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Dissertations / Theses on the topic 'Dapke'

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Published: 5 June 2025

Last updated: 16 July 2025

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1

Holzapfel, Elaine Kester. "The Paleoamerican occupation of Darke County, Ohio, and environs." Virtual Press, 2001. http://liblink.bsu.edu/uhtbin/catkey/1204195.

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This thesis develops and executes a method of comprehensively discovering accessible Paleoamerican archaeological materials from a restricted geographic area, analyzing the data collected, and comparing them within a larger sphere of interaction. The restricted area was Darke County, in west-central Ohio. The study area was familiar to the writer both in field experience and knowledge of collections held by local residents. A total of 115 diagnostic points and additional tools were located, examined, photographed, and measured.On the basis of point typology three stages of Paleoamerican occupation were identified, Early (11, 500 to 10, 500 B. P.), Middle (11,000 to 10, 500 B. P.), and Late (10,500 to 10,000 B. P.). The Early Paleoamerican stage was marked by Clovis fluted and Unfluted fluted points, the Middle by the Cumberland point, and the Late by Agate Basin, Transitional, Plano Lanceolate, and Hi-Lo points. The sources of raw materials were identified and changes of habitat through time were described.The abundant data recovered and analyzed by the approach used in this study from just one Ohio county indicates that extensive data is available but has yet to be recorded and analyzed for Paleoamerican occupation throughout Midwestern United States.<br>Department of Anthropology

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2

Lin, Yao. "Control of DAPK-1 degradation." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/4189.

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DAPK-1 is calcium-calmodulin regulated protein kinase involved in multiple cellular pathways including apoptosis, autophagy, cell survival and motility. The cytokine TNF-α has been reported to induce the degradation of DAPK-1. Here I identified the protease cathepsin B as a novel binding partner of DAPK-1 that protects DAPK-1 from TNF-α induced degradation. Using deletion mutants of DAPK-1, I mapped the cathepsin B binding domain on DAPK-1 to amino acids 836-947. Overexpression of this mini-protein DAPK-1(836-947) facilitated degradation of full-length DAPK-1 and apoptosis induced by TNFR-1. Moreover, siRNA mediated knock-down of DAPK-1 enhanced TNF-α induced apoptosis, confirming the role of DAPK-1 as a survival factor in the TNF-α signalling pathway. In addition, a splice variant of DAPK-1, which I have called s-DAPK-1, was discovered. s-DAPK-1 shares part of DAPK-1’s ankyrin repeats region and cytoskeletal binding domain, and possesses an unique tail region, which contains a cleavage site at its first two amino acids. Unlike DAPK-1, s-DAPK-1 does not contribute to apoptosis induced by high level of MEK/ERK signalling, but it does mimic DAPK-1’s function to induce membrane blebbing. The proteolytically processed form of s-DAPK-1 is more active in the induction of membrane blebbing, which may be due to its higher stability compared to that of full-length s-DAPK-1, suggesting that the tail region can control s-DAPK-1 stability and activity. Co-transfection of s-DAPK-1 and DAPK-1 leads to reduction in DAPK-1 expression level, suggesting a role for s-DAPK-1 to regulate DAPK-1 stability. The kinase domain of DAPK-1 is the region required for s-DAPK-1 to promote DAPK-1 degradation. Surprisingly, s-DAPK-1 does not bind directly to DAPK-1, suggesting that the interaction is indirect and mediated by as yet unidentified accessory proteins. Finally, the experiments with proteasome and lysosome inhibitors indicated that s-DAPK-1 induces DAPK-1 degradation via both lysosome and proteasome pathways.

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3

Flynn, Patrick G. "Activation of Non-Muscle Myosin IIB Helps Mediate TNF-Alpha Cell Death Signaling." Scholarly Repository, 2010. http://scholarlyrepository.miami.edu/oa_dissertations/369.

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TNF-alpha can stimulate a variety of kinases with the ability to activate non-muscle myosin II. As a result, increases in actin filament formation and actomyosin contractility (AMC) have been reported in response to TNF-alpha. These events are thought to play an important role in mediating TNF-alpha induced apoptosis but how they do so is unclear. In this study we prevented non-muscle myosin II activation in response to TNF-alpha by treating cells with the myosin light chain kinase (MLCK) inhibitor ML-7 or through isoform specific siRNA knockdown of myosin IIA and IIB. We found that treatment with ML-7 or knockdown of myosin IIB, but not IIA, impaired the cleavage of caspase 3 and caspase 8 as well as nuclear condensation in response to TNF-alpha. During this cell death process myosin II seemed to function independent of AMC since treatment of cells with blebbistatin or cytochalasin D failed to inhibit TNF-alpha induced caspase cleavage. Immunoprecipitation studies revealed associations of myosin IIB with clathrin and FADD in response to TNF-alpha suggesting a role for myosin IIB in TNFR1 endocytosis and DISC formation. Taken together these findings suggest that myosin IIB activation promotes TNF-alpha cell death signaling in a manner independent of its force generating property.

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4

Nilsson, Ulf. "Nils Dacke och Dackefejden : Forskningens väg till läroboken." Thesis, Växjö University, School of Education, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:vxu:diva-1386.

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5

Dalpke, Raphael [Verfasser]. "Transport Behavior of Tailored Carbon Nanomembranes / Raphael Dalpke." Bielefeld : Universitätsbibliothek Bielefeld, 2020. http://d-nb.info/1220028282/34.

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6

Eriksson, Johan. "Tidens sand blästra fram ett nytt ansikte : En litteraturstudie om Nils Dacke." Thesis, Högskolan i Jönköping, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:hj:diva-38724.

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7

Lehnert, Katrin. ""Arbeit, nein danke"!? : das Bild des Sozialschmarotzers im aktivierenden Sozialstaat." München Utz, 2009. http://deposit.d-nb.de/cgi-bin/dokserv?id=3337703&prov=M&dokv̲ar=1&doke̲xt=htm.

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8

Golgath, Tabea [Verfasser]. ""Langweilige Museen? Nein, danke!" : nachhaltige Vermittlungsmethoden in Ausstellungen / Tabea Golgath." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover (TIB), 2011. http://d-nb.info/1020076135/34.

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9

Lehnert, Katrin. ""Arbeit, nein danke"!? das Bild des Sozialschmarotzers im aktivierenden Sozialstaat." München Utz, 2006. http://d-nb.info/995537054/04.

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10

Kupčinskaitė, Rita, and Rita Kupčinskaitė-Noreikienė. "Genų, susijusių su apoptoze ir dnr pažaidų atitaisymu, metilinimo ypatumai skrandžio onkogenezės pakopiniame procese." Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2013. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2013~D_20130919_143632-54949.

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DNR pažaidų atitaisymas ir apoptozė - dvi pagrindinės grandys, palaikančios žmogaus genomo vientisumą. Sutrikus šiems procesams, ląstelė išgyvena, nepaisant susikaupusių DNR pažaidų ir sudaromas pagrindas tolesnei transformacijai. Tyrimu įvertinome DNR pažaidų atitaisymo funkcijoje dalyvaujančių (hMLH1, MGMT) ir su apoptoze susijusių (DAPK-1, CASP8) genų epigenetinio reguliavimo - metilinimo aspektus pakopiniame skrandžio onkogenezės procese. Šio mokslinio tyrimo metu pirmą kartą buvo nustatytas skirtingas hMLH1 geno metilinimo dažnis atskirose skrandžio anatominėse dalyse atrofiniu pangastritu sergančiųjų audinyje. Įvertinta, kad hMLH1 geno metilinimas sergančiųjų skrandžio vėžiu aplinkiniame nenavikiniame audinyje sietinas su pacientų amžiumi. Išgyvenamumo analizės rezultatai parodė, kad MGMT geno metilinimas agresyvios skrandžio vėžio histologinės formos atveju yra geresnės prognozės rodiklis. Tyrimo metu nustatėme mokslinėje periodikoje neaprašytų tirtųjų genų metilinimo derinių sąsajų su klinikiniais, morfologiniais ir prognoziniais onkologinės ligos ypatumais.<br>DNA repair and apoptosis are two main pathways supporting the integrity of human genome. After the disturbance of these processes the cell survives, despite the accumulation of DNA lesions, and in this way a basis for a subsequent transformation is formed. In our research we evaluated the epigenetic regulation - methylation - aspects of genes participating in DNA repair function (hMLH1 and MGMT) and also of apoptosis-related genes (DAPK-1, CASP8) in relation to a stepwise gastric oncogenesis process. During this investigation a different hMLH1 gene methylation observation frequency in tissues obtained from separate anatomical parts of the stomach in atrophic pangastritis patients was determined for the first time. It was estimated, that hMLH1 gene methylation in tumor-surrounding non-cancerous tissue in gastric cancer patients could be associated with patient age. Results of survival analysis indicated that MGMT gene methylation is an indicator of better prognosis in case of diffuse form of gastric cancer. During the study we determined some additional associations (not described in previous publications) between methylation combinations of analyzed genes and clinical, morphological and prognostic features of oncological illness.

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11

Tong, Amy. "Caenorhabditis Elegans DAPK-1 functions in epidermal damage responses /." Diss., Digital Dissertations Database. Restricted to UC campuses, 2008. http://uclibs.org/PID/11984.

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12

Schönborn, Julia [Verfasser], and Werner [Akademischer Betreuer] Frick. ""Danke für Deinen Eintrag ins Logbuch" : literarische Massenkommunikation im Social Web." Freiburg : Universität, 2015. http://d-nb.info/1120626374/34.

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13

Wayland, Luke. "Sanctifying a Darke Conceit: Seeing the Bible in the Faerie Queene." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:15821957.

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Approaching the poem from the perspective of reception history, the present dissertation seeks to show that the Bible’s role in The Faerie Queene is far more pervasive than has usually been recognized. Rather than see the biblical material as the domain of only certain sections—notably, Book I and perhaps Books II and V—I propose that it is to be seen as a meaningful presence throughout the poem. Indeed, I will argue that it provides a previously unnoticed, unifying structure to the whole. I begin by giving a brief sketch of the Bible in Spenser’s early life. From here, I draw upon the resources of modern biblical scholarship—specifically, Childs’ “canonical approach”—to describe the way Spenser read the Bible and, consequently, the ways in which he alluded to it. I go on to discuss the notions of “typology” and “allegory,” providing the foundation for a discussion of Spenser’s reading not only of the Bible, but of the ongoing narrative of history. Then follows an exploration of the ways Spenser seeks to relate the various legacies of the Classical and biblical past to his Christian, humanist present, which culminates in a description of the Christian canon’s structuring role within the poem. This leads to a reflection on this structure’s significance through consideration of the various instances of books and of reading that occur in Book I. I then take up this theme again in Book III, in the transformation of Malbecco and in the idolatrous Tabernacle-Temple of Busirane. Drawing upon the early modern discourse concerning images and idols, I conclude with a discussion of The Faerie Queene as a unified, poetic sign pointing to the Divine Presence—a function typified in the discarded ending of Book III.

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14

von, Daake Andreas [Verfasser]. "Beitrag zur Kalibrierung und anforderungsbasierten Arbeitsraumoptimierung parallelkinematischer Manipulatoren in Hexapodbauweise / Andreas von Daake." Clausthal-Zellerfeld : Universitätsbibliothek Clausthal, 2012. http://d-nb.info/1024391302/34.

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15

Steinvall, Alexander. "Mot de rovgiriga och mordiska bondehoparna : En komparativ studie mellan upprorsmännensklagomål och krav underDackefejden och det Tyska bondekriget." Thesis, Linnéuniversitetet, Institutionen för kulturvetenskaper (KV), 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-30643.

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The aim of this study is to make a comparative study between the grievances during the Dacke Warand the German Peasant´s War. These two conflicts may have occurred separately, regarding bothgeographical and chronological distances but also share common issues for this comparative study.Less than two decades separates these two conflicts and they were all by their own serious insurrectionsduring their time. While the German Peasant´s War was the greatest uprising in Europe up tothe French Revolution, the Dacke War was the biggest Peasant Rebellion in Scandinavian history.While the German Peasant War has been studied and researched by historians for a relative longtime, the Dacke War has been neglected in research history. If it were not for the Swedish professorLars-Olof Larsson’s studies during foremost in the 1960s, the Dacke War would have been a historicallyuncharted territory of research indeed. This study aims to foremost supplement the unsatisfiedresearch on the Dacke War, but also supplement the research of The German Peasant war, with thiscomparative study. Although is exists a somewhat considerable amount of studies and theories regardinggeneral peasant uprisings and revolts from this period, researchers are still debating themain causes for these violent conflicts. The combination of different geographical and social differencesand insufficient sources makes studies about theses conflicts both problematic and complex.The result of this comparative study, show that both uprisings shared both common and differentkinds of grievances where generally the rebels of the German Peasant´s War had a larger propotionof demands than the rebels of the Dacke War. In Sweden the grievances was largely made up bycomplaints. While the German Peasant´s War was generally more radical and religious motivatedthan the Dacke War, it shared many similarities to each other, especially when it came to economicand economical complaints. While the German Peasants (although not all rebel-groups) made radicaldemands, such as the abolishment of serfdom, the rebels during the Dacke War were more intenton restoring their former rights and customs. Therefore the Swedish peasantry motivated theircomplaints by claiming they had juridical rights and legal claims to motivate rebellion. The Germanpeasants on the other hand, although also sharing the same motives but in somewhat lesser degree,had less legal rights and therefore motivated their demands in religious terms. The reason why thegrievances during the Dacke War mostly can be categorized as complaints instead of demands, maybe explained how influential and political equal the Swedish peasants were as a social group and estatein Swedish society compared to the many peasants living in serfdom in the Holy Roman Empire.This is also why German rebels more often legitimized their demands with religious motive,because they lacked the political power as social group and estate.

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16

Kloos, Bianca [Verfasser], and Alexander [Akademischer Betreuer] Dalpke. "Mechanismen der Pasteurella multocida Toxin vermittelten Modulation des Osteoimmunsystems / Bianca Kloos ; Betreuer: Alexander Dalpke." Heidelberg : Universitätsbibliothek Heidelberg, 2017. http://d-nb.info/1180985826/34.

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17

Rimbach, Katharina [Verfasser], and Alexander [Akademischer Betreuer] Dalpke. "Inhibition of innate immune activation by modifications in bacterial RNA / Katharina Rimbach ; Betreuer: Alexander Dalpke." Heidelberg : Universitätsbibliothek Heidelberg, 2014. http://d-nb.info/1180300270/34.

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18

Klöss, Volker [Verfasser], and Alexander [Akademischer Betreuer] Dalpke. "Cooperation of innate immune cells during Hepatitis C virus infection / Volker Klöss ; Betreuer: Alexander Dalpke." Heidelberg : Universitätsbibliothek Heidelberg, 2017. http://d-nb.info/1180986814/34.

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19

Dake, Jules [Verfasser]. "Experimental investigations of microstructural coarsening in 3D using X-ray microscopy / Jules Dake." Ulm : Universität Ulm, 2020. http://d-nb.info/1208296272/34.

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20

Britschgi, Adrian. "DAPK2, EGCG and autophagy in neutrophil differentiation and retinoic acid-therapy of acute myeloid leukemic cells." [S.l.] : [s.n.], 2009. http://www.zb.unibe.ch/download/eldiss/09britschgi_a.pdf.

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21

Daake, Henning-Felix von [Verfasser]. "Möglichkeiten zur Optimierung der Wirkungsweise bauchemischer Zusatzmittel durch Mechanismen der kontrollierten Wirkstofffreisetzung / Henning-Felix von Daake." Kassel : Kassel University Press, 2016. http://d-nb.info/1109083793/34.

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22

Daake, Gert [Verfasser], and Ulrich [Akademischer Betreuer] Joos. "Permanente und temporäre Erblindung nach operativen Eingriffen am Orbitaboden bei Orbitabodenfrakturen / Gert Daake. Betreuer: Ulrich Joos." Münster : Universitäts- und Landesbibliothek der Westfälischen Wilhelms-Universität, 2012. http://d-nb.info/1027019099/34.

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23

Tucher, Christine [Verfasser], and Alexander [Akademischer Betreuer] Dalpke. "Charakterisierung extrazellulärer Vesikel und Analyse ihrer Bedeutung als Regulatoren der Immunantwort / Christine Tucher ; Betreuer: Alexander Dalpke." Heidelberg : Universitätsbibliothek Heidelberg, 2020. http://d-nb.info/1224684559/34.

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24

Konen, Michael Eugene. "Morphology and distribution of polygonal patterned ground and associated soils in Darke and Miami Counties, Ohio." Connect to resource, 1995. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1170954705.

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REIS, R. S. "Potencialidades dos Genes CD44, DAPK, MGMT e RUNX3 como Biomarcadores Epigenéticos no Câncer Oral." Universidade Federal do Espírito Santo, 2014. http://repositorio.ufes.br/handle/10/4493.

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Made available in DSpace on 2016-08-29T15:34:34Z (GMT). No. of bitstreams: 1 tese_8180_Dissertação_Raquel Reis.pdf: 1748568 bytes, checksum: 359aed01be42e32554969ef4cd5248e8 (MD5) Previous issue date: 2014-10-09<br>Potencialidades dos Genes CD44, DAPK, MGMT e RUNX3 como Biomarcadores Epigenéticos no Câncer Oral

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26

Alves, Catarina Silva de Carvalho Alexandre. "Plano de marketing do lançamento de uma água gourmet." Master's thesis, Instituto Superior de Economia e Gestão, 2011. http://hdl.handle.net/10400.5/10161.

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Mestrado em Marketing<br>Este projecto traduz-se na apresentação de um plano de marketing para o lançamento de uma água gourmet. O produto dá pelo nome de "Danke Cristal" e fará parte da unidade de negócio das águas & cervejas da empresa Sumol+Compal com o crescimento do portefólio da Água Serra da Estrela. O plano de marketing tem como principais objectivos reforçar a presença da marca no mercado das águas engarrafadas, posicionar a marcar no mercado das águas gourmet e, assim, aumentar a quota de mercado da Água Serra da Estrela.<br>This project consists in the presentation of a marketing plan to launch a premium water. The products name is "Danke Crystal" and will be part of the business unit of waters & beers of Sumol+Compal Group, by growing the portfolio of Serra da Estrela Water. The marketing plan has as main objectives to reinforce brand presence on the market of bottled water, place the brand on the premium water market and thereby increase the market share of Serra da Estrela Water.

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27

Steinvall, Alexander. "Slaget vid sjön Hjorten : The unknown battle of the Dacke war which settled the future of Sweden." Thesis, Växjö University, School of Humanities, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:vxu:diva-2415.

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28

Metzdorf, Daniela [Verfasser], and Alexander [Akademischer Betreuer] Dalpke. "Regulation der Toll-like Rezeptor-vermittelten Signaltransduktion durch die hämatopoetische GTPase RhoH / Daniela Metzdorf ; Betreuer: Alexander Dalpke." Heidelberg : Universitätsbibliothek Heidelberg, 2012. http://d-nb.info/1179785797/34.

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29

Soussi, Hedi. "Obésité et méta-inflammation : rôle du système lysosomal-autophagique et des protéines associées." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066273/document.

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L'obésité se caractérise par une accumulation excessive de masse grasse ainsi qu'un état inflammatoire chronique évoluant à bas bruit. Parmi les processus biologiques susceptibles de contribuer aux altérations méta-inflammatoires caractéristiques de l'obésité, nous étudions l'autophagie. Les données, relatives à la première étude, indiquent une diminution de l'activité autophagique adipocytaire des sujets obèses comparée aux sujets non-obèses. Les analyses transcriptomiques du laboratoire indiquent une forte diminution de l'expression du gène codant la Death Associated Protein Kinase 2 (DAPK2), chez les sujets obèses. De façon intéressante, l'inhibition de cette kinase induit une diminution de l'activité autophagique tandis qu'une surexpression augmente le processus dans des lignées adipocytaires. Nous observons également une restauration partielle et concomitante de l'activité autophagique et de l'expression génique de DAPK2 après perte de poids induite par chirurgie bariatrique chez les sujets obèses. L'ensemble de ces données montre un lien entre l'expression de DAPK2 et l'activité autophagique dans les adipocytes. La seconde étude est focalisée sur la lipase lysosomale (LIPA).. L'analyse de la topologie de son expression au cours de l'obésité n'indique pas de modulation d'expression génique. Néanmoins, une corrélation inverse entre l'adiposité et l'expression de la lipase lyosomale a été mise en évidence, suggérant un lien avec le stockage de lipides dans un contexte physiopathologique. Globalement, nos travaux indiquent des altérations adipocytaires du système lysosomal-autophagique, au cours de l'obésité<br>Obesity is characterized by excessive accumulation of body fat and a chronic inflammatory condition evolving low noise. In this context, storage and nutritional metabolic sensing represent a real challenge to systemic and cellular level. Among the biological processes that may contribute to alterations meta-inflammatory characteristics of obesity, we are studying autophagy. This lysosomal process, related to nutritional flow as well as the regulation of pro-inflammatory signaling, allows the degradation dysfunctional organelles.The data relating to the first study indicate a decrease in adipocyte autophagic activity in obese subjects compared to non-obese subjects, and an inverse correlation between adipocyte hypertrophy and autophagic activity, suggesting a link with the lipid storage. The laboratory transcriptomic analyzes indicate a strong decrease in the expression of the gene encoding the Death Associated Protein Kinase 2 (DAPK2), in obese subjects. Interestingly, inhibition of this kinase induces a reduction of autophagic activity while overexpression increases the process of adipocyte cell lines. We also observe a partial and concomitant restoration of autophagic activity and gene expression after DAPK2 weight loss induced by bariatric surgery in obese subjects, strengthening the role of this kinase in regulating autophagy and adipocyte homeostasis. All these data show a link between the expression of DAPK2 and autophagic activity in adipocytes, suggesting that a lack of regulation of this kinase activity could help adipocyte dysfunction observed in obesity . The second study focused on the lysosomal lipase (LIPA). This protein, located at the interface of the immunological and metabolic regulation, participates in the catabolism of lipids. The analysis of the topology of its expression during obesity does not indicate a modulation of gene expression. However, an inverse correlation between adiposity and the expression of lyosomale lipase was demonstrated, suggesting a link with the storage of lipids in a pathophysiologic context. Overall, our work indicates adipocyte alterations of lysosomal-autophagic system during obesity. This type of alteration is present in several tissues, pharmacological approach could thus be envisaged in a systemic therapeutic context

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Eberle, Mariel-Esther [Verfasser], and Alexander [Akademischer Betreuer] Dalpke. "Induction and properties of SOCS1 in myeloid cells by activation of Dectin-1 / Mariel-Esther Eberle ; Betreuer: Alexander Dalpke." Heidelberg : Universitätsbibliothek Heidelberg, 2012. http://d-nb.info/1179785487/34.

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Gandesiri, Muktheshwar [Verfasser], and Robert [Akademischer Betreuer] Slany. "LBH589-induced DAPK activation triggers apoptosis and autophagy in human colon tumor cells / Muktheshwar Gandesiri. Betreuer: Robert Slany." Erlangen : Universitätsbibliothek der Universität Erlangen-Nürnberg, 2013. http://d-nb.info/1033029874/34.

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Chakilam, Saritha [Verfasser], and Wolfgang [Akademischer Betreuer] Kreis. "Negative regulation between DAPK and STAT3 in intestinal epithelial cells under TNF-stimulus / Saritha Chakilam. Betreuer: Wolfgang Kreis." Erlangen : Universitätsbibliothek der Universität Erlangen-Nürnberg, 2013. http://d-nb.info/1033029866/34.

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Schlegel, Christoph Richard. "DAPK2 is a novel modulator of trail-induced apoptosis and it regulates oxidative stress in cancer cells by preserving mitochondrial function." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/44460.

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Targeting molecules involved in Tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) -mediated signalling has been hailed by many as a potential magic bullet to efficiently kill cancer cells, with little side effects on normal cells. Indeed, initial clinical trials showed that antibodies against TRAIL receptors, death receptor (DR) 4 and DR5 are well tolerated by cancer patients. Despite the initial efficacy issues in the clinical setting, novel approaches to trigger TRAIL-mediated apoptosis are being developed and its clinical potential is being reappraised. Unfortunately, many patients develop resistance to TRAIL-induced apoptosis and there is thus impetuous for identifying additional resistance mechanisms that may be targetable and usable in combination therapies. Here, we show that the death associated protein kinase (DAPK) 2 is a modulator of TRAIL signalling. DAPK2 is a serine/threonine kinase that belongs to the DAPK family. Like DAPK1, it has been implicated in programmed cell death, the regulation of autophagy and developmental processes. Ablation of DAPK2 using RNAi causes phosphorylation of NF-κB and its transcriptional activity in several cancer cell lines. This then leads to the induction of a variety of NF-κB target genes, which includes DR4 and DR5. DR4 and DR5 protein expression is correspondingly increased on the cell surface and this leads to the sensitisation of resistant cells to TRAIL-induced killing. As DAPK2 is a kinase, it is imminently druggable and our data thus offer a novel avenue to overcome TRAIL-resistance in the clinic. We have additionally identified a new role for DAPK2 in the regulation of mitochondrial integrity. RNAi-mediated depletion of DAPK2 leads to a number of metabolic changes, including a significantly decreased rate of oxidative phosphorylation in combination with an overall destabilised mitochondrial membrane potential. This phenotype is further corroborated by an increase in the production of mitochondrial superoxide anions and general oxidative stress. This role of DAPK2 is completely novel and could impact significantly on the understanding of DAPK2's function in physiology and disease.

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Ulrich, Sebastian [Verfasser]. "The death-associated protein kinase 1 (DAPK1) : prognostic relevance in pediatric acute lymphoblastic leukemia (ALL) and evaluation as a therapeutic target / Sebastian Ulrich." Ulm : Universität Ulm, 2018. http://d-nb.info/1155238540/34.

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Lahlali, Thomas. "Virus de l'hépatite C, Nétrine-1 et réponse aux protéines mal repliées en contexte hépatique." Thesis, Lyon 1, 2014. http://www.theses.fr/2014LYO10301.

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Les connaissances actuelles en pathologie hépatique suggèrent que HCV n'est pas directement oncogénique mais expose les patients au risque de cancer du foie dans un contexte inflammatoire associé à une réponse UPR (Unfolded Protein Response) et une régénération hépatique. La nétrine-1, le ligand canonique de la famille des DRs (Récepteurs à dépendance), est une protéine anti-apoptotique impliquée dans le développement, l'inflammation et la tumorigenèse. Les DRs induisent l'apoptose en absence de leurs ligands. A ce jour, il n'existe aucune donnée reliant le concept de DR et les virus oncogènes. Au cours de ma thèse, j'ai contribué à démontrer que la fonctionnalité des DRs était altérée au cours de l'infection par HCV in vitro et in vivo. Nous avons montré que la surexpression de la nétrine-1 augmente l'infectivité des virions et promeut leur entrée via l'activation et la diminution du recyclage de l'EGFR. De son coté, HCV augmente l'expression de la nétrine-1 suite à l'activation de l'épissage de son ARN pré-messager. Nous avons aussi montré que l'expression du récepteur à la nétrine-1, UNC5A, était diminuée au cours de l'infection suite à des diminutions transcriptionnelle et traductionnelle. Dans ce cadre, la nétrine-1 joue le rôle de facteur proviral en inhibant une potentielle voie de signalisation antivirale induite par le récepteur UNC5A non lié. Nous avons ensuite voulu savoir quelles conséquences cette surexpression de nétrine-1 pourrait avoir en physiopathologie hépatique en contexte non infectieux. Un stress du RE (Réticulum Endoplasmique) est observé au cours de l'infection par HCV. Le stress du RE entraîne l'activation de la réponse UPR qui induit l'apoptose médiée par la DAPK1 en cas de stress prolongé. Le fait que le récepteur UNC5B active aussi l'apoptose via l'activation de la DAPK1 nous a conduit à étudier l'implication de la nétrine-1 dans la survie cellulaire au cours de la réponse UPR en contexte hépatique. Nous avons démontré à la fois in vitro et in vivo que l'expression de la nétrine-1 pourrait protéger les cellules contre l'apoptose induite par la réponse UPR suite à sa liaison aux récepteurs UNC5A et C qui entraîne l'inhibition de la DAPK1. De nombreuses études ont également reporté des rôles de la nétrine-1 dans l'inflammation et la néoangiogenèse. Nous avons montré que la nétrine-1 inhibe la migration transendothéliale hépatique des PBMCs (Peripheral Blood Mononucleated Cells) et accélère la tubulogenèse des cellules endothéliales intrasinusoïdales hépatiques. Dans leur ensemble, mes travaux de thèse suggèrent que la nétrine-1 via ses récepteurs UNC5s joue des rôles délétères en pathophysiologie hépatique favorables à la persistance virale et à la résistance à la mort cellulaire<br>Current knowledge in hepatic pathology suggests that HCV is not directly oncogenic but puts patients at risk for liver cancer in a context associated with a chronic inflammation, UPR (Unfolded Protein Response) and liver regeneration. Netrin-1, the canonical ligand of the DR (Dependence Receptor) family, is an antiapoptotic secreted factor implicated in development, cancer and cancer-associated inflammatory diseases. DRs induce cell death when unbound. No data linking the DR system to oncogenic viruses are available to date. During the first part of my PhD, I contributed to demonstrate that HCV infection alters DR functionality both in vitro and in vivo. We found that Netrin-1 conditions HCV virion infectivity and promotes virion entry by increasing the activation and decreasing the recycling of the EGFR. In turn, HCV increases Netrin-1 expression through enhanced Netrin-1 pre-mRNA splicing. The Netrin-1 UNC5A receptor expression was decreased upon HCV infection through diminished transcription and translation. In this setting, Netrin-1 acts as a proviral factor by inhibiting a putative antiviral signaling pathway conveyed by the unbound UNC5A receptor. In this context, we wanted to determine what consequences such Netrin-1 up-regulation could induce in non-infectious hepatic pathophysiology. Chronic ER (endoplasmic reticulum) stress is observed during HCV infection. ER stress leads to UPR activation which triggers apoptosis via DAPK1 activation upon prolonged stress. The fact that the UNC5B receptor induces apoptosis through DAPK1 activation led us to investigate Netrin-1 implication in cell survival upon UPR in the liver. During the second part of my PhD, I have demonstrated both in vitro and in vivo in mice that Netrin-1 translation during UPR could protect cells against UPR-related cell death after binding to UNC5A and C, in a DAPK1-mediated fashion. Several studies have also identified Netrin-1 roles in inflammation and neo-angiogenesis. We found that Netrin-1 inhibits hepatic transendothelial migration of PBMCs (Peripheral Blood Mononucleated Cells) and accelerates tubulogenesis of liver sinusoidal endothelial cells. Netrin-1’s role in a hepatic inflammation and neoangiogenesis, both events being tightly associated with viral hepatitis, remains to be thoroughly elucidated. Altogether, our results suggest that Netrin-1 plays UNC5-dependent deleterious roles in hepatic pathophysiology, leading to viral persistence as well as resistance to cell death

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Bezuidenhout, Andries Jacobus. "Die drukking van dakke : ruimtelikheid en morele agentskap in Gert Vlok Nel se digbundel "om te lewe is onnatuurlik” en “Veelvuldige gebruike vir huishoudelike toestelle”." Thesis, Stellenbosch : Stellenbosch University, 2013. http://hdl.handle.net/10019.1/79962.

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Thesis (MA)--Stellenbosch University, 2013.<br>AFRIKAANSE OPSOMMING: Die eerste gedeelte van hierdie tesis ondersoek die ruimtelike basis vir morele agentskap in Gert Vlok Nel se digbundel om te lewe is onnatuurlik. As teoretiese raamwerk word daar van die teoloog/letterkundige Wesley Kort, die letterkundige/sosioloog Irma du Plessis en die radikale geograaf David Harvey se werk gebruik gemaak. Kwessies soos die (i) wisselwerking tussen omvattende, sosiale en intieme ruimtes deur narratiewe ruimtelikheid in poësie, (ii) die onstandvastigheid van die onderskeid tussen private en openbare ruimtes en (iii) verkillende vorms van ruimtelikheid, soos absolute, relatiewe en relasionele ruimtes, asook materiële ruimte, gerepresenteerde ruimte en ruimtes van representasie kom aan die bod. Daar word aangevoer dat Gert Vlok Nel se bewustelike plasing van homself as randfiguurdigter binne die Afrikaanse literêre sisteem as vorm van morele agentskap gesien kan word. Verder word getoon dat, as om te lewe is onnatuurlik in geheel en as familiekroniek gelees word, die onderskeid tussen private en openbare ruimtes waar geweld en trauma plaasvind ondergrawe word en sodoende politieke magskwessies as persoonliketiese kwessies herdefinieer. Laastens word argument gevoer dat, alhoewel die sprekerdigter in die bundel (“Gert”, of “Gertjie”) op die oog af gebrekkige agentskap blyk te toon, die besonderse tydruimtelike plasing van die spreker-digter die moontlikheid vir verruiming van agentskap skep en sodoende die idee van versplinterde subjek uitdaag. Hierdie akademiese opstel hou verband met die kreatiewe gedeelte van die tesis, digbundel getiteld Veelvuldige gebruike vir huishoudelike toestelle, waarin huishoudelike ruimtes as vertrekpunt gebruik word om kwessies soos morele verantwoordbaarheid, kreatiewe aandadigheid, post-koloniale manlikheid, sosiale verandering en trauma te ondersoek.<br>ENGLISH ABSTRACT: The first part of this thesis investigates the spatial grounds for moral agency in Gert Vlok Nel’s collection of poems om te lewe is onnatuurlik [“to live is unnatural”]. The works of theologian/literary theorist Wesley Kort, literary theorist/sociologist Irma du Plessis and radical geographer David Harvey are used as theoretical framing. Matters such as (i) the interplay between encompassing, social and intimate spaces through narrative spatiality in poetry, (ii) flawed distinctions between private and public space, and (iii) different forms of spatiality, such as absolute, relative and relational space, as well as material space, represented space and spaces of representation are explored. It is argued that Gert Vlok Nel’s conscious positioning of himself as poetic outsider within the Afrikaans literary system can be seen as a form of moral agency. Furthermore, it is pointed out that a reading of om te lewe is onnatuurlik in its entirety, as family chronicle, destabilises the distinction between private and public spaces where violence and trauma occur, thereby recasting political power as questions of personal ethics. Finally it is argued that, although the narrator-poet in die collection (“Gert”, or “Gertjie”) seems to lack agency, the peculiar spatio-temporal placing of the narrator-poet nevertheless opens up room for the possibility of agency and by doing this, challenges the idea of a splintered subject. This academic essay is related to the creative part of this thesis, a collection of poems titled Veelvuldige gebruike vir huishoudelike toestelle [“Multiple uses for domestic appliances”], in which household space is used as a vantage point from which to interrogate issues such as moral responsibility, creative complicity, postcolonial masculinities, social change and trauma.

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Ivanovska, Jelena [Verfasser], and Robert [Akademischer Betreuer] Slany. "Interplay of DAPK signalling pathway with LIMK, cofilin complex in TNF-induced apoptosis in HCT116 colorectal cancer cells / Jelena Ivanovska. Betreuer: Robert Slany." Erlangen : Universitätsbibliothek der Universität Erlangen-Nürnberg, 2013. http://d-nb.info/1035540754/34.

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Daske, Thomas [Verfasser], Weizsäcker Robert K. [Akademischer Betreuer] [Gutachter] von, and Michael [Gutachter] Kurschilgen. "The Impact of Other-Regarding Preferences on Moral Hazard and Adverse Selection / Thomas Daske ; Gutachter: Robert K. von Weizsäcker, Michael Kurschilgen ; Betreuer: Robert K. von Weizsäcker." München : Universitätsbibliothek der TU München, 2017. http://d-nb.info/1147565791/34.

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Arlt, Dorothee [Verfasser], Jens [Akademischer Betreuer] Wolling, Wolfgang [Akademischer Betreuer] Schweiger, and Oliver [Akademischer Betreuer] Quiring. "Laufzeitverlängerung von Atomkraftwerken – Nein, Danke!? : Eine kommunikationswissenschaftliche Studie zum Einfluss medialer Kommunikation auf Einstellungen gegenüber Atomkraft / Dorothee Arlt. Gutachter: Wolfgang Schweiger ; Oliver Quiring. Betreuer: Jens Wolling." Ilmenau : Universitätsbibliothek Ilmenau, 2013. http://d-nb.info/1046241567/34.

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40

Bittner, Marietta. "Klassenbeste in Physik oder Informatik? Klassenbester in Deutsch oder Englisch? Nein danke - das passt nicht zu mir! Von der Stimmigkeit zwischen "geschlechtsspezifischer" Sozialisationserfahrung in der Schule und geschlechtersegregativer Arbeitsmarktstruktur." [S.l. : s.n.], 2006. http://nbn-resolving.de/urn:nbn:de:swb:14-1181125042903-96038.

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Gheit, Henda [Verfasser], Heidi [Gutachter] Foth, Andreas [Gutachter] Simm, and Bettina [Gutachter] Grasl-Kraupp. "Role of carcinogens factors in epigenetic silencing of Rassf1a, DAPK, p16, MT1A genes in human lung / Henda Gheit ; Gutachter: Heidi Foth, Andreas Simm, Bettina Grasl-Kraupp." Halle (Saale) : Universitäts- und Landesbibliothek Sachsen-Anhalt, 2021. http://nbn-resolving.de/urn:nbn:de:gbv:3:4-1981185920-385631.

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El, Chamaa Marwan [Verfasser], and Holger [Akademischer Betreuer] Daske. "Essays on Implied Cost of Capital Estimation and Implementation for Corporates and Banks: In Association with Customer Satisfaction, Equity Market Discipline and an Estimation Approach / Marwan El Chamaa. Betreuer: Holger Daske." Mannheim : Universitätsbibliothek Mannheim, 2015. http://d-nb.info/1082205419/34.

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43

Bittner, Marietta. "Klassenbeste in Physik oder Informatik? Klassenbester in Deutsch oder Englisch? Nein danke - das passt nicht zu mir! Von der Stimmigkeit zwischen "geschlechtsspezifischer" Sozialisationserfahrung in der Schule und geschlechtersegregativer Arbeitsmarktstruktur." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2007. http://nbn-resolving.de/urn:nbn:de:swb:14-1181125042903-96038.

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Der soziale Geschlechterdualismus bestimmt als auf dem Arbeits- wie dem Ausbildungsmarkt gültiges Strukturierungsprinzip über Lebenschancen und –risiken. Das heißt zugleich, dass die Makro-Berufsfeldklassifizierungen als „männlich“ oder „weiblich“ ein Element der sozialen Ordnung der Geschlechter darstellen, die sich durch die kulturelle Annahme „geschlechtsspezifischer“ Neigungen, Begabungen, Kompetenzen und Verhaltensweisen (als für die Berufswahl relevanter Faktoren) legitimiert. Die Schule aber ist ein Teil unseres kulturellen Systems. Die vorliegende Studie hinterfragte darum die Verzahnung des Bildungs- und Beschäftigungssystems aus dem sozialkonstruktivistischen Blickwinkel der „geschlechtsspezifischen“ schulischen Sozialisation und stellte somit die Frage nach deren Bedeutung für das -makrostatistisch betrachtet- geschlechtstypische Berufswahlverhalten der Geschlechter. Im Vordergrund der explorativen Studie stand es dabei herauszufinden, welche berufswahlrelevanten schulischen Einflussfaktoren existieren und wie wesentlich diese Einflussfaktoren für die Berufswahlentscheidung sind. An der quantitativen Untersuchung beteiligten sich bundesweit 33 Schulen (8 Hauptschulen, 9 Realschulen, 5 Gesamtschulen, 11 Gymnasien) bzw. 1513 aus diesen Schulen rekrutierte Befragte (737 Schülerinnen und 776 Schüler der jeweils letzten beiden Klassenstufen der beteiligten Schulformen), die mit Hilfe eines im Internet bereitgestellten elektronischen Erhebungsbogens befragt wurden. Die Untersuchungsergebnisse dokumentierten, dass auch -mit den kulturellen Geschlechterrollen in Kontext stehende- schulische Sozialisationsvorgänge das geschlechtsrollennonkonforme oder aber geschlechterrollenadäquate Berufswahlverhalten von Schülerinnen und Schülern (durch sich auf der curricularen, interaktionalen, strukturellen bzw. berufsorientierenden Ebene ereignende Alltagseinflüsse) prägen. Denn sowohl das schulischerseits mitbeeinflusste fachliche Selbstkonzept als auch das unter anderem von seiten der Schule geformte soziale Selbstkonzept tragen entsprechend den in der Untersuchung ermittelten Korrelationen dazu bei, dass die Berufsfindung geschlechtsrollenorientiert oder eben gerade nicht geschlechtsrollenorientiert verläuft. Da die Schule als zentrale Sozialisationsinstanz nach den Untersuchungsergebnissen nicht nur gemäß ihrem pädagogischen Auftrag durch die gezielte Vermittlung von Fachkompetenzen ohne Ansehen des Geschlechtes auf die Integration in den Ausbildungs- bzw. Arbeitsmarkt vorbereitet und hierfür für beide Geschlechter prinzipiell gleiche Voraussetzungen schafft, sondern im schulischen Rahmen auch berufswahlrelevante Lernprozesse über kulturelle Normen von „Weiblichkeit“ und „Männlichkeit“ stattfinden, die mit der „geschlechtsspezifischen“ Segregation des Ausbildungs- und Arbeitsmarktes korrespondieren, ergibt sich hier ein deutlicher Handlungsbedarf im Sinne eines veränderten schulischen Verständnisses für die Kompetenzvermittlung zur perspektivischen Integration in das Beschäftigungssystem. Diesem Handlungsbedarf nach einem (per Festschreibung der Koedukation) nicht nur theoretischen, sondern auch in der alltäglichen Praxis verankerten Selbstverständnis der Schule als androgyner Lehr- und Lernraum für alle Altersklassen wird in den aus dem Erhebungsbogen abgeleiteten pädagogisch-sozialpädagogischen Schlussfolgerungen Rechnung getragen. Des weiteren verweisen die Schlussfolgerungen auf das bildungspolitische Erfordernis, die Koedukation bundeseinheitlich!- tatsächlich bildungsprogrammatisch (und nicht nur wie bisher primär pragmatisch) zu verankern und ihren emanzipatorischen pädagogischen Auftrag in einer Bildungs- und Erziehungstheorie detailliert auszuformulieren, um dergestalt kontinuierlich (über die Schuljahre) und systematisch (also fächerübergreifend) den schulischen Beitrag zum Gelingen einer wahrhaft selbstbestimmten Berufswahl von Jugendlichen zu leisten – gerade in Zeiten demographisch und globalisierungsbedingter Umbrüche, die nicht nur eine raschere Ausbreitung neuer beruflicher Vorbilder für Frauen und Männer gestatten, sondern sie geradezu bedingen. Die methodischen Schlussfolgerungen der Erhebung sind in einem Konzept für die sozialwissenschaftliche Nutzung des Internets zu Befragungszwecken zusammengefasst. (Dissertation zum Thema: „Zur Stimmigkeit zwischen „geschlechtsspezifischer“ Sozialisationserfahrung in der Schule und geschlechter-segregativer Arbeitsmarktstruktur“)

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44

Bittner, Marietta. "Klassenbeste in Physik oder Informatik? Klassenbester in Deutsch oder Englisch? Nein danke - das passt nicht zu mir! Von der Stimmigkeit zwischen "geschlechtsspezifischer" Sozialisationserfahrung in der Schule und geschlechtersegregativer Arbeitsmarktstruktur." Doctoral thesis, Technische Universität Dresden, 2005. https://tud.qucosa.de/id/qucosa%3A24823.

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Abstract:

Der soziale Geschlechterdualismus bestimmt als auf dem Arbeits- wie dem Ausbildungsmarkt gültiges Strukturierungsprinzip über Lebenschancen und –risiken. Das heißt zugleich, dass die Makro-Berufsfeldklassifizierungen als „männlich“ oder „weiblich“ ein Element der sozialen Ordnung der Geschlechter darstellen, die sich durch die kulturelle Annahme „geschlechtsspezifischer“ Neigungen, Begabungen, Kompetenzen und Verhaltensweisen (als für die Berufswahl relevanter Faktoren) legitimiert. Die Schule aber ist ein Teil unseres kulturellen Systems. Die vorliegende Studie hinterfragte darum die Verzahnung des Bildungs- und Beschäftigungssystems aus dem sozialkonstruktivistischen Blickwinkel der „geschlechtsspezifischen“ schulischen Sozialisation und stellte somit die Frage nach deren Bedeutung für das -makrostatistisch betrachtet- geschlechtstypische Berufswahlverhalten der Geschlechter. Im Vordergrund der explorativen Studie stand es dabei herauszufinden, welche berufswahlrelevanten schulischen Einflussfaktoren existieren und wie wesentlich diese Einflussfaktoren für die Berufswahlentscheidung sind. An der quantitativen Untersuchung beteiligten sich bundesweit 33 Schulen (8 Hauptschulen, 9 Realschulen, 5 Gesamtschulen, 11 Gymnasien) bzw. 1513 aus diesen Schulen rekrutierte Befragte (737 Schülerinnen und 776 Schüler der jeweils letzten beiden Klassenstufen der beteiligten Schulformen), die mit Hilfe eines im Internet bereitgestellten elektronischen Erhebungsbogens befragt wurden. Die Untersuchungsergebnisse dokumentierten, dass auch -mit den kulturellen Geschlechterrollen in Kontext stehende- schulische Sozialisationsvorgänge das geschlechtsrollennonkonforme oder aber geschlechterrollenadäquate Berufswahlverhalten von Schülerinnen und Schülern (durch sich auf der curricularen, interaktionalen, strukturellen bzw. berufsorientierenden Ebene ereignende Alltagseinflüsse) prägen. Denn sowohl das schulischerseits mitbeeinflusste fachliche Selbstkonzept als auch das unter anderem von seiten der Schule geformte soziale Selbstkonzept tragen entsprechend den in der Untersuchung ermittelten Korrelationen dazu bei, dass die Berufsfindung geschlechtsrollenorientiert oder eben gerade nicht geschlechtsrollenorientiert verläuft. Da die Schule als zentrale Sozialisationsinstanz nach den Untersuchungsergebnissen nicht nur gemäß ihrem pädagogischen Auftrag durch die gezielte Vermittlung von Fachkompetenzen ohne Ansehen des Geschlechtes auf die Integration in den Ausbildungs- bzw. Arbeitsmarkt vorbereitet und hierfür für beide Geschlechter prinzipiell gleiche Voraussetzungen schafft, sondern im schulischen Rahmen auch berufswahlrelevante Lernprozesse über kulturelle Normen von „Weiblichkeit“ und „Männlichkeit“ stattfinden, die mit der „geschlechtsspezifischen“ Segregation des Ausbildungs- und Arbeitsmarktes korrespondieren, ergibt sich hier ein deutlicher Handlungsbedarf im Sinne eines veränderten schulischen Verständnisses für die Kompetenzvermittlung zur perspektivischen Integration in das Beschäftigungssystem. Diesem Handlungsbedarf nach einem (per Festschreibung der Koedukation) nicht nur theoretischen, sondern auch in der alltäglichen Praxis verankerten Selbstverständnis der Schule als androgyner Lehr- und Lernraum für alle Altersklassen wird in den aus dem Erhebungsbogen abgeleiteten pädagogisch-sozialpädagogischen Schlussfolgerungen Rechnung getragen. Des weiteren verweisen die Schlussfolgerungen auf das bildungspolitische Erfordernis, die Koedukation bundeseinheitlich!- tatsächlich bildungsprogrammatisch (und nicht nur wie bisher primär pragmatisch) zu verankern und ihren emanzipatorischen pädagogischen Auftrag in einer Bildungs- und Erziehungstheorie detailliert auszuformulieren, um dergestalt kontinuierlich (über die Schuljahre) und systematisch (also fächerübergreifend) den schulischen Beitrag zum Gelingen einer wahrhaft selbstbestimmten Berufswahl von Jugendlichen zu leisten – gerade in Zeiten demographisch und globalisierungsbedingter Umbrüche, die nicht nur eine raschere Ausbreitung neuer beruflicher Vorbilder für Frauen und Männer gestatten, sondern sie geradezu bedingen. Die methodischen Schlussfolgerungen der Erhebung sind in einem Konzept für die sozialwissenschaftliche Nutzung des Internets zu Befragungszwecken zusammengefasst. (Dissertation zum Thema: „Zur Stimmigkeit zwischen „geschlechtsspezifischer“ Sozialisationserfahrung in der Schule und geschlechter-segregativer Arbeitsmarktstruktur“)

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Dabke, Partha [Verfasser], Anibh Martin [Akademischer Betreuer] Das, Wolfgang [Akademischer Betreuer] Löscher, and Karin [Akademischer Betreuer] Weißenborn. "Mechanism of Ketogenic Diet: Impact of Beta – Hydroxybutyrate and Decanoic Acid on Sirtuins, Energy Metabolism and Cellular Lipids in a Murine Hippocampal Neuronal Cell Model / Partha Dabke ; Anibh Martin Das, Wolfgang Löscher, Karin Weißenborn." Hannover : Stiftung Tierärztliche Hochschule Hannover, 2020. http://d-nb.info/1224883012/34.

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Doumont, Gilles. "Identification et caractérisation de nouveaux médiateurs de l'activité biologique de la protéine suppresseur de tumeur p53." Doctoral thesis, Universite Libre de Bruxelles, 2005. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/211022.

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Le suppresseur de tumeur p53 permet à la cellule de se défendre contre différentes formes de stress. Il joue un rôle de barrière s'opposant à la tumorigenèse: en effet la perte de p53 chez la souris prédispose grandement ces animaux à développer des tumeurs; de même le locus p53 est inactivé dans près de 50% des tumeurs humaines.<p>p53 constitue un facteur de transcription qui se lie à des séquences particulières de l'ADN et active l'expression des gènes adjacents. L'expression orchestrée de ces gènes conduit, directement ou indirectement et suivant le contexte cellulaire, soit à la mort de la cellule soit à l'inhibition de la division cellulaire.<p>Les mécanismes moléculaires médiant ces deux activités biologiques essentielles de p53, de même que les mécanismes influençant le choix de la réponse cellulaire, sont encore mal compris. L'importance de p53 dans ce choix reste également à démontrer.<p>Afin de contribuer à la compréhension de ces mécanismes, le modèle murin déficient pour Mdm4, un régulateur négatif de l'activité de p53, a été choisi. L'inactivation de Mdm4 chez la souris conduit en effet à l'activation ectopique de p53 in vivo et l'induction de deux types de réponse: apoptose dans le neuroépithélium et arrêt de la prolifération cellulaire dans les tissus non neuronaux. Le profil d'expression des gènes dans les tissus neuronaux et non neuronaux a donc été comparé entre embryons de souris sauvage et mdm4-/- par la technique d'hybridation de biopuces à ADN. Les résultats obtenus suggèrent que le type de réponse dépend du type cellulaire et non de p53 lui-même. En effet les profils d'expression des gènes dans les tissus neuronaux (conditions d'apoptose) et non neuronaux (conditions d'arrêt de la prolifération cellulaire) chez l'embryon de souris mdm4-/- sont comparables.<p><p>Nous nous sommes ensuite particulièrement intéressés à deux nouveaux gènes dont l'expression est augmentée dans les embryons mdm4-/-. Dans un premier temps, leur induction transcriptionnelle chez l'embryon de souris mdm4-/- a été confirmée par différentes techniques et il a été vérifié qu'ils constituaient tous deux des cibles directes de p53 induites suite à un stress génotoxique.<p>Le premier gène code Dapk1, une protéine suppresseur de tumeur pro-apoptotique présentant une activité de type sérine/thréonine kinase. Ce travail a permis d'établir que Dapk1 participait à une boucle de rétroaction du contrôle de l'activité de p53.<p>Le deuxième gène identifié code la protéine Ptprv, un récepteur transmembranaire présentant une activité de type tyrosine phosphatase. En vue d'étudier la signification physiologique de l'induction transcriptionnelle de ptprv suite à l'activation de p53, des expériences effectuées à partir de matériel biologique issu de souris déficientes pour Ptprv ont été réalisées. Ces expériences confirment le rôle essentiel de Ptprv comme médiateur de l'arrêt du cycle cellulaire en phase G1 induit par p53 suite à un stress génotoxique, à la fois in vitro et in vivo. Par contre, Ptprv ne semble pas influencer l'apoptose induite suite à l'activation de p53. Ce travail a également permis d'établir le rôle essentiel de Ptprv dans la suppression de tumeurs induites chez la souris par activation constitutive de l'oncogène Ras.<p><br>Doctorat en sciences, Spécialisation biologie moléculaire<br>info:eu-repo/semantics/nonPublished

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Blue, Emily Keller. "Death-Associated Protein Kinase Regulates Vascular Smooth Muscle Cell Signaling and Migration." Thesis, 2011. http://hdl.handle.net/1805/2518.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>Cardiovascular disease is the number one cause of death for Americans. New treatments are needed for serious conditions like atherosclerosis, as it can lead to stroke and heart attack. Many types of cells contribute to the progression of cardiovascular disease, including smooth muscle cells that comprise the middle layers of arteries. Inappropriate growth and migration of smooth muscle cells into the lumen of arteries has been implicated in vascular diseases. Death associated protein kinase (DAPK) is a protein that has been found to regulate the survival and migration of cancer cells, but has not been well characterized in vascular cells. The objective of this work was to determine the signaling pathways that DAPK regulates in smooth muscle cells. These studies have focused on smooth muscle cells isolated from human coronary arteries (HCASM cells). We have determined that HCASM cells depleted of DAPK exhibit more rapid migration, showing that DAPK negatively regulates migration of vascular cells. Results from a focused RT-PCR array identified matrix metalloproteinase 9 (MMP9) as a gene that is increased in cells depleted of DAPK. MMP9 is an important enzyme that degrades collagen, a component of the extracellular matrix through which smooth muscle cells migrate during atherosclerosis. We found that DAPK regulates phosphorylation of the NF-kappa B transcription factor p65 at serine 536, a modification previously found to correlate with increased nuclear levels and activity of p65. In DAPK-depleted HCASM cells, there was more phosphorylation of p65, which causes increased MMP9 promoter activity. Additional experiments were conducted using transgenic mice in which the DAPK gene has been deleted. By studying these mice, we have determined that under some circumstances DAPK augments maximal MMP9 levels in mouse carotid arteries which have been injured by ligation surgery via other signaling pathways. MMP9 has been previously implicated as a protein that promotes vascular diseases such as atherosclerosis. Our research in identifying DAPK as a regulator of MMP9 expression identifies a new target for treatment of vascular diseases like atherosclerosis.

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Chen, Chun-Hau. "Bi-directional signals transduced by DAPK-ERK interaction promote the apoptotic effect of DAPK." 2004. http://www.cetd.com.tw/ec/thesisdetail.aspx?etdun=U0001-2411200422583800.

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Chen, Chun-Hau, and 陳俊豪. "Bi-directional signals transduced by DAPK-ERK interaction promote the apoptotic effect of DAPK." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/47922186222590929126.

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博士<br>國立臺灣大學<br>分子醫學研究所<br>93<br>Death-associated protein kinase (DAPK) is a death domain (DD)-containing serine/threonine kinase identified by its participation in the interferon-��-induced apoptosis. Subsequent studies revealed a broad involvement of DAPK in apoptosis induced by a variety of stimuli and the DD of DAPK positively regulates this pro-apoptotic effects. In an attempt to identify molecules that mediate the pro-apoptotic effect of DAPK through interacting with its DD, we performed a yeast-two hybrid screen using the DD of DAPK as bait. Both extracellular signal-regulated kinase 1 (ERK1) and ERK2 were recovered from this screen. We demonstrate that DAPK specifically interacts with ERK1 and ERK2 both in vitro and in vivo and this interaction is mediated by a consensus ERK docking sequence located in the DD of DAPK. Furthermore, an ERK consensus phosphorylation site was identified at S735 of DAPK, implying that DAPK is a substrate of ERK. Indeed, using various in vitro and in vivo analyses, we demonstrate that ERK phosphorylates DAPK mainly at S735 residue, and, more importantly, this phosphorylation leads to an elevation of DAPK kinase activity by decreasing the Km value of catalytic reaction. In addition to uncovering the role of ERK in regulating DAPK, a reverse direction of regulation was identified in this thesis: that is, the blockage of ERK nuclear translocation and nuclear signaling by DAPK. Thus, these findings collectively establish a reciprocal regulation between DAPK and ERK. As ERK nuclear signaling contributes in part to its anti-apoptotic function, we hypothesize that the interplay between DAPK and ERK could constitute a positive feedback loop that ultimately promotes the apoptotic effect of DAPK. Indeed, we show that ERK activation could promote the anoikis/apoptosis inducibility of DAPK in cells overexpressing DAPK. Furthermore, disruption of endogenous ERK-DAPK interaction by overexpressing the DD of DAPK attenuates the Fas-induced, DAPK-mediated apoptosis. Finally, in a physiological apoptosis system, we found that the upregulation of ERK-DAPK complex formation and consequent enhancement of their reciprocal regulation correlate well with the apoptosis cell fate. Furthermore, either deactivation of endogenous ERK or downregulation of endogenous DAPK in this system efficiently blocks apoptosis, thus providing physiological evidence for the apoptosis promoting function of ERK-DAPK complex. In conclusion, these results indicate that bi-directional signalings between DAPK and ERK contribute to the apoptosis-promoting function of the DD of DAPK.

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CHOU, TING-FANG, and 周定芳. "The Role of DAPK in Th17 Development." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/7ys8qe.

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博士<br>國防醫學院<br>生命科學研究所<br>104<br>Death-associated protein kinase (DAPK) is known for its tumor suppressor function. Here we show that DAPK also inhibits T helper 17 (Th17) and prevents Th17-mediated pathology in a mouse model of autoimmunity. We identified that DAPK specifically downregulates hypoxia-inducible factor 1(HIF-1), the transcription factor dictating the differentiation of Th17 cells, in a novel process. In contrast to the predominant nuclear localization of HIF-1 in many cell types, HIF-1 is located in both the cytoplasm and nucleus in T cells, allowing for a cytosolic DAPK-HIF-1interaction DAPK also binds prolyl hydroxylase domain protein 2 (PHD2) and increases HIF-1-PHD2 association. DAPK promotes the proline hydroxylation and proteasome degradation of HIF-1. Consequently, DAPK-deficiency led to excess HIF-1 accumulation and IL-17 expression. Th1 cell differentiation and T-bet expression, in contrast, were not significantly altered. We further found that experimental autoimmune encephalomyelitis, a model for T-cell mediated autoimmune disease, was exacerbated in Dapk-/- mice, while T cell-specific transgenic expression of active DAPK suppressed disease induction, illustrating the suppressive effect of DAPK in T cells. Additional knockout of HIF-1 restored the normal differentiation of Dapk-/- Th17 cells and prevented EAE generation. Our results reveal a novel mechanism of inhibition of Th17 generation involving DAPK-mediated degradation of cytoplasmic HIF-1, and suggest that raising DAPK levels could be used for treatment of Th17-associated inflammatory diseases.

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