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Grabner, René. "MPICH-G2." Thesis, Universitätsbibliothek Chemnitz, 2003. http://nbn-resolving.de/urn:nbn:de:swb:ch1-200300470.
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The paper gives an overview on installation and usage of the Grid-enabled MPI implementation MPICH-G2. Performance results of MPICH-G2 in several environments are presented<br>Die Arbeit gibt einen Überblick über die Installation und Nutzung der Grid-fähigen MPI-Implementation MPICH-G2. Performance-Ergebnisse von MPICH-G2 in verschiedenen Umgebungen werden gezeigt
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Grabner, René. "MPICH-G2." [S.l. : s.n.], 2002. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB10547296.
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Sa, Earp Henrique N. "Instantons on G2-manifolds." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.506933.
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Baraglia, David. "G2 geometry and integrable systems." Thesis, University of Oxford, 2009. http://ora.ox.ac.uk/objects/uuid:30cf9c7c-157e-4204-b68b-08f6e199ef36.
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We study the Hitchin component in the space of representations of the fundamental group of a Riemann surface into a split real Lie group in the rank 2 case. We prove that such representations are described by a conformal structure and class of Higgs bundle we call cyclic and we show cyclic Higgs bundles correspond to a form of the affine Toda equations. We also relate various real forms of the Toda equations to minimal surfaces in quadrics of arbitrary signature. In the case of the Hitchin component for PSL(3,R) we provide a new proof of the relation to convex RP²-structures and hyperbolic affine spheres. For PSp(4,R) we prove such representations are the monodromy for a special class of projective structure on the unit tangent bundle of the surface. We prove these are isomorphic to the convex-foliated projective structures of Guichard and Wienhard. We elucidate the geometry of generic 2-plane distributions in 5 dimensions, work which traces back to Cartan. Nurowski showed that there is an associated signature (2,3) conformal structure. We clarify this as a relationship between a parabolic geometry associated to the split real form of G₂ and a conformal geometry with holonomy in G₂. Moreover in terms of the conformal geometry we prove this distribution is the bundle of maximal isotropics corresponding to the annihilator of a spinor satisfying the twistor-spinor equation. The moduli space of deformations of a compact coassociative submanifold L in a G₂ manifold is shown to have a natural local embedding as a submanifold of H2(L,R). We consider G2-manifolds with a T^4-action of isomorphisms such that the orbits are coassociative tori and prove a local equivalence to minimal 3-manifolds in R^{3,3} = H²(T⁴,R) with positive induced metric. By studying minimal surfaces in quadrics we show how to construct minimal 3-manifold cones in R^{3,3} and hence G₂-metrics from equations that are a set of affine Toda equations. The relation to semi-flat special Lagrangian fibrations and the Monge-Ampere equation is explained.
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Walpuski, Thomas. "Gauge theory on G2–manifolds." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/14365.
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In their seminal paper [DT98] Donaldson–Thomas pointed out the possibility of an enumerative invariant for G2–manifolds obtained by counting certain connections, called G2– instantons. This putative invariant is sometimes referred to as the G2 Casson invariant, since it should be formally similar to the Casson invariant for 3–manifolds. In this thesis I prove existence results for G2–instantons on G2–manifolds arising from Joyce’s generalised Kummer construction [Joy96b, Joy00] as well as the twisted connected sum construction [Kov03,CHNP12b]. These yield a number of concrete examples of G2–instantons and may, in the future, help to compute the G2 Casson invariant. Moreover, I show how to construct families of G2–instantons that bubble along associative submanifolds. From this construction it follows that a naïve count of G2–instantons cannot yield a deformation invariant of G2–manifolds. Nevertheless, there can still be hope for a G2 Casson invariant by counting G2–instantons as well as associative submanifolds (and objects in between) with carefully chosen weights. I present a promising proposal for the definition of these weights in the low energy SU(2)–theory.
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Silva, Julio César Conegundes da 1986. "G2 e as álgebras normadas." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/305803.
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Orientador: Luiz Antonio Barrera San Martin<br>Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Matemática, Estatística e Computação Científica<br>Made available in DSpace on 2018-08-21T14:02:28Z (GMT). No. of bitstreams: 1
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Previous issue date: 2012<br>Resumo: ...Observações: Por apresentar basicamente fórmulas, o resumo, na íntegra, poderá ser visualizado no texto completo da tese digital<br>Abstract: ...Note: The complete abstract is available with the full electronic document<br>Mestrado<br>Matematica<br>Mestre em Matemática
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Elin, Fjellheim. "BOTTLENECK-HYPOTHESIS G2 ÅARJELSAEMIEN LOHKEHTIMMESNE." Thesis, Umeå universitet, Institutionen för språkstudier, 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-155144.
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Funksjonelle morfologije haastadihks munnjien orreme mubpiengïelen soptsestæjjine. Lohkehtæjjine leam vueptiestamme learohkh aaj seamma haestemh vuesehteminie gosse funksjonelle morfologijem lierieh jïh utnieh. Daennie mastereksamenetjaalegisnie gihtjem mejtie Bottleneckhypotese, Slabakova:n (2016) mietie, daejtie haestiemidie vaestede mubpiengïelen lohkehtimmesne, gosse saemien veljie morfologije mohte daaroen goh voestesgïele. Daennie tjaalegisnie sïjhtem vuartasjidh guktie mubpiengïelen soptsestæjjah objeektem mïerhkesjieh jïh guktie verbaalem subjeekten mietie sojjehtieh. Bottleneckhypotese gihtjie mah aelhkie mubpiengïelen lohkehtimmesne jïh mah geerve. Dan gaavhtan gihtjem mejtie aelhkemes subjeekte-verbaale kongruensem darjodh jallh objeektem mïerhkesjidh. Manne goerehtimmiem dorjeme, guktie pryövem vaastoeh dïsse åadtjodh. Manne mubpiengïelen soptsestæjjah nöörjen jïh sveerjen raedtesne gihtjeme. Dej illeldahkh leah referansedåehkien illeldahki vööste viertiestamme. Referansedåehkesne feadtagïelen soptsestæjjah, gïeh aaj aerpiegïelen soptsestæjjah. Dan gaavhtan vaenie åarjelsaemien soptsestæjjah jïh vaenie åarjelsaemien learohkh skuvline, dle vaenie goerehtimmielïhtsegh aaj sjïdti mov goerehtæmman. Læjhkan goerehtimmien illeldahkh Bottleneckhypotesem dåarjelieh. Stuerebh haestemh lohkehtimmesne jijhtieh gusnie voestesgïele jïh mubpiengïele joekehtedtieh duhtie mubpeste. Vaenebh haestemh jijhtieh gosse vaenie joekehtassh gïeli gaskem. Slabakova (2016) jeahta dle vihkeles dejtie haestiemidie mubpiengïelen lohkehtimmesne gaavnedh, jïh Slabakova juvnehte mijjieh tjiehtebe dej haestemigujmie skuvlesne barkedh jeanatjommes tïjjen. Goerehtimmiedåehkiej gaskemedtien illeldahkh vuesiehtieh haastadihks objeektem mïerhkesjidh, destie ij gååvnesh daaroengïelesne. Ij badth goerehtimmiedåehkide haastadihks nominatijvem utnedh, dan gaavhtan mahte seammalaakan gåabpaginie gïeline nominatijvem utnedh. Ij leah seamma kreajnas mejtie aelhkebe verbh subjeekti mietie sojjehtidh goh objeekth mïerhkesjidh, jalhts nemhtie aaj muvhtene våajnoes. Montrul (2016) aaj dam illeldahkem dåarjele gosse aerpiegïelen veljie morfologije jïh mubpiengïelen, goh jienebelåhkoegïele, dle vaenie funksjonelle morfologije. Montrul aerpiegïelen soptsestæjjaj haestemh iktedamme, jïh jeahta dle geervebe dam nominaale morfologijem haalvedh enn verbaale morfologijem. Daate goerehtimmie vuesehte referansedåehkie, åarjelsaemien aerpiegïelen soptsestæjjajgujmie, ij badth seamma illeldahkh vuesiehtieh goh jeatjah 5 aerpiegïelen soptsestæjjah veartanisnie. Daan goerehtimmien referansedåehkien illeldahkh feadtagïelen daltesisnie. Daate murreds, kaanna dan åvteste saemien gïele båatsose veadtaldihkie jïh båatsoe vihkeles mijjen jieliemisnie jïh kultuvresne. Men im leah daan bïjre goerehtamme.<br>Funksjonell morfologi har vært en utfordring for meg som andrespråkstaler, og som lærer så ser jeg at elevene har utfordringer når funksjonell morfologi skal læres og brukes. I denne mastereksamensoppgaven spør jeg om Flaskehalshypotesen, presentert av Slabakova (2016), kan gi oss svar på disse utfordringene i andrespråksopplæringen, når sørsamisk har rik funksjonell morfologi i motsetning til førstespråket norsk. Jeg har avgrenset oppgaven til markering av direkte objekt, og samsvarsbøyning mellom subjekt og verbal i sørsamisk. Da Flaskehalshypotesen spør om hva som er vanskelig i andrespråksopplæringen og hva som er lett, så har jeg valgt markering av direkte objekt og samsvarsbøyning, for å se om dette er like utfordrende eller om noe er enklere enn det andre. For å få svar på dette så har jeg gjort en undersøkelse blant andrespråkstalere av sørsamisk både på norsk og svensk side. Deres resultater er målt mot en referansegruppe av morsmålstalere, som per definisjon også er arvspråkstalere. Da det er få sørsamiske talere og få sørsamiske elever i skolen, så blir utvalget lite. Men likevel gir undersøkelsens resultater støtte til Flaskehalshypotesen. Der førstespråket og andrespråket skiller seg ad, så oppstår det større utfordringer i språkopplæringen. Det skaper lite eller mindre utfordringer for elevene der språkene skiller seg lite. Slabakova (2016) er opptatt av å finne utfordringene i andrespråksopplæringen, og hun gir en klar anbefaling om at det er her vi må bruke størsteparten av tiden i klasserommet. Ut i fra gruppenes gjennomsnittlige resultater så er det liten tvil om at markering av direkte objekt er blant de større utfordringene i andrespråksopplæringen, i motsetning til bruk av nominativ hvor norsk og samisk ikke skiller seg nevneverdig fra hverandre. Om markering av objektskasus er vanskeligere enn samsvarsbøyning mellom subjekt og verbal er ikke like entydig, selv om det langt på vei viser det i denne undersøkelsen. Dette funnet støttes av Montrul (2016), som har sammenfattet arvspråkstalernes utfordringer med å produsere arvspråkets morfologi når arvspråket har rik morfologi, og andrespråket, som er majoritetsspråket, har lite funksjonell morfologi. Hun påpeker at det er vanskeligere å få den nominale morfologien på plass enn den verbale morfologien. Denne undersøkelsen viser at referansegruppen med de sørsamiske arvspråkstalerne ikke oppviser samme resultater som arvspråkstalere generelt sett. De ligger på nivå med innfødte talere. Dette er interessant, og en viktig faktor kan være at sørsamisk språk har stått sterkt i båatsoeh/reindriften, en viktig del av vår livsform og kultur. Men det ligger utenfor denne oppgaven å gi svar på det.
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Janesch, Oscar Ricardo. "Grupo G2 de automorfismos de ostónicos." reponame:Repositório Institucional da UFSC, 1990. https://repositorio.ufsc.br/handle/123456789/111255.
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Sauer, Rica [Verfasser]. "Untersuchung des G2/M Checkpoints in Fanconi-Anämie-Zellen durch Analyse der Chromosomeninstabilität in G2-Phase und Mitose / Rica Sauer." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1031096809/34.
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Stewart, Nancy G. "P53 control over cell cycle progression at G2." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ32022.pdf.
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Erazo, Jorge G. "An emulator system for the MC146805F2/G2 microprocessors." Ohio : Ohio University, 1985. http://www.ohiolink.edu/etd/view.cgi?ohiou1184001657.
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Gronlund, Anne Lentz. "Regulatory mechanisms of the plant G2 M transition." Thesis, Cardiff University, 2007. http://orca.cf.ac.uk/54650/.
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The cell cycle is the life of a cell from one mitotic division to the next. In yeast and animals the transition from G2 to mitosis is regulated by the Weel kinases and Cdc25 phosphatases. Phosphoregulation of G2/M is also maintained by 14-3-3 proteins, which function in a wide range of additional processes including signal transduction and stress responses. The scope of this thesis was to investigate how the plant G2/M checkpoint functions and how features of the yeast and animal G2/M model apply to the plant model. A better knowledge of the mechanisms that regulate AtCDC25 and AtWEEl activities was achieved by identifying interaction partners for the two proteins. Both proteins interact with proteins involved in protein biosynthesis, cell division and plant stress responses leading to many hypotheses about the localization, regulation and function of both AtCDC25 and AtWEEl. Moreover, AtWEEl interacts with proteins involved in ubiquitin-mediated degradation, which might be the mechanism regulating WEE1 protein levels (Chapter 4). Additionally, AtWEEl interacts with 14-3-3 proteins and its interaction with 14-3-3 was confirmed in vivo in plant cells (Chapter 5). Furthermore, greater insights into the role of WEE 1 in cell cycle regulation and plant development were obtained by investigation of the biochemistry of <italic>N. tabacum</italic> WEE1 during the cell cycle of synchronized <italic>N. tabacum</italic> BY-2 cells showing that both WEE1 protein level and kinase activity are sensitive indicators for the timing of mitosis (Chapter 6). Moreover, <italic>A. thaliana </italic> weel T-DNA insertion lines were characterized Under standard growth conditions the T-DNA insertions in the WEE1 gene only mildly affect the plant root development. However, exposure to hydroxyurea results in a hypersensitivity response leading to a reduced primary root length and decreased rate of lateral root production linking AtWEEl with both stress responses and plant development (Chapter 7).
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Lehouritis, Panos. "Bacterial directed enzyme prodrug therapy using carboxypeptidase G2." Thesis, Institute of Cancer Research (University Of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429988.
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Davy, Clare Elizabeth. "Analysis of HPV16 E1^E4 induced G2 arrest." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268394.
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Jauregui, Jeff Loren. "Solving for Volume-Minimizing Cycles in G2-Manifolds." Scholarship @ Claremont, 2005. https://scholarship.claremont.edu/hmc_theses/170.
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M-theory, a generalization of string theory, motivates the search for examples of volume minimizing cycles in Riemannian manifolds of G2 holonomy. Methods of calibrated geometry lead to a system of four coupled nonlinear partial differential equations whose solutions correspond to associa- tive submanifolds of R7, which are 3-dimensional and minimize volume in their real homology classes. Several approaches to finding new solutions are investigated, the most interesting of which exploits the quaternionic structure of the PDE system. A number of examples of associative 3-planes are explicitly given; these may possibly be projected to nontrivial volume minimizing cycles in, for example, the G2-manifold R6 × S1.
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Oakes, Vanessa Louise. "Cyclin A/CDK2 regulates multiple G2 phase pathways." Thesis, Queensland University of Technology, 2012. https://eprints.qut.edu.au/63534/1/Vanessa_Oakes_Thesis.pdf.
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The cell cycle is a carefully choreographed series of phases that when executed successfully will allow the complete replication of the genome and the equal division of the genome and other cellular content into two independent daughter cells. The inability of the cell to execute cell division successfully can result in either checkpoint activation to allow repair and/or apoptosis and/or mutations/errors that may or may not lead to tumourgenesis.
Cyclin A/CDK2 is the primary cyclin/CDK regulating G2 phase progression of the cell cycle. Cyclin A/CDK2 activity peaks in G2 phase and its inhibition causes a G2 phase delay that we have termed 'the cyclin A/CDK2 dependent G2 delay'. Understanding the key pathways that are involved in the cyclin A/CDK2 dependent G2 delay has been the primary focus of this study.
Characterising the cyclin A/CDK2 dependent G2 delay revealed accumulated levels of the inactive form of the mitotic regulator, cyclin B/CDK1. Surprisingly, there was also increased microtubule nucleation at the centrosomes, and the centrosomes stained for markers of cyclin B/CDK1 activity. Both microtubule nucleation at the centrosomes and phosphoprotein markers were lost with short-term treatment of CDK1/2 inhibition. Cyclin A/CDK2 localised at the centrosomes in late G2 phase after separation of the centrosomes but before the start of prophase. Thus G2 phase cyclin A/CDK2 controls the timing of entry into mitosis by controlling the subsequent activation of cyclin B/CDK1, but also has an unexpected role in coordinating the activation of cyclin B/CDK1 at the centrosome and in the nucleus. In addition to regulating the timing of cyclin B/CDK1 activation and entry into mitosis in the unperturbed cell cycle, cyclin A/CDK2 also was shown to have a role in G2 phase checkpoint recovery.
Known G2 phase regulators were investigated to determine whether they had a role in imposing the cyclin A/ CDK2 dependent G2 delay. Examination of the critical G2 checkpoint arrest protein, Chk1, which also has a role during unperturbed G2/M phases revealed the presence of activated Chk1 in G2 phase, in a range of cell lines. Activated Chk1 levels were shown to accumulate in cyclin A/CDK2 depleted/inhibited cells. Further investigations revealed that Chk1, but not Chk2, depletion could reverse the cyclin A/CDK2 dependent G2 delay. It was confirmed that the accumulative activation of Chk1 was not a consequence of DNA damage induced by cyclin A depletion. The potential of cyclin A/CDK2 to regulate Chk1 revealed that the inhibitory phosphorylations, Ser286 and Ser301, were not directly catalysed by cyclin A/CDK2 in G2 phase to regulate mitotic entry. It appeared that the ability of cyclin A/CDK2 to regulate cyclin B/CDK1 activation impacted cyclin B/CDK1s phosphorylation of Chk1 on Ser286 and Ser301, thereby contributing to the delay in G2/M phase progression.
Chk1 inhibition/depletion partially abrogated the cyclin A/CDK2 dependent G2 delay, and was less effective in abrogating G2 phase checkpoint suggesting that other cyclin A/CDK2 dependent mechanisms contributed to these roles of cyclin A/CDK2. In an attempt to identify these other contributing factors another G2/M phase regulator known to be regulated by cyclin A/CDK2, Cdh1 and its substrates Plk1 and Claspin were examined. Cdh1 levels were reduced in cyclin A/CDK2 depleted/inhibited cells although this had little effect on Plk1, a known Cdh1 substrate. However, the level of another substrate, Claspin, was increased. Cdh1 depletion mimicked the effect of cyclin A depletion but to a weaker extent and was sufficient at increasing Claspin levels similar to the increase caused by cyclin A depletion. Co-depletion of cyclin A and Claspin blocked the accumulation of activated Chk1 normally seen with cyclin A depletion alone. However Claspin depletion alone did not reduce the cyclin A/CDK2 dependent G2 delay but this is likely to be a result of inhibition of S phase roles of Claspin.
Together, these data suggest that cyclin A/CDK2 regulates a number of different mechanisms that contribute to G2/M phase progression. Here it has been demonstrated that in normal G2/M progression and possibly to a lesser extent in G2 phase checkpoint recovery, cyclin A/CDK2 regulates the level of Cdh1 which in turn affects at least one of its substrates, Claspin, and consequently results in the increased level of activated Chk1 observed. However, the involvement of Cdh1 and Claspin alone does not explain the G2 phase delay observed with cyclin A/CDK2 depletion/inhibition. It is likely that other mechanisms, possibly including cyclin A/CDK2 regulation of Wee1 and FoxM1, as reported by others, combine with the mechanism described here to regulate normal G2/M phase progression and G2 phase checkpoint recovery. These findings support the critical role for cyclin A/CDK2 in regulating progression into mitosis and suggest that upstream regulators of cyclin A/CDK2 activation will also be critical controllers of this cell cycle transition.
The pathways that work to co-ordinate cell cycle progression are very intricate and deciphering these pathways, required for normal cell cycle progression, is key to understanding tumour development. By understanding cell cycle regulatory pathways it will allow the identification of the pathway/s and their mechanism/s that become affected in tumourgenesis. This will lead to the development of better targeted therapies, inferring better efficacy with fewer side effects than commonly seen with the use of traditional therapies, such as chemotherapy. Furthermore, this has the potential to positively impact the development of personalised medicines and the customisation of healthcare.
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Guerrra, Ponce Mariela. "Plan estratégico para Grey Group Perú y plan de Marketing para las unidades estratégicas de negocio G2 RR.PP y G2 CRM." Bachelor's thesis, Universidad Peruana de Ciencias Aplicadas - UPC, 2013. http://hdl.handle.net/10757/274057.
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Guerra, Ponce Mariela. "Plan estratégico para Grey Group Perú y plan de marketing para las unidades estratégicas de negocio G2 RR.PP y G2 CRM." Bachelor's thesis, Universidad Peruana de Ciencias Aplicadas (UPC), 2012. http://hdl.handle.net/10757/301431.
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El tema que abordará la siguiente tesis gira en torno a la búsqueda y aplicación de las estrategias de marketing más adecuadas para vender dos de los servicios que ofrece Grey Group Perú, que son G2 Relaciones Públicas (RR.PP) y G2 Customer Relationship Management (CRM), ambas pertenecientes a la unidad de negocio G2 que ofrece los servicios de BTL. Asimismo, en el presente trabajo se verá desarrollado el plan estratégico de Grey Group Perú, para poder determinar los planes de marketing de las unidades mencionadas. La hipótesis propuesta sostiene una estrategia de penetración de mercado para G2 RR.PP y de desarrollo de producto para G2 CRM. Con estas estrategias se pretende captar y conservar clientes rentables y de esta manera generar rentabilidad para la empresa. Este trabajo muestra el desarrollo del proyecto, que expone el marco conceptual del plan estratégico y plan operativo; la empresa, sus servicios y su situación en el mercado, la propuesta del plan estratégico para Grey Group Perú y los planes de marketing para G2 RR.PP y G2 CRM; así como el costo beneficio de ambas unidades.<br>Tesis
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Fitzgerald, J. G. M. "Weyl modules for groups of type B2 and G2." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.257653.
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In this thesis we determine the submodule structure of a number of Weyl modules for algebraic groups with root systems B2 and G2. We use the Jantzen sum formula to find the composition factors of Weyl modules and go on to use homomorphisms between Weyl modules, given by H.H. Andersen, and the comparison of two filtrations of tensor products of Weyl modules to establish submodule structure. A computer program in the Prolog language is given which calculates the Jantzen sum formula. In addition we find one 2-dimensional Ext group for simple modules for type G2 in characteristic greater than or equal to 7.
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Arenas, Ruben. "Constructing a Matrix Representation of the Lie Group G2." Scholarship @ Claremont, 2005. https://scholarship.claremont.edu/hmc_theses/166.
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We define the Lie group G2 and show several equivalent ways to view G2. We do the same with its Lie algebra g2. We identify a new basis for g2 using Bryant’s view of g2 and geometric considerations we develop. We then show how to construct a matrix representation of G2 given our particular basis for g2. We examine the geometry of 1 and 2-parameter subgroups of G2. Finally, we suggest an area of further research using the new geometric characterization we developed for g2.
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Mazzei, Mitch. "Nonclassical Effects in Electromagnetically Induced Transparency." Miami University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=miami1565254688578434.
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Carrassa, Laura. "Molecular mechanisms regulating the G2 checkpoint induced after DNA damage." Thesis, Open University, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434262.
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Pogorelsky, Bárbara Seelig. "Subálgebras coideais à direita dos grupos quânticos de tipo G2." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2009. http://hdl.handle.net/10183/17568.
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Nesta tese descrevemos as sub algebras coideais a direita que contêm todos elementos group-like dos grupos quânticos multiparâmetro U+ q (g) e Uq(g), onde g e uma algebra de Lie simples de tipo G2, no caso em que o parâmetro principal de quantização q não e raiz da unidade. Se q possui ordem multiplicativa nita t, t > 4, t (diferente) 6, a mesma classicação vale para as sub algebras coideais a direita homogêneas da versão multiparâmetro do grupo quântico de Lusztig uq(g).<br>In this thesis we describe the right coideal subalgebras containing all group-like elements of the multiparameter quantum groups U+ q (g) and Uq(g), where g is a simple Lie algebra of type G2, while the main parameter of quantization q is not a root of 1. If the multiplicative order t of q is nite, t > 4, t (diferent) 6, then the same classi cation remains valid for homogeneous right coideal subalgebras of the multiparameter version of the small Lusztig quantum group uq(g).
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Masala, Giovanni Batista. "Trigonométrie et polyèdres dans les variétés de Grassmann G2 (Rn)." Mulhouse, 1996. http://www.theses.fr/1996MULH0427.
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On donne un système complet d'invariants orthogonaux permettant de déterminer la classe d'isométries d'un triplet. Ces résultats sont par la suite appliqués aux quadruplets et aux N-uples de plans. Certains cas particuliers sont étudiés, comme les quadruplets et triplets réguliers
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Crosby, Meredith Ellen. "G2 Phase Cell Cycle Regulation by E2F4 Following Genotoxic Stress." Case Western Reserve University School of Graduate Studies / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=case1136934596.
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Lossaint, Gérald. "Mécanismes orchestrant la sortie du cycle cellulaire opérant en G2." Thesis, Montpellier 2, 2010. http://www.theses.fr/2010MON20040/document.
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La dérégulation du système de surveillance qui bloque la prolifération lorsque l'intégrité du génome est compromise fait partie intégrante de la cancérogenèse. Nous cherchons à décortiquer les mécanismes qui, en phase G2, orchestrent l'arrêt du cycle cellulaire, irréversible, en présence des lésions de l'ADN (sénescence) ou réversible (quiescence), en absence de signaux mitogéniques ou confluence. L'objectif du premier volet fut d'élucider les rôles respectifs de l'inhibiteur de CDK (CKI) p21Waf1 et des kinases Chk1 et Chk2 dans l'arrêt en G2 dû au stress génotoxique menant à la sénescence. Nous avons montré que dans les cellules humaines normales cet arrêt nécessite l'action de p21 et Chk1 tandis que Chk2 n'est pas requise. Au contraire, dans plusieurs lignées cancéreuses, malgré la présence de p53, ce rôle de p21 est compromis à cause d'une activation inefficace de la kinase ATM. Par conséquent, en dépit d'une forte activation de Chk1 bloquant la mitose, ces cellules ne parviennent pas à initier la sénescence (Lossaint et al., soumis). L'objectif du deuxième volet fut de mettre en évidence le programme déclenchant la quiescence lors de confluence ou en absence de sérum. Les travaux antérieurs de l'équipe ont montré que cette décision pouvait être prise avant la mitose même si l'arrêt du cycle n'a lieu qu'en phase G1 suivante. En étudiant les fibroblastes synchronisés nous avons trouvé que la quiescence est précédée par l'inhibition pré-mitotique de la phosphorylation de pRb due à une diminution de cycline D1 et une stabilisation du CKI p27Kip1 (Chassot et al., 2008). De plus, nos résultats récents montrent que la présence de sérum entre le point R et la mitose est requise pour initier la réplication de l'ADN au cycle suivant. Les travaux futurs devraient élucider comment différentes voies de signalisation, via la voie cycline D-pRb, affectent divers composants de l'appareil de réplication de l'ADN pour inhiber la progression du cycle de façon réversible ou irréversible<br>Cancer is a multi-step process resulting from abrogation of several barriers to uncontrolled proliferation. They include inhibitory pathways with appropriate checkpoints that lead to reversible (quiescence) or irreversible (senescence, apoptosis) block of cell proliferation. We are especially interested in pathways orchestrating cell cycle exit that operate in the G2 phase. The first objective of this thesis was to decipher mechanisms that prevent mitosis in response to DNA damage. We found that Cdk inhibitor p21Waf1 plays a crucial role in blocking mitotic onset in normal cells; acting in tandem with checkpoint kinase Chk1, p21 inactivates mitotic Cdks and inhibits pRb phosphorylation, thereby irreversibly blocking mitotic entry. In contrast, in p53-proficient transformed cells, the induction of p21 in G2 is impaired, most likely because of deficient ATM activation. While, in some cases, Chk1 hyper-activation prevents mitosis, the absence of p21 compromises the senescence program from G2. Finally, we showed that Chk2 is dispensable for G2 arrest in both non-transformed and transformed cells (Lossaint et al., submitted). Our second objective was to elucidate the pathways that induce quiescence (G0). This reversible cell cycle exit occurs in G1, requires pRb family members and p27Kip1-dependent Cdk inactivation. Based on observations obtained in our team and the data in the literature, we hypothesized that reversible cell cycle exit program might be launched before mitosis. By using an in vitro wounding model, we showed that confluence-driven quiescence is preceded by pre-mitotic CDK inhibition by p27, cyclin D1 downregulation and reduced pre-mitotic pRb phosphorylation (Chassot et al., 2008). Moreover, our results obtained in synchronized fibroblasts that were serum-starved after release from G1/S block suggest that cyclin D1 might stimulate proliferation by keeping pocket proteins phosphorylated during G2/M progression (Lossaint et al., in preparation)
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BERTINI, EFREM. "Yap is regulated by phosphorylation at the G2/M transition." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/1192.
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La proteina umana Yap è un co-fattore trascrizionale ed è stata di recente oggetto di molti studi per la sua capacità di interagire con molti fattori di trascrizione. Questa capacità ha condotto molti ricercatori a fornire diverse interpretazioni sulla sua funzione, descrivendola sia come una proteina con attività onco-soppressiva, e sia come un fattore oncogenico. Inoltre, recenti studi hanno indicato un suo ruolo nella differenziazione cellulare e nella regolazione della dimensione di organi, in particolare del fegato. Tuttavia, il ruolo di questa proteina nella regolazione del ciclo cellulare è rimasto finora elusivo. Con il lavoro svolto durante il periodo di dottorato e riportato di seguito, mostriamo che Yap viene fosforilata in mitosi e forniamo alcune indicazioni su un suo possibile ruolo in questa fase del ciclo. In particolare, abbiamo notato che la proteina viene de-fosforilata prima dell’uscita dalla mitosi suggerendo un suo ruolo come co-fattore nella trascrizione nell’imminente nuovo ciclo cellulare, e abbiamo quindi fornito le basi per un indagine più approfondita di tale evento.<br>Yap is a small protein that acts as a co-activator of transcription. It has been shown to interact with many and diverse transcription factors and as a result of these promiscuous interactions, Yap has been described to have a role in many cellular events, including apoptosis, proliferation, and differentiation. For this reason, it is described to have a role both in tumor suppression and transformation. However, the function of Yap in the regulation of the cell cycle has not been investigated so far. Here we demonstrate that Yap is phosphorylated at the G2/M, both in physiologic mitotic cells and in cells arrested in mitosis by microtubules-targeting drugs. We show that Yap is not recruited onto the chromatin during mitosis and does not localize to any mitotic organelles. In addition, we have noticed that de-phosphorylation of Yap occurs before the entry into G1. These data give an indication that Yap may have a role in the exit from mitosis, and place a solid foundation for characterizing the function(s) of Yap during this event.
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Joioso, Aparecido Luciano Breviglieri. "Aplicação de computação em grade a simulações computacionais de estruturas semicondutoras." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/76/76132/tde-24042008-114210/.
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Neste trabalho foi avaliada a utilização da grid computing em aspectos importantes para simulações em Física Computacional. Em particular, para aplicações de diagonalização de matrizes de grande porte. O projeto de código aberto Globus Toolkit foi utilizado para comparar o desempenho da biblioteca paralela de álgebra linear ScaLAPACK em duas versões baseadas na biblioteca de passagem de mensagens, a versão tradicional MPICH e a versão desenvolvida para um ambiente de grid computing MPICH-G2. Várias simulações com diagonalização de matrizes complexas de diversos tamanhos foram realizadas. Para um sistema com uma matriz de tamanho 8000 x 8000 distribuída em 8 processos, nos nós de 64 bits foi alcançado um speedup de 7,71 com o MPICH-G2. Este speedup é muito próximo do ideal que, neste caso, seria igual a 8. Foi constatado também que a arquitetura de 64 bits tem melhor desempenho que a de 32 bits nas simulações executadas para este tipo de aplicação<br>This work evaluates the use of grid computing in essential issues related to Computational Physics simulations. In particular, for applications with large scale matrix diagonalization. The Globus Toolkit open source project was used to compare the performance of the linear algebra parallel library ScaLAPACK in two different versions based on the message passing library, the traditional version MPICH and its version developed for a grid computing environment MPICH-G2. Several simulations within large scale diagonalization of complex matrix were performed. A 7.71 speedup was reached with the MPICH-G2 for a 8000 x 8000 size matrix distributed in 8 processes on 64 bits nodes. This was very close to the ideal speedup, that would be in this case, 8. It was also evidenced that the 64 bits architecture has better performance than the 32 bits on the performed simulations for this kind of application.
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Gregoire, Chloé. "Espace de modules de G2-fibrés principaux sur une courbe algébrique." Phd thesis, Université Montpellier II - Sciences et Techniques du Languedoc, 2010. http://tel.archives-ouvertes.fr/tel-00539858.
Full textAbstract:
L'objet de cette thèse est l'étude de l'espace de modules des G2-fibrés principaux sur une courbe complexe projective connexe lisse, où G2 désigne le groupe de Lie exceptionnel de plus petit rang. Le groupe G2 est caractérisé via trois approches différentes, la première étant celle où G2 est défini comme le groupe des automorphismes de l'algèbre complexe des octaves de Cayley. Les différentes réductions et extensions que peut admettre un G2-fibré principal sont étudiées ainsi que la relation entre la stabilité d'un G2-fibré principal et celle du fibré vectoriel qui lui est associé. L'espace de modules des G2-fibrés principaux semi-stables est analysé. Nous obtenons notamment une caractérisation de son lieu lisse, une décomposition explicite de son lieu singulier en trois composantes connexes et une analyse de l'espace de Verlinde de niveau 1 pour le groupe G2.
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Leão, Maria João de Lemos Pinto Estrela. "Modulation of G2/M cell cycle checkpoints by Epstein-Barr virus." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414473.
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Blakemore, Louise Margaret. "Curcumin-induced G2/M cell cycle arrest in colorectal cancer cells." Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/9809.
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Curcumin, a diet-derived chemopreventive and chemotherapeutic agent has been shown to induce G2/M cell cycle arrest, and previous studies suggested that microtubule depolymerisation may be linked to M-phase arrest. However, mechanisms involved have not been elucidated and often non-physiological concentrations of curcumin were used. The goal of this study was to characterise in more detail curcumin-induced cell cycle arrest using a panel of human colorectal cancer cell (CRC) lines, HT-29, SW480, HCT116 p53+/+, HCT116 p53-/- and HCT116 p21-/-. Using physiologically relevant concentrations of curcumin (5-10μM), achievable in the gut tissue following oral ingestion, cell cycle analysis showed that treatment for 12 hours results in significant G2/M arrest in all five cell lines. Curcumin treatment significantly increased the number of cells in M phase in 4 out of the 5 lines tested for this duration, and those with microsatellite instability (HCT116) were found to have a higher mitotic index than those with chromosomal instability. Pre-treatment with caffeine abrogated mitotic arrest in these cell lines, indicating the involvement of the ATM/ATR kinases. Activating phosphorylation of the Chk1 kinase was increased and total protein levels of CDC25C reduced, further implicating the DNA damage pathway in the induction of arrest. Higher levels of HSP70 were also found, indicating proteotoxic stress such as proteasomal inhibition. Image analysis revealed impaired mitotic progression, and significantly higher levels of mitotic spindle abnormalities following curcumin treatment. Aurora B mislocalisation and significantly lower levels of centrosomal separation were found in the HCT116 p53+/+ line. Furthermore, the high levels of pH2A.X staining seen in curcumin-treated mitotic but not interphase cells suggest that aberrant mitosis may result in DNA damage. This proteotoxic and genotoxic stress incurred following curcumin treatment may contribute to the upregulation of NKG2D ligands on the cell surface, leading to CRC lysis and enhancement of the anti-cancer immune response.
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Quinn, Jennifer E. "BRCA1 mediated G2/M cell cycle arrest in response to taxol." Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326034.
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Melton, R. G. "Physiological properties of carboxypeptidase G2 : Polymer conjugates and their clinical application." Thesis, Birmingham City University, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374679.
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Ahmad, Syed Saif. "Deciphering the role of BRCA2 at the damage-induced G2 checkpoint." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/278013.
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Loss of DNA damage-induced G2 checkpoint control is associated with genome instability, tumour formation and the therapeutic response of tumours to genotoxic agents. The large 3418 residue protein encoded by BRCA2 – heterozygous germline mutations in which predispose to cancer - has recently been implicated in G2 checkpoint maintenance. However, the mechanistic basis of BRCA2’s role in the G2 checkpoint remains unknown. The overall aim of my research is to understand the mechanism by which BRCA2 regulates the G2 checkpoint. Domain mapping studies, using overlapping fragments encoding the full-length BRCA2 protein, carried out in our laboratory suggest that BRCA2’s function at the G2 checkpoint is mediated through regions that span BRCA2 amino acids (aa) 1-454 and aa 2438-2824. My research has focused on understanding how these two regions contribute to G2 checkpoint function through the interrogation of two novel interactions of BRCA2 mediated at these regions. My experiments have identified that BRCA2 interacts with the serine/threonine kinase ATR (aa 2438-2824) and the deSUMOylase SENP1 (aa 1-454). ATR is known to play a key role at the G2 checkpoint and my results identify that loss of BRCA2 leads to a reduction in ATR activity at sites of damage. This leads to a downstream attenuation in the phosphorylation of Chk1 – an important effector protein of the G2 checkpoint. BRCA2 is known to function in DNA repair and is recruited to sites of DNA damage, where it displaces RPA bound to exposed single-strand DNA. RPA is required to localise and activate ATR during the G2 checkpoint and therefore I hypothesise that BRCA2’s role at the checkpoint is to substitute for RPA and mediate ATR activation. I have also shown that SENP1 interacts with BRCA2 at a region within the N-terminus (aa 290-454). SUMOylation has been increasingly recognised as an important post-translational modification (PTM) in the context of the DNA damage response, and SENP1 is involved in reversing this PTM. I have shown that BRCA2 is SUMOylated. Moreover, I have shown that loss of SENP1 prevents BRCA2 from being recruited to chromatin in a timely manner after DNA damage and that SENP1 depletion exacerbates the loss of G2 checkpoint maintenance seen in BRCA2 deficiency. Taken together, this work reveals novel insights into the mechanism by which BRCA2 maintains genomic stability through enforcement of the G2 checkpoint. This new knowledge has the potential to translate into a better understanding of how mutations in BRCA2 may lead to cancer.
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Tao, Yungan. "Interruption of G2-M and mitotic checkpoint : Influence on tumor radiosensitivity." Paris 11, 2008. http://www.theses.fr/2008PA11T062.
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Huang, Yehong. "The Kinetics of G2 and M Transitions Regulated by B Cyclins." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1386197228.
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Grégoire, Chloé. "Espace de modules des G2-fibrés principaux sur une courbe algébrique." Thesis, Montpellier 2, 2010. http://www.theses.fr/2010MON20086.
Full textAbstract:
L'objet de cette thèse est l'étude de l'espace de modules des G_2-fibrés principaux sur une courbe complexe projective connexe lisse, où G_2 désigne le groupe de Lie exceptionnel de plus petit rang. Le groupe G_2 est tout d'abord présenté comme le groupe des automorphismes de l'algèbre complexe des octaves de Cayley. D'autres définitions sont ensuite proposées. Les différentes réductions et extensions que peut admettre un G_2-fibré principal sont étudiées ainsi que la relation entre la stabilité d'un G_2-fibré principal et celle de son fibré vectoriel associé. L'espace de modules des G_2-fibrés principaux semistables est analysé. Nous obtenons notamment une caractérisation de son lieu lisse, une décomposition explicite de son lieu singulier en trois composantes connexes et une analyse de l'espace de Verlinde de niveau 1 pour le groupe G_2<br>This thesis studies the moduli space of principal G_2-bundles over a smooth connected projective curve, where G_2 is the exceptional Lie group of smallest rank. The group G_2 is first introduced as the group of automorphisms of the complex algebra of the Cayley numbers. Other equivalent definitions are also proposed. We study the reductions and extensions that a principal G_2_bundle can admit, as well as the link between a principal G_2-bundle and its associated vector bundle in relation to the notion of (semi)stability. The moduli space of semistable principal G_2-bundles is analysed. We notably obtain a characterisation of its smooth locus, with an explicit decomposition of its singular locus into three connected componants. We also give an analysis of the Verlinde space of G_2 at level 1
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Dufour, Quentin. "Une construction de métriques quaternion-kählériennes à partir du groupe G2." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066142/document.
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Le théorème central de cette thèse est une construction de métriques quaternion-kählériennes sur des variétés de dimension 8 modelées sur l'espace symétrique de type non-compact G2/SO(4). Cette construction s'inscrit dans la lignée des constructions de LeBrun (1989) et de Biquard (2000) pour lesquelles d'un côté les variétés quaternion-kählériennes construites possèdent un modèle homogène qui est un espace symétrique de type non-compact G/K, et d'un autre côté, les données initiales peuvent s'interpréter comme étant des déformations d'un bord de Furstenberg G/P où P est un sous-groupe parabolique de G. Ces constructions nous amènent ainsi à penser qu'il existe une correspondance générale entre des déformations de bords de Furstenberg G/P et des variétés quaternion-kählériennes.Ces déformations d'espaces G/P sont des variétés munies de géométries paraboliques. Après une présentation de la théorie des géométries paraboliques donnée dans la première partie, nous nous consacrerons, dans la deuxième partie à la correspondance précédemment supposée. En observant la construction de LeBrun (1989), nous réduirons les candidats pour une généralisation de cette construction à deux cas dont celui de l'espace G2/SO(4) et du parabolique P fixant une droite isotrope de R^{3,4}. Dans la dernière partie, nous donnerons justement la construction des métriques quaternion-kählériennes dont les données initiales sont des géométries paraboliques de type (G2,P). Cette construction passe par la construction d'espaces des twisteurs dans lesquels nous déformons des courbes doubles. Les variétés quaternion-kählériennes construites sont des ouverts des espaces de déformation de ces courbes<br>The main theorem of this thesis is a construction of quaternionic Kählerian metrics over a 8-manifolds modelled on the non-compact Riemannian symmetric space G2/SO(4). This construction is in line with LeBrun?s construction (1989) and Biquard?s construction (2000) for which, on one side, the quaternionic Kählerian manifolds constructed have a homogeneous model which is a non-compact Riemannian symmetric space G/K , and in the other side, the initial data can be seen as deformations of a Furstenberg boundary G/P with P a parabolic sub-group of G. These constructions lead us to think about a general correspondence between the deformations of Furstenberg boundaries and quaternionic Kählerian manifolds. Those deformation of G/P space are manifolds with parabolic geometries. After a presentation of the theory of parabolic geometries given in the first part, we will focus on the previous supposed correspondence in the second part. Observing LeBrun?s construction (1989), we will reduce the candidates for a generalisation of this construction to two cases among which the one of the space G2/SO(4) with the parabolic sub-group P stabilizing an isotropic line in R^{3,4}. In the last part, we will precisely give the construction of quaternionic Kählerian metrics with initial data some parabolic geometries of type (G2,P). This construction begins with the construction of twistor spaces where we will deform some double curve named ribbon. The quaternionic Kählerian manifolds constructed will be some open set in the space of deformation of these curves
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Li, Tzu Hao. "Open Platform Semi-Passive Ultra High Frenquency Radio Frequency Identi." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20060.
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Radio frequency identi cation (RFID) is a rapidly emerging technology that enables au-
tomatic remote identi cation of objects. Passive and semi-passive RFID systems can be
distinguished from other forms of wireless systems, because the RFID tags (transponders)
communicate by way of backscatter. In addition, passive tags derive their energy from
the RF energy emitted by the reader. RFID technology can provide a fully automated
data capture and analysis system.
Compared to a passive RFID system, an open platform semi-passive UHF RFID
tag can provide identi cation, security, low-power (compared to a wireless sensor net-
work(WSN)), medium range and medium processing speed. However, the eld of semi-
passive RFID is still under development, and has yet there are no open development
platforms available.
This thesis develops a prototype of a semi-passive UHF RFID tag that is compatible
with the leading UHF RFID standard EPCglobal Gen 2 Class 1. I alsot has the
exible
I2C and analog digital converter(ADC) interface, which allows the additional of external
analog and digital sensors. The sensor data can be read by microcontroller and stored at
memory. Standard reader can get sensor data by sending QUERY and READ command
to tag.
Test results of our open platform semi-passive UHF RFID tag demonstrated that it
can achieve a read rate above 50% when an open platform semi-passive UHF RFID tag
is placed four meters from the reader antenna and the reader output power is set to 21
dBm. In addition, the proposed semi-passive open platform RFID tag consumes very
little power (4.9 mA in 2V with system frequency set to 8MHz).
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Persico, Angela. "The Role of Golgi Fragmentation in the Regulation f G2/Prophase Transition." Thesis, Open University, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.520741.
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Thanasoula, Maria. "ATM/ATR-dependent responses to dysfunctional telomeres at the G2/M transition." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:b9f806e3-88e5-4dc4-b2e9-8ecf854249d1.
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Mammalian telomeres are nucleoprotein complexes at the end of chromosomes containing a specific protein complex, called shelterin. Shelterin protects chromosome ends from the DNA damage response (DDR), by facilitating the formation of a telomeric capping structure, called the T-loop. During their elongation in S phase, telomeres become transiently uncapped and can be sensed as DNA damage in G2 phase. This leads to the recruitment of DDR factors, such as phosphorylated histone H2AX (γH2AX), to the telomeres forming the so-called, telomere dysfunction-induced foci (TIFs). My PhD work described here, indicates that DNA damage occurring during interphase can persist after entry into mitosis, indicated by the detection of γH2AX at a subset of mitotic telomeres in human and mouse cells. This accumulation of γH2AX to mitotic telomeres is ATM-dependent and the γH2AX-labelled uncapped telomeres that persist, are shorter than the average telomere length for the entire cell population. Most importantly, my work suggests that telomere uncapping, naturally occurring or artificially induced, is detected by two parallel ATM/ATR-dependent pathways at the G2/M transition: a p53/p21-dependent pathway through the ATM/ATR-mediated phosphorylation of p53 at Ser15 and a CHK1/CHK2-dependent pathway that acts through negative regulation of CDC25 phosphatases. In particular, telomere uncapping triggered by TRF2 depletion leads to CHK2-dependent CDC25A degradation, while POT1 depletion results in CHK1-mediated CDC25A and CDC25C degradation. Both pathways act as sensors of unprotected telomeres at the G2/M transition and block cell cycle progression through inhibition of CDK1/Cyclin B complex, allowing telomere re-capping before entry into mitosis. This mechanism protects telomere integrity by the maintenance of a cell cycle stage conducive for capping reactions and thereby prevents genomic instability induced by telomere dysfunction. Finally, I studied the cellular functions of 3 poorly characterised shelterin components, TRF1, RAP1 and TPP1, in telomere protection. TRF1 and to a lesser extent RAP1 were shown to be important for telomere protection by suppressing DDR at the telomeres, while TPP1 was shown to be mainly responsible for the recruitment of the catalytic subunit of telomerase, TERT , to the chromatin, contributing to telomere maintenance. In conclusion, my work on both human and mouse models, reveals an important part of the DDR pathways activated by dysfunctional telomeres, as well as the molecular mechanisms underlying the cell cycle specific regulation of telomere capping, which ensures that only cells with intact telomeres enter mitosis.
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Serafin, Antonio Mendes. "Chemosensitivity of prostatic tumour cell lines under conditions of G2 block abrogation." Thesis, Cape Technikon, 2000. http://hdl.handle.net/20.500.11838/2245.
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Thesis (MTech (Biomedical Technology))--Cape Technikon, 2011.<br>Cancer of the prostate gland is now recognised as one of the principal medical problems in males.
In the USA, cancer of the prostate is the second most commonly diagnosed cancer after skin cancer
and the second most common cause of death from cancer after lung cancer. In South Africa,
prostate cancer is the second most common cancer, with an estimated annual incidence of 19.1 per
LOO000 men (Sitas, 1994). However, this incidence is probably under-estimated, due to incomplete
records. Comparison of the incidence of prostate cancer in the different racial groups shows that it
is the second most common malignancy in the White, Black (African) and Mixed (Coloured) race
groups, and the fourth most common malignancy in Asian (Indian) men in South Africa.
Metastatic prostate cancer is refractory to hormone therapy and remains incurable. Hence, novel
therapeutic approaches are needed. These anticancer drugs can be tested in tumour cell lines, and
cell culture methods also permit testing of optimum conditions.
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Bauchat, Jean-Luc. "Étude du raccordement géométrique G2 de surfaces rationnelles mises sous forme (SBR)." Lille 1, 1992. http://www.theses.fr/1992LIL10039.
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Le travail présenté est une contribution à l'étude des raccordements géométriques G1 et G2 entre surfaces rationnelles mises sous forme (SBR): il s'agit de construire une surface composite régulière formée de surfaces (SBR) convenablement raccordées. Une définition des raccords géométriques G1 et G2 entre deux surfaces est proposée. Les conditions analytiques obtenues conduisent, lorsqu'elles sont appliquées au cas de deux surfaces qui sont des PiOméga-projetées, à des conditions nécessaires et suffisantes portant sur les paramétrisations des surfaces «au-dessus». Ces CNS sont traduites en termes de vecteurs massiques pour exprimer les raccords G1 et G2 entre deux (SBR) rectangulaires ou triangulaires qui, par définition, sont des PiOméga-projetées de surfaces polynomiales. Plusieurs exemples illustrent en détail les résultats obtenus: le raccordement géométrique G2 de deux quadriques et le raccordement d'une (SBR) rectangulaire à une (SBR) triangulaire. Les relations obtenues permettent de traduire un problème continu de géométrie différentielle par des conditions portant sur les réseaux massiques de contrôle
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Hirabayashi, Shigeki. "APOBEC3B is preferentially expressed at the G2/M phase of cell cycle." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/264663.
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京都大学<br>新制・課程博士<br>博士(医学)<br>甲第23382号<br>医博第4751号<br>新制||医||1052(附属図書館)<br>京都大学大学院医学研究科医学専攻<br>(主査)教授 伊藤 貴浩, 教授 滝田 順子, 教授 江藤 浩之<br>学位規則第4条第1項該当<br>Doctor of Medical Science<br>Kyoto University<br>DFAM
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Mourgues, Lucas. "Identification d'une nouvelle fonction oncogénique de BMI1 à travers la répression du gène suppresseur de tumeur CCNG2 : une fenêtre thérapeutique potentielle." Thesis, Nice, 2014. http://www.theses.fr/2014NICE4064/document.
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BMI1 est une protéine appartenant à la famille des polycombs impliquée dans la régulation épigénétique de la transcription. Il a été montré que cette protéine est essentielle à la régulation de la prolifération, de la sénescence et du métabolisme ainsi qu’à l’auto-Renouvellement des cellules souches hématopoïétiques et cancéreuses. Ce répresseur transcriptionnel au fort potentiel oncogénique est retrouvé surexprimé dans de nombreux types de cancer ; dans le cas de la Leucémie Myéloïde Chronique (LMC) le niveau d’expression de BMI1 augmente avec l’aggravation de la pathologie. Cependant, les voies de signalisation impliquées dans sa surexpression et le rôle qu’il joue au sein de cette maladie demeurent méconnus. En réprimant l’expression de BMI1 par ARN interférence nous avons pu mettre en évidence que ce polycomb était essentiel à la prolifération cellulaire ainsi qu’au potentiel clonogénique des cellules de LMC. Nous avons également démontré pour la première fois que BMI1 soutenait la croissance tumorale à travers la répression d’un processus autophagique délétère pour la cellule cancéreuse. Une approche transcriptomique nous a permis d’identifier la cible transcriptionnelle impliquée dans ce processus, la Cycline G2. Nous avons, pour finir, trouvé une molécule, via une approche bioinformatique, capable de réinduire l’expression de la Cycline G2 dans les cellules de LMC, l’alexidine dihydrochloride. Cette molécule induit une forte autophagie dans les cellules cancéreuses ainsi que de l’apoptose. Elle s’est également montrée capable de resensibiliser à l’imatinib (un inhibiteur de BCR-ABL) une lignée pourtant résistante<br>The polycomb protein Bmi1 is a major epigenetic regulator. It has been shown that this protein is essential for the regulation of cell proliferation, senescence and metabolism but also self-Renewal of hematopoïetic and cancer stem cells. This transcriptional repressor, with a strong oncogenic potential, is overexpressed in many types of cancer. In case of Chronic Myeloid Leukemia (CML) the expression level of BMI1 is associated with worsening prognosis. However, the signaling pathways involved in its overexpression and its role in this disease remains unclear. By using RNAi to repress BMI1 expression we highlighted that this polycomb was essential for proliferation and clonogenicity of CML cells. We also demonstrated, for the first time, that BMI1 supported tumor growth through repression of deleterious cancer cell autophagy. A transcriptomic approach allowed us to identify a transcriptional target involved in this process: the Cyclin G2. Through a bioinformatic approach, we finally found a molecule capable of expression re-Induction of Cyclin G2 in CML cells : alexidine dihydrochloride. This molecule induced a high level of autophagy as well as apopotosis in cancer cells. It had also been able to re-Sensitize to imatinib a resistant cell line. In conclusion, our results revealed a new role for the polycomb BMI1 in supporting the CML pathology. Moreover, our work allowed the identification of two new approaches for therapeutically targeting this oncogene functions
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Martín, Rodríguez Elena 1989. "Control of G2/M cell cycle transition by a complex of the splicing factors SPF45/SR140/CHERP." Doctoral thesis, Universitat Pompeu Fabra, 2018. http://hdl.handle.net/10803/572042.
Full textAbstract:
A splicing network analysis that captured functional
similarities among spliceosomal components, revealed a
prominent core module containing splicing factors SPF45,
SR140 and CHERP. We report that these factors form a
complex, as they stabilize each other’s protein levels, coimmunoprecipitate
and co-sediment in glycerol gradients.
Depletion of SPF45, SR140 or CHERP in HeLa cells impairs
progression through the G2/M phase of the cell cycle and this
is correlated with decreased cell proliferation and increased
apoptosis. Transcriptome-wide analyses revealed extensive
overlap between alternative splicing events regulated by
SPF45, SR140 or CHERP and that common targets are
enriched in G2/M transition genes. A relevant alternative
splicing change was identified in FOXM1, a key
transcriptional regulator of G2/M transition. Depletion of
SPF45, SR140 or CHERP promotes total or partial inclusion
of FOXM1 exon 9, which disrupts the transactivation domain
and results in a non-functional FOXM1 isoform. We propose
that alternative splicing regulation of FOXM1 contributes to
the cell cycle G2/M phase arrest observed upon SPF45,
SR140 or CHERP knock down and discuss possible
physiological scenarios for this regulation.<br>Un análisis de red de factores de splicing capturó
similaridades funcionales entre componentes del
spliceosoma y reveló un prominente módulo central que
contiene a los factores de splicing SPF45, SR140 y CHERP.
Hemos demostrado que estos factores forman un complejo,
ya que estabilizan mutuamente sus niveles de proteínas, coinmunoprecipitan
y co-sedimentan en gradientes de glicerol.
La depleción de SPF45, SR140 o CHERP en células HeLa
impide la progresión a través de la fase G2/M del ciclo celular
y ello se correlaciona con una disminución de la proliferación
celular y un aumento de la apoptosis. Análisis globales del
transcriptoma han revelado un sustancial solapamiento entre
los eventos de splicing alternativo regulados por SPF45,
SR140 o CHERP y que las dianas comunes están
enriquecidas en genes implicados en la transición G2/M. Se
ha identificado un cambio de splicing alternativo relevante en
FOXM1, un regulador transcripcional clave en la transición
G2/M. La depleción de SPF45, SR140 o CHERP promueve la
inclusión total o parcial del exon 9 de FOXM1, lo que
interrumpe el dominio de transactivación y da lugar a una
isoforma no funcional de FOXM1. Proponemos que la
regulación del splicing alternativo de FOXM1 contribuye al
arresto en la fase G2/M del ciclo celular observado cuando se
deplecionan SPF45, SR140 o CHERP y discutimos posibles
escenarios fisiológicos para esta regulación.
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Schmit, Fabienne. "LINC, a novel protein complex involved in the regulation of G2/M genes." kostenfrei, 2008. http://www.opus-bayern.de/uni-wuerzburg/volltexte/2009/2933/.
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Daviknes, Ingrid Marie Eriksen. "G2 checkpoint siRNA screen in irradiated cancer cells: validation of candidate positive hits." Thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for bioteknologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-14145.
Full textAbstract:
Prior to this project, a high throughput assay was developed in order to perform automated RNAi screens with siRNA- libraries targeting potential regulators of the G2 checkpoint. The libraries were covering the human kinases, phosphatases and DNA repair. The aim of this project was to validate the candidate hits from the phosphatome screen as possible G2 checkpoint regulators. To validate the candidate hits, esiRNAs were applied in order to down regulate the target proteins, and G2 checkpoint abrogation was assayed by flow cytometry analysis. To confirm that the assay did work, the effects of inhibiting WEE1 by the small molecule inhibitor, MK1775, were tested in both U2OS and U2OSp53 cells. Both the early and the late G2 checkpoint were tested for.WEE1 was a hit in the kinome screen, and a well-known regulator of the G2 checkpoint. The samples treated with MK1775, and 6Gy were showing a dose-dependent abrogation of the G2 checkpoint when stained for H3-p and analyzed by flow cytometry.In optimization experiments for esiRNA transfection, Effectene was chosen over Oligofectamine as the preferred transfection reagent. The transfection conditions which were decided to be the most efficient in down regulating the target protein were 5&#956;L esiRNA and 10 &#956;L Effectene. For the validation experiments it was focused on the two phosphatases SSH3 and PTPN7. Western blotting analysis showed that the protein level of SSH3 was reduced to less than 50% at two days following transfection with SSH3 esiRNA.The validation experiment did not show any abrogation of the G2 checkpoint by neither SSH3 nor PTPN7 in irradiated cells. More repetitions of the experiment are needed in order to validate- or reject these as false hits. However, the results from a whole-genome DNA damage response siRNA screen were recently published. Neither PTPN7 nor SSH3 were scoring in this screen. These facts are supporting the results that SSH3 and PTPN7 are false hits.
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Lingner, Carol. "Mitotic cycles in Schizosaccharomyces pombe, analysis of mutants defective in G2/M control." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq20571.pdf.
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Bezerra, Érica Leandro. "G2: um gráfico de controle por atributos no monitoramento da variabilidade de processos." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/3/3136/tde-26092017-135421/.
Full textAbstract:
Quando há interesse em monitorar a variância de uma característica da qualidade de interesse através de gráfico de controle por variáveis, o gráfico S2 é a alternativa mais usual. Entretanto, há situações onde mensurar a característica da qualidade é caro, consome mais tempo por unidade de inspeção, requer maior esforço dos operadores quanto à obtenção dos dados ou envolve ensaios destrutivos. Nestes casos, a classificação da variável contínua em categorias através de um dispositivo torna-se uma alternativa interessante. A avaliação pode ser mais rápida, a análise e o equipamento utilizado podem ser mais simples, de modo que o custo final da inspeção seja menor. O objetivo do trabalho é propor um gráfico de controle por atributos para monitoramento da variabilidade. Para tanto a estatística GS2 é calculada e gráfico sinaliza se GS2 > LC, LC limite de controle determinado de modo que minimize o ARL1, fixado um valor de ARL0. Como resultado a performance do gráfico GS2 é comparada ao gráfico S2 em termos de ARL1.<br>In cases aiming at monitoring the variance of a products quality characteristics using a variable control chart, chart S2 is the most used alternative. However, in some situations, this solution can be expensive, demand more time per individual inspected unit, demand greater efforts from operators to acquire data or involve destructive tests. In such cases, the use of a gauge measurement tool to classify the continuous variable into categories, becomes an interesting alternative. The assessment can be faster, the analysis and the tool used can be simple, resulting in less costly final inspections. This work proposes the use of an attribute control chart to monitor variability. Statistics GS2 is calculated and control chart signalize if GS2 > CL, whereas CL is the determined control limit, minimizing ARL1 for a fixed value of ARL0. GS2 control chart performance is compared to S2 chart based on ARL1.