Gotowe bibliografie tematyczne / Dot1x

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Gotowa bibliografia na temat „Dot1x”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 15 lutego 2022

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Artykuły w czasopismach na temat "Dot1x"

Zhang, Wenzheng, Zhiyuan Yu, Hongyu Wu, Lihe Chen, Qun Kong та Bruce C. Kone. "An Af9 cis-element directly targets Dot1a to mediate transcriptional repression of the αENaC gene". American Journal of Physiology-Renal Physiology 304, № 4 (2013): F367—F375. http://dx.doi.org/10.1152/ajprenal.00537.2011.

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The epithelial Na+ channel subunit-α ( αENaC) of the distal nephron is essential for salt balance. We previously demonstrated that the histone methyltransferase Dot1a and its protein partner Af9 basally repress αENaC transcription in mouse inner medullary collecting duct type 3 (mIMCD3) cells and link aldosterone-elicited chromatin modifications to αENaC transcriptional activation. Af9 DNA-binding activity has never been demonstrated, and whether and where Af9 binds to the αENaC promoter to target Dot1a are unknown. The present study sought to identify functional Af9 cis-element(s) in the −57/

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Zhang, Long, Lihe Chen, Chao Gao, et al. "Loss of Histone H3 K79 Methyltransferase Dot1l Facilitates Kidney Fibrosis by Upregulating Endothelin 1 through Histone Deacetylase 2." Journal of the American Society of Nephrology 31, no. 2 (2019): 337–49. http://dx.doi.org/10.1681/asn.2019070739.

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BackgroundThe progression rate of CKD varies substantially among patients. The genetic and epigenetic contributions that modify how individual patients respond to kidney injury are largely unknown. Emerging evidence has suggested that histone H3 K79 methyltransferase Dot1l has an antifibrotic effect by repressing Edn1, which encodes endothelin 1 in the connecting tubule/collecting duct.MethodsTo determine if deletion of the Dot1l gene is a genetic and epigenetic risk factor through regulating Edn1, we studied four groups of mice: wild-type mice, connecting tubule/collecting duct–specific Dot1l

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Wysocki, Robert, Ali Javaheri, Stéphane Allard, Fei Sha, Jacques Côté, and Stephen J. Kron. "Role of Dot1-Dependent Histone H3 Methylation in G1 and S Phase DNA Damage Checkpoint Functions of Rad9." Molecular and Cellular Biology 25, no. 19 (2005): 8430–43. http://dx.doi.org/10.1128/mcb.25.19.8430-8443.2005.

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ABSTRACT We screened radiation-sensitive yeast mutants for DNA damage checkpoint defects and identified Dot1, the conserved histone H3 Lys 79 methyltransferase. DOT1 deletion mutants (dot1Δ) are G1 and intra-S phase checkpoint defective after ionizing radiation but remain competent for G2/M arrest. Mutations that affect Dot1 function such as Rad6-Bre1/Paf1 pathway gene deletions or mutation of H2B Lys 123 or H3 Lys 79 share dot1Δ checkpoint defects. Whereas dot1Δ alone confers minimal DNA damage sensitivity, combining dot1Δ with histone methyltransferase mutations set1Δ and set2Δ markedly enha

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Wu, Aiwei, Junhong Zhi, Tian Tian, et al. "DOT1L complex regulates transcriptional initiation in human erythroleukemic cells." Proceedings of the National Academy of Sciences 118, no. 27 (2021): e2106148118. http://dx.doi.org/10.1073/pnas.2106148118.

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DOT1L, the only H3K79 methyltransferase in human cells and a homolog of the yeast Dot1, normally forms a complex with AF10, AF17, and ENL or AF9, is dysregulated in most cases of mixed-lineage leukemia (MLLr), and has been believed to regulate transcriptional elongation on the basis of its colocalization with RNA polymerase II (Pol II), the sharing of subunits (AF9 and ENL) between the DOT1L and super elongation complexes, and the distribution of H3K79 methylation on both promoters and transcribed regions of active genes. Here we show that DOT1L depletion in erythroleukemic cells reduces its g

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Singer, Miriam S., Alon Kahana, Alexander J. Wolf, et al. "Identification of High-Copy Disruptors of Telomeric Silencing in Saccharomyces cerevisiae." Genetics 150, no. 2 (1998): 613–32. http://dx.doi.org/10.1093/genetics/150.2.613.

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Abstract The ends of chromosomes in Saccharomyces cerevisiae initiate a repressive chromatin structure that spreads internally and inhibits the transcription of nearby genes, a phenomenon termed telomeric silencing. To investigate the molecular basis of this process, we carried out a genetic screen to identify genes whose overexpression disrupts telomeric silencing. We thus isolated 10 DOT genes (disruptor of telomeric silencing). Among these were genes encoding chromatin component Sir4p, DNA helicase Dna2p, ribosomal protein L32, and two proteins of unknown function, Asf1p and Ifh1p. The coll

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Kim, Wootae, Ranah Kim, Geunyeong Park, Jong-Wan Park, and Ja-Eun Kim. "Deficiency of H3K79 Histone Methyltransferase Dot1-like Protein (DOT1L) Inhibits Cell Proliferation." Journal of Biological Chemistry 287, no. 8 (2011): 5588–99. http://dx.doi.org/10.1074/jbc.m111.328138.

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Kim, Wootae, Minji Choi, and Ja-Eun Kim. "The histone methyltransferase Dot1/DOT1L as a critical regulator of the cell cycle." Cell Cycle 13, no. 5 (2014): 726–38. http://dx.doi.org/10.4161/cc.28104.

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Puddu, Fabio, Magda Granata, Lisa Di Nola, et al. "Phosphorylation of the Budding Yeast 9-1-1 Complex Is Required for Dpb11 Function in the Full Activation of the UV-Induced DNA Damage Checkpoint." Molecular and Cellular Biology 28, no. 15 (2008): 4782–93. http://dx.doi.org/10.1128/mcb.00330-08.

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ABSTRACT Following genotoxic insults, eukaryotic cells trigger a signal transduction cascade known as the DNA damage checkpoint response, which involves the loading onto DNA of an apical kinase and several downstream factors. Chromatin modifications play an important role in recruiting checkpoint proteins. In budding yeast, methylated H3-K79 is bound by the checkpoint factor Rad9. Loss of Dot1 prevents H3-K79 methylation, leading to a checkpoint defect in the G1 phase of the cell cycle and to a reduction of checkpoint activation in mitosis, suggesting that another pathway contributes to Rad9 r

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Wood, Adam, Jessica Schneider, and Ali Shilatifard. "Cross-talking histones: implications for the regulation of gene expression and DNA repair." Biochemistry and Cell Biology 83, no. 4 (2005): 460–67. http://dx.doi.org/10.1139/o05-116.

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The regulation of chromatin structure is essential to life. In eukaryotic organisms, several classes of protein exist that can modify chromatin structure either through ATP-dependent remodeling or through the post-translational modification of histone proteins. A vast array of processes ranging from transcriptional regulation to DNA repair rely on these histone-modifying enzymes. In the last few years, enzymes involved in the post-translational modification of histone proteins have become a topic of intense interest. Our work and the work of several other laboratories has focused largely on un

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Jo, Stephanie Y., Eric M. Granowicz, Ivan Maillard, Dafydd Thomas, and Jay L. Hess. "Requirement for Dot1l in murine postnatal hematopoiesis and leukemogenesis by MLL translocation." Blood 117, no. 18 (2011): 4759–68. http://dx.doi.org/10.1182/blood-2010-12-327668.

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Abstract Disruptor of telomeric silencing 1-like (Dot1l) is a histone 3 lysine 79 methyltransferase. Studies of constitutive Dot1l knockout mice show that Dot1l is essential for embryonic development and prenatal hematopoiesis. DOT1L also interacts with translocation partners of Mixed Lineage Leukemia (MLL) gene, which is commonly translocated in human leukemia. However, the requirement of Dot1l in postnatal hematopoiesis and leukemogenesis of MLL translocation proteins has not been conclusively shown. With a conditional Dot1l knockout mouse model, we examined the consequences of Dot1l loss in

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Rozprawy doktorskie na temat "Dot1x"

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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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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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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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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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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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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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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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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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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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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Części książek na temat "Dot1x"

Bon, Corentin, Yang Si, and Paola B. Arimondo. "Targeting DOT1L for mixed-lineage rearranged leukemia." In Histone Modifications in Therapy. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-816422-8.00005-2.

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De Vos, Dirk, Hanneke Vlaming, Barbara M. Bakker, and Fred van Leeuwen. "Modeling Distributive Histone Modification by Dot1 Methyltransferases." In Epigenetics and Systems Biology. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-803075-2.00006-4.

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Streszczenia konferencji na temat "Dot1x"

Guppy, Brent, and Kirk McManus. "Abstract 117: DOT1L is a human chromosome stability gene." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-117.

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Klopp, Adam, Jack Schultz, and Ali Tajaddini. "Passenger Vehicle Characterization, Modeling, Validation, and Sensitivity Analysis." In 2018 Joint Rail Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/jrc2018-6194.

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As part of the vehicle qualification process, the Federal Railroad Administration (FRA) currently requires in its track and passenger equipment safety standards that a validated vehicle model be used to demonstrate safe dynamic vehicle response to allowable track geometry variations. Transportation Technology Center, Inc. (TTCI) was contracted by FRA to characterize, model, and analyze a high speed passenger vehicle in order to provide guidance related to the vehicle qualification process. The overall objective of the project was to evaluate methods required to demonstrate the validity of a ve

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Zhang, Yaqi, Yinu Wang, Guangyuan Zhao, and Daniela Matei. "Abstract A80: Targeting ovarian cancer stem cell by Dot1L inhibition." In Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research; September 13-16, 2019; Atlanta, GA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.ovca19-a80.

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Richon, Victoria M. "Abstract SY02-01: Targeting the histone methyltransferase DOT1L inMLL-rearranged leukemia." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-sy02-01.

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Berghen, Nathalie, Ellen De Langhe, and Rik Lories. "AB0200 INHIBITION OF DOT1L ACTIVITY IN HUMAN SKIN FIBROBLASTS: A TRANSCRIPTOME ANALYSIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.1023.

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Grigsby, Sierrah Marie, Jennifer Chase, Bridget Waas, et al. "Abstract 1380: Towards peptidomimetics to target DOT1L recruitment in MLL-AF9 leukemia." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1380.

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Riedel, Simone, Jessica Haladyna, Brett Stevens, et al. "Abstract IA11: Meningioma-1 cooperates with MLL and DOT1L to induce leukemia." In Abstracts: AACR Special Conference: Advances in Pediatric Cancer Research: From Mechanisms and Models to Treatment and Survivorship; November 9-12, 2015; Fort Lauderdale, Florida. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.pedca15-ia11.

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Wong, Matthew, Andrew Tee, Giorgio Milazzo, et al. "Abstract LB-080: The histone methyltransferase DOT1L promotes neuroblastoma by regulating gene transcription." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-lb-080.

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Gibbons, Garrett, Chenxi Shen, Andrew Muntean, Stephanie Jo, Jay Hess, and Zaneta Nikolovska-Coleska. "Abstract A158: Therapeutic strategies for targeting histone methyltransferase DOT1L in MLL rearranged leukemia." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a158.

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Lumba, Bhavna, and Charles S. Hemenway. "Abstract 278: Role of AF4 and Dot1 in MLL-AF9 mediated leukemogenesis." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-278.

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