant l'accès aux informations génétiques via la régulation épigénétique.L’épigénétique est l’ensemble des modifications de l’expression des gènes n’entraînant pas de modifications dans la séquence d’ADN, qui m
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10

Spurr, Sophie S. "Design, synthesis and evaluation of novel small molecule inhibitors of the histone methyltransferase DOT1L and ubiquitination facilitator Keap1." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10038412/.

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This thesis details the design, synthesis and evaluation of novel small molecule inhibitors of the histone methyltransferase DOT1L and the ubiquitination facilitator Keap1. The thesis is in two parts as outlined below. Part 1: The first part of this thesis details efforts towards identification of novel small molecule inhibitors of DOT1L, a histone methyltransferase which has been implicated in the development and proliferation of mixed lineage leukaemias (MLL). This work aims to optimise the drug-like properties of published DOT1L inhibitors while retaining potency, through further exploratio
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11

Dindar, Gülcin [Verfasser], and Christian [Gutachter] Janzen. "Molecular basis for product-specificity of DOT1 methyltransferases in Trypanosoma brucei / Gülcin Dindar. Gutachter: Christian Janzen." Würzburg : Universität Würzburg, 2014. http://d-nb.info/1102827541/34.

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12

Gassen, Alwine. "Functional analysis of DOT1-dependent histone H3 lysine 76 methylation during cell cycle progression in Trypanosoma brucei." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-151275.

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13

Eisenhuth, Nicole Juliana [Verfasser], Christian J. [Gutachter] Janzen, Klaus [Gutachter] Brehm, and Falk [Gutachter] Butter. "Novel and conserved roles of the histone methyltransferase DOT1B in trypanosomatid parasites / Nicole Juliana Eisenhuth ; Gutachter: Christian J. Janzen, Klaus Brehm, Falk Butter." Würzburg : Universität Würzburg, 2021. http://d-nb.info/1225296048/34.

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14

Raul, Sanjay Kumar [Verfasser], Steven A. [Akademischer Betreuer] Johnsen, Thomas [Gutachter] Meyer, and Michael [Gutachter] Zeisberg. "The histone methyltransferase DOT1L is required for DNA damage recognition and repair / Sanjay Kumar Raul ; Gutachter: Thomas Meyer, Michael Zeisberg ; Betreuer: Steven A. Johnsen." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2017. http://d-nb.info/1135778256/34.

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15

Gassen, Alwine [Verfasser], and Michael [Akademischer Betreuer] Boshart. "Functional analysis of DOT1-dependent histone H3 lysine 76 methylation during cell cycle progression in Trypanosoma brucei / Alwine Gassen. Betreuer: Michael Boshart." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2012. http://d-nb.info/1029662096/34.

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16

Rendeiro, André Figueiredo. "Regulation of Oikopleura dioica's alternative cell cycle modes." Master's thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/13425.

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Mestrado em Biologia Molecular e Celular<br>The eukaryotic cell cycle is one of the most studied biological processes. However, variations of the canonical cell cycle have been discovered and found to be more predominant than previously expected. Endoreplication and endocycling - two such variants - produce polyploid cells, conferring advantages in growth and genotoxic stress. Although some of the regulatory principles of these cycles are being discovered, little is known about how cells can transition from a mitotic cell cycle to them. Recently, it has been proposed that methylation of
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17

Parsons, Michelle L. "The Role of SIR4 in the Establishment of Heterochromatin in the Budding Yeast Saccharomyces cerevisiae." Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31028.

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Heterochromatin in the budding yeast Saccharomyces cerevisiae is composed of polymers of the SIR (Silent Information Regulator) complex bound to nucleosomal DNA. Assembly of heterochromatin requires all three proteins of the Sir complex: the histone deacetylase Sir2, and histone binding proteins Sir3 and Sir4. Heterochromatin establishment requires passage through at least one cell cycle, but is not dependent on replication. Inhibition of chromatin modifying enzymes may be a mechanism for how cells limit assembly. Dot1 dependent methylation of H3K79 is suggested to inhibit de novo assembly. Ha
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18

Eisenhuth, Nicole Juliana. "Novel and conserved roles of the histone methyltransferase DOT1B in trypanosomatid parasites." Doctoral thesis, 2021. https://doi.org/10.25972/OPUS-21993.

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The family of trypanosomatid parasites, including the human pathogens Trypanosoma brucei and Leishmania, has evolved sophisticated strategies to survive in harmful host environments. While Leishmania generate a safe niche inside the host’s macrophages, Trypanosoma brucei lives extracellularly in the mammalian bloodstream, where it is constantly exposed to the attack of the immune system. Trypanosoma brucei ensures its survival by periodically changing its protective surface coat in a process known as antigenic variation. The surface coat is composed of one species of ‘variant surface glycoprot
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19

Raul, Sanjay Kumar. "The histone methyltransferase DOT1L is required for DNA damage recognition and repair." Doctoral thesis, 2016. http://hdl.handle.net/11858/00-1735-0000-002B-7D2D-A.

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20

"The role of histone H3K79 methyltransferase Dot1l in renal development, injury and repair." Tulane University, 2013.

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21

Dindar, Gülcin. "Molecular basis for product-specificity of DOT1 methyltransferases in Trypanosoma brucei." Doctoral thesis, 2014. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-102524.

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Post-translational histone modifications (PTMs) such as methylation of lysine residues influence chromatin structure and function. PTMs are involved in different cellular processes such as DNA replication, transcription and cell differentiation. Deregulations of PTM patterns are responsible for a variety of human diseases including acute leukemia. DOT1 enzymes are highly conserved histone methyltransferases that are responsible for methylation of lysine 79 on histone H3 (H3K79). Most eukaryotes contain one single DOT1 enzyme, whereas African trypanosomes have two homologues, DOT1A and DOT1B, w
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22

"Characterization of specific roles for AF4 and Dot1 in transformation mediated by MLL-AF9 leukemic oncoprotein." Tulane University, 2011.

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Chromosomal translocations involving the mixed-lineage leukemia (MLL) gene lead to acute myeloid or lymphoid leukemias that are often associated with poor prognosis, particularly in infants. The translocations result in in-frame fusion between MLL and one of the over sixty known partner genes that are heterogeneous in nature. AF4 and AF9 are two of the most common MLL fusion partners. Importantly, they also interact specifically with each other in subnuclear foci. An AF4-mimetic peptide which disrupts the AF4-AF9 interaction is able to cause necrotic cell death in leukemic cell lines harboring
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