Dissertations / Theses on the topic 'Polo kinases'
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Michel, Daniel R. "Cytoskeletal Architecture and Cell Motility Remain Unperturbed in Mouse Embryonic Fibroblasts from Plk3 Knockout Mice." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1446546516.
Full textPrimot, Aline. "Etude de la régulation de deux protéines kinases : : GSK-3 et polo." Rennes 1, 2001. http://hal.upmc.fr/tel-01117984.
Full textRandall, Catherine Leah. "Genetic dissection of polo-like kinase 1's functions in human cell division /." Access full-text from WCMC, 2009. http://proquest.umi.com/pqdweb?did=1692357351&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.
Full textLong, Thavy. "Caractérisation structurale et régulation de l'activité de deux Polo-like kinases de Schistosoma mansoni : SmPlk1 et SmSak." Lille 2, 2010. http://www.theses.fr/2010LIL2S007.
Full textSchistosomiasis is the most important helminthic infection in term of morbidity and mortality in many developing countries and represents the second parasitic disease to malaria. The evidence for praziquantel (PZQ) resistance, the only drug currently used to treat the disease, led the World Health Organization (WHO) to consider as a priority the finding of novel therapeutic targets. Egg production is responsible for disease transmission by complex trematodes parasites but also for the pathology of schistosomiasis. My PhD work contributes to a better understanding of the complex mechanisms that regulate schistosome reproduction. One particularity of schistosomes is that the sexual development of females requires a permanent contact with the male, allowing a level of fecundity exceptionally high. Therefore, the molecular mechanisms implied in this hyperfecundity are obvious targets for the control of schistosomiasis. Polo kinases are serine/threonine kinases, belonging to the Polo-like kinase family (Plks) whose members are conserved from yeast to mammals. During last years, human Plks have been extensively studied and considered as major targets for cancer because of their dramatic overexpression in proliferating cells and many tumors. In silico researches have led us to the characterization in S. Mansoni, SmPlk1, homologous to human Plk1. SmPlk1 was abundantly transcribed in parasite stages containing germinal cells expected to undergo frequent cell divisions, and particularly in the reproductive organs of adult worms suggesting a potential role of SmPlk1 in division processes. We have shown that SmPlk1 induced resumption of meiosis in oocytes of Xenopus. Moreover, the specific Plk1- inhibitor BI 2536 used in clinical trials, induces morphological aberrations in reproductive organs and inhibits oogenesis and spermatogenesis in paired worms, indicating a role of SmPlk1 in gamete multiplication and differentiation in S. Mansoni parasites and so the possibility that this kinase could be a novel potential target for schistosomiasis treatment. In parallel to this work, we recently identified a second Plk in S. Mansoni, SmSak different for its structure and its functions, and notably its role in the centriole duplication. Moreover, we identified a potential activator of Plk, SmSLK (S. Mansoni Ste-20 like kinase) able to activate specifically SmPlk1 in particular conditions. Indeed, two original mechanisms, one dependent on caspases and the other one dependent on antisense RNA, could regulate the kinase activity of SmSLK and therefore, the activity of SmPlk1
MONTANI, FRANCESCA. "MOLECULAR MECHANISMS UNDERLYING CDC14 ACTIVATION DURING MITOTIC EXIT IN SACCHAROMYCES CEREVISIAE." Doctoral thesis, Università degli Studi di Milano, 2012. http://hdl.handle.net/2434/214785.
Full textDahmene, Manel. "Caractérisation de la voie de dégradation de l'α-synucléine catalysée par la Polo-Like Kinase 2." Master's thesis, Université Laval, 2018. http://hdl.handle.net/20.500.11794/28320.
Full textParkinson's disease is a chronic neurological disease characterized by the progressive degeneration of the dopaminergic neurons of the substantia nigra pars compacta. A second neuropathological feature of this disease is the accumulation of intracellular aggregates called Lewy bodies. These aggregates are formed by a pre-synaptic protein, α-synuclein (α-syn). This pathological accumulation interferes with the vital metabolic pathways of neurons such as synaptic transmission and mitochondrial activity, leading to cell death. Consequently, promoting the elimination of the toxic forms, reducing the expression of the native form and decreasing the probability of aggregate formation could be a therapeutic strategy of interest for the treatment of Parkinson's disease and other related disorders. Recently, we have described a novel α-syn degradation pathway that is catalyzed by the enzymatic activity of Polo-like kinase 2 (PLK2). However, the cellular mechanism and the identity of the molecules involved are still unknown. So, my work has focused on studying this pathway and its various steps that lead to remove the toxic effect of α-syn. In this thesis we show that, in addition to PLK2, PLK3, another member of the PLK family, is able to phosphorylate α-syn at S129 and induce its elimination. In addition, we declare that this action requires a physical interaction between the 2 proteins (α-syn and PLK2) involving the N-terminal domain and that a poly-ubiquitination step is essential for the autophagic degradation of the α-syn and PLK2 complex. This effect of PLK2 is also observed on mutated forms of α-syn such as α-syn A30P, α-syn A53T and is more pronounced in the case of the α-syn E46K mutant. The characterization of this elimination pathway offers new opportunities for the development of treatments that allow, in a specific and selective manner, the degradation of α-syn and thus the reduction of its toxic forms.
Pearson, John Robert. "Metazoan polo-like kinases : their conservation and function during the specialised cell cycles of oogenesis and early embryogenesis." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620065.
Full textBrassac, Thierry. "Analyse fonctionnelle de la kinase "Polo-like" lors de l'entrée et de la sortie de phase M des ovocytes de Xénope." Montpellier 2, 2000. http://www.theses.fr/2000MON20056.
Full textRawal, C. "ROLE OF POLO KINASE CDC5 AND SLX4-RTT107 COMPLEX IN CHECKPOINT SIGNALING DURING DNA DAMAGE IN S. CEREVISIAE." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/335192.
Full textRenner, Annelies. "Mise au point de tests "preuve de principe" pour l'étude des inhibiteurs de la Plk1 et caractérisation de la Plk1 en tant que cible dans le traitement des leucémies aigües myéloïdes." Toulouse 3, 2008. http://thesesups.ups-tlse.fr/430/.
Full textPolo-like kinase 1, a major regulator of mitosis, is found overexpressed in many cancers and its overexpression correlates with a bad prognosis. Experimentally, the constitutive expression of Plk1 induces transformation of NIH3T3 cells and confer them the ability to initiate new tumours in athymic mice. In addition, Plk1 depletion in cancer cells induces apoptosis, suggesting that Plk1 may be a new pharmacological target in anticancer therapies. The first aim of my thesis was to generate molecular and cellular tools in order to characterize the activity of Plk1 inhibitors, evaluate the implication of Plk1 in different steps of cell division and to find new partners Plk1. We generated inducible cell lines allowing the expression of wild type and mutants' forms (inactivated, overactivated) of Plk1, and the analysis of their impact on growth, proliferation, cell cycle and also on known substrates of Plk1. As expected, the higher the activity of Plk1 is, the best its impact on these biological processes. We have tested on these inducible cell lines several inhibitors of Plk1, and developed an assay allowing a rapid and highly efficient evaluation of the effect of these inhibitors on the Plk1 pathway. The Luminex methodology was used on cell extracts in order to assess the activity of Plk1 on its downstream effectors. This methodology appears to be very efficient to analyse the effects of putative Plk1 inhibitors in cellulo. The second aim of my thesis was to analyse the status and role of Plk1 in a malignant hemopathy, Acute Myeloid Leukemia (AML). AML is a clonal hemopathy characterized by a block in differentiation and by an uncontrolled proliferation of immature leukemic cells. Molecular mechanisms involved in the dysregulation of cell cycle in AML are still poorly understood. We have characterized the expression and the role of Plk1 in AML cell lines and primary cells and analysed the consequences of a specific Plk1 inhibition in this pathology. .
Martino, Lisa. "Rôle et régulation de la kinase PLK-1 lors de l'entrée en mitose dans l'embryon de Caenorhabditis elegans." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC225.
Full textDuring cell division, a mother cell duplicates (interphase) and then segregate its genetic material equally between the two daughter cells (mitosis). Between these two stages, the cell undergoes a drastic reorganization governed by the major actor Cdk1-Cyclin B, leading to mitotic entry. The activation of this kinase is regulated by an auto-amplification loop where the first molecules of Cdk1-Cyclin B stimulate activation of the following. Plk1 kinase has been shown to initiate this self-amplification loop by stimulating activators and repressing upstream Cdk1-Cyclin B inhibitors. For this kinase to be fully active, it must itself be activated by Aurora A, in the presence of its coactivator Bora. It is crucial to understand how all these actors coordinate in space and time to trigger mitotic entry because a disruption could lead to a segregation of anarchic DNA, leading to the formation of tumors and the appearance of cancers. During my thesis, I first contributed to demonstrate a conserved mechanism of Plk1 activation in human cells and in C. elegans (PLK-1), involving the coactivator Bora or SPAT-1 in C. elegans. We have shown that the phosphorylation of SPAT-1 by Cdk1-Cyclin B induces its interaction with PLK-1, which promotes the phosphorylation of PLK-1 by Aurora A and thus its activation in vitro. This phosphory-dependent mechanism of SPAT-1 is important in vivo for controlling the entry into mitosis over time. In addition, activation of Plk1 in vitro with human proteins strongly suggests conservation of the mechanism. We then showed that the phosphorylation of Bora and SPAT-1 by Cdk1 on residues S41, S112, S137 and S119, S190, T229 respectively, is necessary for their interaction with Plk1 / PLK-1, then triggering the activation of Plk1 / PLK-1 and mitotic entry. These results demonstrate that phosphorylated Bora / SPAT-1 is part of the self-amplification loop of Cdk1-Cyclin B via the activation of Plk1, ultimately enabling irreversible activation of the actors of mitotic entry. Subsequently, I focused on the role of PLK-1 in nuclear envelope breakdown using the C. elegans early embryo as a model system. After demonstrating that PLK-1 is crucial for the nuclear envelope breakdown in embryos, I observed a localization of PLK-1 to the nuclear envelope before its rupture and I identified a nucleoporin complex involved in this process. Indeed, NPP-1, NPP-4 and NPP-11 whose function is to regulate nucleo-cytoplasmic transport, also have a second role in the recruitment of PLK-1 to nuclear pores. PLK-1 interacts with its phosphorylated substrates by two types of Plk1-dependent and independent priming mechanisms, involving another upstream kinase such as Cdk1-Cyclin B for example. I have shown that the recruitment of PLK-1 to the pores depends on both mechanisms, thus requiring coordination between Cdk1-Cyclin B and PLK-1. Once PLK-1 is at the center of the nuclear pore, it can probably phosphorylate many nucleoporins and participate in the disassembly of pores, leading to tnuclear envelope breakdown
Stokes, Jamie Edward. "Small molecule approaches targeting the Polo-box domain of Polo-like kinase 1." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648778.
Full textDonaldson, M. M. "Multiple roles of polo kinase in Drosophila melanogaster." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598595.
Full textAbraham, Anne. "Polo-like kinase interacting proteins in fission yeast." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/10699.
Full textReindl, Wolfgang. "Inhibition of polo-like kinase 1 by small molecules targeting the polo-box domain." kostenfrei, 2008. http://mediatum2.ub.tum.de/doc/650458/650458.pdf.
Full textNguyen, Annie, Vijay Gokhale, and Gregory Rogers. "Therapeutic Molecular Targeting of Polo-Like Kinase 4 for Cancer Treatment." The University of Arizona, 2015. http://hdl.handle.net/10150/614130.
Full textObjectives: Two characterized peptide substrates were assayed with human Polo-like kinase 4 to determine phosphorylation activity. A pilot library of Type-II kinase inhibitors designed to fit into the ATP-binding pocket will be screened to determine HsPlk4 inhibition activity, which will help characterize a novel drug compound. Methods: Two peptide substrates of varying concentrations (2 uM, 1 uM, and 0.5 uM) were each combined with serial dilutions of HsPlk4 (1.25 uM, 0.625 uM, 0.313 uM, 0.156 uM, 0.078 uM, and 0.039 uM). EZ Reader detected phosphorylation activity by measuring fluorescence of both substrate and product, which separated at respective time points based on electrophoresis. The subsequent part of the experiment will be to inhibit the kinase activity with molecular inhibitors. Results: The results showed HsPlk4 activity with the modified PLKtide, (5FAM)KKKTPSDSLYDDGLSKK(CONH2). All reactions with the various concentrations of substrate 1 and HsPlk4 showed phosphorylation activity. The reaction started within the first 10 minutes, quickly reaching maximal phosphorylation of substrate. No p-values were calculated due to lack of data. Conclusions: No overall conclusions can be drawn based on the current results. Results showed the reaction reached its saturation point, so methods need to be refined to obtain data within the first 10 minutes. HsPlk4 phosphorylation of PLKtide confirmed the presumption that PLK family is a conserved family of Ser/Thr kinases. There are practical limitations for obtaining good kinetics data depicting enzyme activity, such as having EZ Reader quickly sample the reaction.
Eckerdt, Frank. "Funktionelle Charakterisierung von Interaktionspartnern der Polo-like-Kinase 1 (Plk1)." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=96938193X.
Full textZhang, Yun [Verfasser], and Andreas [Gutachter] Gießl. "Novel insights into the aberrant activation of fibroblasts in systemic sclerosis - Casein kinase 2, Poly(ADP-ribose)-Polymerase 1, and Janus kinase1 mediated transactivation of Janus kinase2 as novel players / Yun Zhang ; Gutachter: Andreas Gießl." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2016. http://d-nb.info/1114499722/34.
Full textSchmidt, Andreas. "Functional characterization of a novel Xenopus polo-like kinase interacting protein." Diss., lmu, 2006. http://nbn-resolving.de/urn:nbn:de:bvb:19-59773.
Full textRobert, Kin Yip Cheng. "Structural and functional studies of the mitotic Polo-like kinase 1." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432557.
Full textNeutzner, Melanie. "Regulatoren des Zellteilungszyklus der Hefe Saccharomyces cerevisiae : die Polo-Kinase Cdc5 und der Ubiquitinierungsfaktor Hct1 /." [S.l. : s.n.], 2003. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB10605153.
Full textWarnke, Silke. "Funktionelle Charakterisierung der humanen Polo-Kinase Plk2-Snk im Zell- und Centrosomenzyklus." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=971267154.
Full textHabedanck, Robert. "The Human Polo-like Kinase 4 is a Regulator of Centrosome Duplication." Diss., lmu, 2006. http://nbn-resolving.de/urn:nbn:de:bvb:19-57757.
Full textSeeburg, Daniel P. (Daniel Philip). "The role of Polo-like kinase 2 in synaptic function and plasticity." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/38993.
Full textIncludes bibliographical references.
Homeostatic forms of plasticity keep the spiking output of neurons within an optimal range in the face of changing activity levels of the surrounding network, but little is known about the underlying molecular mechanisms, particularly during heightened activity. We report in Chapter 2 that in hippocampal neurons experiencing elevated activity, the activity-inducible protein kinase, Polo-like kinase 2 (Plk2), was required for synaptic scaling in dissociated culture and for reducing membrane excitability in slice culture-two principal compensatory mechanisms underlying homeostatic plasticity. Inhibition of Plk2 activity in slice culture during elevated activity resulted in increased dendritic spine size and density as well as a "run-up" in synaptic strength that prevented subsequent LTP. Thus, the homeostatic functions of Plk2 allow synapses to remain within a modifiable range during prolonged heightened network activity. In Chapter 3, we show that the homeostatic prevention of run-up during elevated activity also depended on CDK5, which acted as a "priming" kinase for the phospho-dependent binding of PIk2 to its substrate SPAR, a postsynaptic RapGAP.
(cont.) Overexpression of SPAR strengthened synapses, whereas RNAi knockdown of SPAR weakened synapses and disrupted homeostasis. Thus CDK5-dependent recruitment of Plk2 to SPAR, followed by Plk2-mediated degradation of SPAR, constitutes a likely molecular mechanism for Plk2-dependent homeostatic plasticity in neurons.
by Daniel P. Seeburg.
Ph.D.
Argunhan, Bilge. "Interplay between Dbf4-dependent Cdc7 kinase and polo-like kinase unshackles mitotic recombination mechanisms by promoting synaptonemal complex disassembly." Thesis, University of Sussex, 2016. http://sro.sussex.ac.uk/id/eprint/59019/.
Full textWestendorf, Jens. "Regulation of Polo-like kinase 4 via phosphorylation and ubiquitin-dependent proteolytic degradation." Diss., lmu, 2009. http://d-nb.info/1000276333/34.
Full textGheghiani, Lilia. "Mécanisme de contrôle de l'entrée en mitose par Polo-like kinase 1 (PlK1)." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066385/document.
Full textA main requirement of the cell cycle is a tight coordination between the completion of the replication process and entry into mitosis in order to maintain genetic integrity and the identity and survival of cell progeny. All somatic cells reproducibly execute an intermediate G2 phase of constant duration during successive cell divisions in a given cell type. However the molecular mechanisms controlling precisely its duration during unperturbed cell cycle remains poorly characterized. In this context, the main objective of my PhD project was to decipher signaling pathways controlling entry into mitosis during normal cell cycles as well as their spatiotemporal regulation. CyclinB1-Cdk1, the universal master mitotic driver, is under the control of direct inhibitors (Wee1 and Myt1) and activators (Cdc25A, B and C). Previously, it was determined that CyclinB1-Cdk1 is suddenly activated in very late G2 phase, suggesting that a rapid modification in the equilibrium between its opposite regulators is reproducibly taking place in late G2 by poorly elucidated mechanisms. During my PhD, I investigated the potential role of Polo-like kinase 1 (Plk1) in the initial activation of CyclinB1-Cdk1. Even though its roles during mitosis are well characterized, its contribution for the regulation of entry into mitosis remains controversial. At the molecular level, Plk1 was shown to phosphorylate at least in vitro, several regulators of CyclinB1-Cdk1 including Cdc25B&C, and Wee1 and Myt1. However, it remains largely unknown if these phosphorylation events are taking place in vivo and whether they significantly contribute to the activation process of CyclinB1-Cdk1 leading to mitotic entry
Pahlavan, Golbahar. "Polo-like kinase 1(Plk1) et la maturation méiotique de l'ovocyte de souris." Paris 7, 2001. http://www.theses.fr/2001PA077229.
Full textUllrich, Andrea [Verfasser]. "Expressionsmuster der Polo-like-Kinase 1 und 3 im humanen Magenadenokarzinom / Andrea Ullrich." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2010. http://d-nb.info/1024007022/34.
Full textZhu, Kaiyuan, and 祝开元. "Polo-like kinase 1 (Plk1) phosphorylates VCP T76 during mitosis for the fragmentation of Golgi in mammalian cell." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208019.
Full textMyer, David. "Role of the Mammalian Polo-Like Kinase 3(Plk3) in Cell Cycle Regulation and DNA Damage Checkpoints." University of Cincinnati / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1141395911.
Full textLee, Cathy. "Molecular targeting of polo-like kinase 1 (PLK1) for the treatment of brain tumours." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44820.
Full textZalles, Nicole. "Effects of MicroRNA modulation of PLK1 in Breast Cancer in combination with PLK1 inhibitor NMS-P937." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1554130079416561.
Full textSpänkuch-Schmitt, Birgit. "Funktionelle Studien zur Hemmung von PLK1 (Polo-like-Kinase 1) in vitro und in vivo." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968909922.
Full textTriscott, Joanna Catherine Caprio. "Polo-like kinase 1 as a prognostic and therapeutic target in high-grade brain tumors." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/54512.
Full textMedicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate
Patel, Avinash. "Exploiting classical and chemical genetics to interrogate the polo kinase phospho-proteome of fission yeast." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/exploiting-classical-and-chemical-genetics-to-interrogate-the-polo-kinase-phosphoproteome-of-fission-yeast(c6666a88-fb38-47f2-bfc8-62c864823073).html.
Full textKlebba, Joseph Earl. "A Comprehensive Analysis of Polo-like Kinase 4's Regulation and Role in Centriole Biogenesis." Diss., The University of Arizona, 2014. http://hdl.handle.net/10150/318808.
Full textLabella, Sara. "Characterization of the functions of polo-like kinase 2 during meiotic chromosome pairing in C. elegans." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114400.
Full textLes deux cycles de division cellulaire qui constituent la méiose représentent un processus conservé au cours de l'évolution des espèces qui permet de créer les gamètes nécessaires à la reproduction sexuelle. Compte tenu de l'importance de ce processus dans la formation de toute nouvelle vie, il est essentiel pour les cellules méiotiques d'assurer la séparation correcte des chromosomes homologues lors de la première division de méiose (MI), puis des chromatides sœurs lors de la deuxième division de méiose (MII) afin d'éviter aneuploïdie des gamètes et infertilité. Au cours de la méiose I, les chromosomes maternels et paternels homologues se reconnaissent et s'alignent sur toute leur longueur (appariement). Dans de nombreux organismes cette première étape aboutit à la formation du complexe synaptonémal (SC) qui stabilise davantage leurs interactions. Puisque la formation du SC est indépendante de l'homologie des chromosomes, les processus d'appariement et de synapse doivent être dûment coordonnés pour que la formation du SC n'ait lieu qu'après vérification de l'homologie. Pendant le processus d'appariement des chromosomes chez le nématode C. elegans, une extrémité de chaque chromosome (les centres d'appariement, PC) interagit avec l'enveloppe nucléaire (NE) et génère vraisemblablement leur mouvement à l'intérieur du noyau par le biais d'une connexion au cytosquelette via l'enveloppe nucléaire, un processus bien conservé des levures aux mammifères. La fonction du mouvement des chromosomes et la façon dont il est établi et réglementé est encore mal comprise dans tout système. Je présente dans ce manuscrit ma contribution à la compréhension du mécanisme et de la fonction précise de ce processus dans le mouvement des chromosomes lors de la méiose chez C.elegans.Mon travail initial a porté sur la caractérisation d'une protéine polo-like kinase 2 (PLK-2). PLK-2 se localise au niveau des centres d'appariement associés à l'enveloppe nucléaire au début de la méiose; son absence perturbe gravement l'appariement des homologues et conduit à la formation de synapse non-homologue. Des travaux antérieurs avaient montré que à l'entrée en méiose l'enveloppe nucléaire est réorganisée de telle façon que les complexes protéiques SUN-1/ZYG-12 qui permettent de créer la liaison physique entre le cytosquelette à l'extérieur du noyau et les chromosomes à l'intérieur s'agrègent entre eux au voisinage des centres d'appariement des chromosomes. J'ai montré que c'est l'activité de PLK-2 qui préside à la réorganisation de ces complexes SUN-1/ZYG-12 dans l'enveloppe nucléaire, et que ces complexes sont directement nécessaires au mouvement des chromosomes durant le processus d'appariement. Par mutagénèse dirigée j'ai créé une protéine PLK-2 sans activité kinase, et j'ai ainsi pu démontrer qu'une réaction de phosphorylation par PLK-2 est essentielle au mouvement des chromosomes; en son absence les chromosomes forment des synapses non homologues. La découverte et l'étude d'un allèle non nul de plk-2 (vv44) a aussi permis de comprendre que le mouvement des chromosomes n'est pas suffisant à la reconnaissance des homologues, puisque dans ces mutants vv44 les chromosomes, bien que mobiles, ne créent pas de réorganisation des complexes SUN-1/ZYG-12 dans l'enveloppe nucléaire et forment aussi des synapses non homologues. Une analyse détaillée du mouvement des chromosomes dans ces mutants montre que les chromosomes se séparent plus rapidement que dans le type sauvage. Je propose donc un modèle dans lequel la formation des agrégats SUN-1/ZYG-12 n'est pas nécessaire au mouvement des chromosomes mais bien à leur rétention entre eux. Ainsi il existe un équilibre des forces entre les agrégats qui contraignent les extrémités des chromosomes dans un micro-environnement et les forces du cytosquelette qui permettent de séparer les chromosomes non homologues; cet équilibre offre une fenêtre d'opportunité pour tester l'homologie des chromosomes.
McKenzie, Lynsey. "G2/M checkpoint associated repression of polo-like kinase-1 mediated by the tumour suppressor, p53." Thesis, University of Dundee, 2010. https://discovery.dundee.ac.uk/en/studentTheses/fea09569-1f92-4084-8dbe-d85de3c86c6d.
Full textDedieu, Fabien. "Régulation de l'expression du facteur eIF4GII par le protéasome : rôle de la Polo-like Kinase Snk." Toulouse 3, 2007. http://thesesups.ups-tlse.fr/131/.
Full textThe eukaryotic translation initiation factors (eIF) 4GI and eIF4GII are scaffolding proteins critical for the assembly of translation initiation complexes. EIF4GI and eIF4GII are the target of different signaling pathways, and a recent report indicates that they may possess distinct functions. Here we show that the polo like kinase (Plk) 2 interacts directly with eIF4GII. In the cell, Plk2 targets eIF4GII to destruction. Plk2-dependent degradation of eIF4GII is sensitive to proteasome inhibition and necessitates both a physical interaction with and ubiquitination of Plk2 (but not that of eIF4GII), suggesting that Plk2 acts as a specific adaptor for the proteasome. We also show that both eIF4GII and Plk2 are destructed by the proteasome upon oxidative stress. Furthermore, although eIF4GI also interacts with Plk2, Plk2 does not target eIF4GI to destruction suggesting that eIF4GI binding to Plk2 may serve another function. Thus, we propose that Plk2 can control translation initiation rates at least through the regulation of eIF4GII cellular content
Tavernier, Nicolas. "Régulation de SPAT-1/Bora, l'activateur de la polo-kinase, dans l'embryon précoce de Caenorhabditis elegans." Paris 7, 2013. http://www.theses.fr/2013PA077133.
Full textThe mechanism of cell division, called mitosis, is a fundamental process by which a mother cell gives two daughter cells. Many cancers can be attributed to the disruption of the process of cell division. To ensure a division, a large number of biochemical reactions is put in. These reactions are the result of the activity of a myriad of proteins involved very temporarily and in a specific order. The coordination of these reactions is tightly regulated. In order to elucidate the functioning of these mechanisms, we use Caenorhabditis elegans early embryos as a model organism. The advantages of this system are many. First, the scientific community has a plethora of tools (gene silencing by RNA interference, proteomics, mutant libraries, fully sequenced and annotated genome) to work effectively. Second, we study the process of cell divisions in the context of development where cell divisions are coordinated with polarity. This brings us strongly of what is happening within a structured contrast to analyzes of individual cells in tissue culture. Finally, the cost of use is rather low. The fact that the cell cycle is an extremely well-preserved in the world living mechanism can transpose most often discovered human model, but also to clarify and supplement the concepts developed from studies in other model organisms and thus greatly accelerate research
Thrum, Stephan. "In vitro-Versuche mit dem Polo like-Kinase 1 Hemmstoff BI 2536 an Zelllinien von Gallenwegskarzinomen." Doctoral thesis, Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-134869.
Full textCLAUDI, CECILIA. "POLO-LIKE KINASE CDC5 CONTRIBUTES TO MITOTIC SPINDLE ELONGATION VIA THE KINESIN-5 MOTOR PROTEIN CIN8." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/607694.
Full textReindl, Wolfgang [Verfasser], Horst [Akademischer Betreuer] Kessler, Thorsten [Akademischer Betreuer] Berg, and Bernhard [Akademischer Betreuer] Küster. "Inhibition of Polo-like Kinase 1 by Small Molecules Targeting the Polo-Box Domain / Wolfgang Reindl. Gutachter: Bernhard Küster ; Horst Kessler. Betreuer: Horst Kessler ; Thorsten Berg." München : Universitätsbibliothek der TU München, 2008. http://d-nb.info/1054351910/34.
Full textChumduri, Cindrilla. "Mechanism of cell death in Burkitt lymphomas." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2010. http://dx.doi.org/10.18452/16086.
Full textApoptosis resistance is the major cause of chemotherapy failure in most kinds of cancers, including Burkitt lymphomas (BL). To elucidate molecular mechanisms regulating the development of apoptosis resistance, a panel of 15 BL cell lines was investigated for apoptosis induction upon treatment with microtubule inhibitors taxol, nocodazole and vincristine. Significant differences were observed in the extent of apoptosis induction among BL cell lines examined. Interestingly, cell lines exhibiting resistance to taxol- or nocodazole-induced apoptosis, showed development of polyploidy (>4N) and vice versa, displaying an inverse relationship between apoptosis and polyploidy induction. Further, in sensitive cell lines taxol-induced apoptosis was accompanied by caspase activation, Bid cleavage and Mcl-1 down-regulation. In contrast, most apoptosis resistant cell lines exhibited a loss of Bax and Bak expression and showed prolonged mitotic arrest with >4N DNA content upon treatment. To gain mechanistic insights into microtubule inhibitor-induced cell death, the role of the mitotic kinase PLK1 was addressed. Dominant negative PLK1 mutant induced apoptosis, however, failed to show synergism in induction of apoptosis in combination with microtubule inhibitors. This indicates that PLK1 inhibition and spindle toxins might trigger a similar mitotic stress pathway. Conversely, overexpression of wildtype PLK1 promoted cell cycle progression in cells treated with taxol. Remarkably, inhibition of apoptosis in sensitive cell lines by caspase inhibition promoted polyploidy confirming the inverse relationship between apoptosis and polyploidization. Considering targets to induce Bax/Bak independent caspase activation would be of great importance to avoid undesirable events leading to chromosomal imbalances in treating resistant cancers.
Reynolds, Nicola. "Functional dissection of the conserved domains of polo-like kinase and its interacting proteins in fission yeast." Thesis, University of Edinburgh, 2001. http://hdl.handle.net/1842/11305.
Full textVidanes, Genevieve M. "Suppression of the DNA damage checkpoint by the Saccharomyces cerevisiae polo-like kinase, CDC5, to promote adaptation." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2009. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3352477.
Full textPina-Mimbela, Ruby Melisa. "Association of Polyphosphate (poly P) Kinases with Campylobacter jejuni Invasion and Survival in Human Epithelial Cells." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1385978458.
Full textHyland, Paula Lisa. "Sequence analysis of the adenine phosphoribosyltransferase gene locus in wild-type and thymidine kinase-deficient friend erythroleukaemia cells." Thesis, University of Ulster, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390158.
Full textAhmadi, Pour Malek. "Role of the mitotic Polo-like kinase PLK1 in the control of the interferon induction pathway mediated by the mitichondria-bound MAVS protein and the IKKε protein kinase." Paris 6, 2009. http://www.theses.fr/2009PA066318.
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