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Relevant bibliographies by topics / Polo kinases

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Academic literature on the topic 'Polo kinases'

Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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Journal articles on the topic "Polo kinases"

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Archambault, Vincent, and Mar Carmena. "Polo-like kinase-activating kinases." Cell Cycle 11, no. 8 (April 15, 2012): 1490–95. http://dx.doi.org/10.4161/cc.19724.

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von Schubert, Conrad, and Erich A. Nigg. "Polo-like kinases." Current Biology 23, no. 6 (March 2013): R225—R227. http://dx.doi.org/10.1016/j.cub.2013.01.066.

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Lee, Kyung S., Tallessyn Z. Grenfell, Frederic R. Yarm, and Raymond L. Erikson. "Mutation of the polo-box disrupts localization and mitotic functions of the mammalian polo kinase Plk." Proceedings of the National Academy of Sciences 95, no. 16 (August 4, 1998): 9301–6. http://dx.doi.org/10.1073/pnas.95.16.9301.

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Members of the polo subfamily of protein kinases play pivotal roles in cell proliferation. In addition to the kinase domain, polo kinases have a strikingly conserved sequence in the noncatalytic domain, termed the polo-box. The function of the polo-box is currently undefined. The mammalian polo-like kinase Plk is a functional homologue ofSaccharomyces cerevisiaeCdc5. Here, we show that Plk localizes at the spindle poles and cytokinetic neck filaments. Without impairing kinase activity, a conservative mutation in the polo-box disrupts the capacity of Plk to complement the defect associated with acdc5–1temperature-sensitive mutation and to localize to these subcellular structures. Our data provide evidence that the polo-box plays a critical role in Plk function, likely by directing its subcellular localization.

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Carmena, Mar, Miguel Ortiz Lombardia, Hiromi Ogawa, and William C. Earnshaw. "Polo kinase regulates the localization and activity of the chromosomal passenger complex in meiosis and mitosis in Drosophila melanogaster." Open Biology 4, no. 11 (November 2014): 140162. http://dx.doi.org/10.1098/rsob.140162.

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Cell cycle progression is regulated by members of the cyclin-dependent kinase (CDK), Polo and Aurora families of protein kinases. The levels of expression and localization of the key regulatory kinases are themselves subject to very tight control. There is increasing evidence that crosstalk between the mitotic kinases provides for an additional level of regulation. We have previously shown that Aurora B activates Polo kinase at the centromere in mitosis, and that the interaction between Polo and the chromosomal passenger complex (CPC) component INCENP is essential in this activation. In this report, we show that Polo kinase is required for the correct localization and activity of the CPC in meiosis and mitosis. Study of the phenotype of different polo allele combinations compared to the effect of chemical inhibition revealed significant differences in the localization and activity of the CPC in diploid tissues. Our results shed new light on the mechanisms that control the activity of Aurora B in meiosis and mitosis.

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Garuti, L., M. Roberti, and G. Bottegoni. "Polo-Like Kinases Inhibitors." Current Medicinal Chemistry 19, no. 23 (July 1, 2012): 3937–48. http://dx.doi.org/10.2174/092986712802002455.

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Song, Sukgil, Tallessyn Z. Grenfell, Susan Garfield, Raymond L. Erikson, and Kyung S. Lee. "Essential Function of the Polo Box of Cdc5 in Subcellular Localization and Induction of Cytokinetic Structures." Molecular and Cellular Biology 20, no. 1 (January 1, 2000): 286–98. http://dx.doi.org/10.1128/mcb.20.1.286-298.2000.

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ABSTRACT Members of the polo subfamily of protein kinases play pivotal roles in cell proliferation. In addition to the kinase domain, polo kinases have a strikingly conserved sequence in the noncatalytic C-terminal domain, termed the polo box. Here we show that the budding-yeast polo kinase Cdc5, when fused to green fluorescent protein and expressed under its endogenous promoter, localizes at spindle poles and the mother bud neck. Overexpression of Cdc5 can induce a class of cells with abnormally elongated buds in a polo box- and kinase activity-dependent manner. In addition to localizing at the spindle poles and cytokinetic neck filaments, Cdc5 induces and localizes to additional septin ring structures within the elongated buds. Without impairing kinase activity, conservative mutations in the polo box abolish the ability of Cdc5 to functionally complement the defect associated with a cdc5-1 temperature-sensitive mutation, to localize to the spindle poles and cytokinetic neck filaments, and to induce elongated cells with ectopic septin ring structures. Consistent with the polo box-dependent subcellular localization, the C-terminal domain of Cdc5, but not its polo box mutant, is sufficient for subcellular localization, and its overexpression appears to inhibit cytokinesis. These data provide evidence that the polo box is required to direct Cdc5 to specific subcellular locations and induce or organize cytokinetic structures.

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Dai, Wei. "Polo-like kinases, an introduction." Oncogene 24, no. 2 (January 2005): 214–16. http://dx.doi.org/10.1038/sj.onc.1208270.

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Eckerdt, Frank, Juping Yuan, and Klaus Strebhardt. "Polo-like kinases and oncogenesis." Oncogene 24, no. 2 (January 2005): 267–76. http://dx.doi.org/10.1038/sj.onc.1208273.

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Berg, Tobias, Gesine Bug, Oliver G. Ottmann, and Klaus Strebhardt. "Polo-like kinases in AML." Expert Opinion on Investigational Drugs 21, no. 8 (June 6, 2012): 1069–74. http://dx.doi.org/10.1517/13543784.2012.691163.

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Hagan, Iain M. "The spindle pole body plays a key role in controlling mitotic commitment in the fission yeast Schizosaccharomyces pombe." Biochemical Society Transactions 36, no. 5 (September 19, 2008): 1097–101. http://dx.doi.org/10.1042/bst0361097.

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Commitment to mitosis is regulated by a conserved protein kinase complex called MPF (mitosis-promoting factor). MPF activation triggers a positive-feedback loop that further promotes the activity of its activating phosphatase Cdc25 and is assumed to down-regulate the MPF-inhibitory kinase Wee1. Four protein kinases contribute to this amplification loop: MPF itself, Polo kinase, MAPK (mitogen-activated protein kinase) and Greatwall kinase. The fission yeast SPB (spindle pole body) component Cut12 plays a critical role in modulating mitotic commitment. In this review, I discuss the relationship between Cut12 and the fission yeast Polo kinase Plo1 in mitotic control. These results indicate that commitment to mitosis is co-ordinated by control networks on the spindle pole. I then describe how the Cut12/Plo1 control network links growth control signalling from TOR (target of rapamycin) and MAPK networks to the activation of MPF to regulate the timing of cell division.

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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.

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Primot, Aline. "Etude de la régulation de deux protéines kinases : : GSK-3 et polo." Rennes 1, 2001. http://hal.upmc.fr/tel-01117984.

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Nous avons étudié 2 protéines kinases : GSK-3 et Polo. La "Glycogen Synthase Kinase-3" intervient dans divers processus cellulaires. Nous avons démontré que GSK-3 peut être purifiée par chromatographie d'affinité sur axine fixée sur des billes de séraphose. Nous avons cloné le gène d'une protéine homologue de GSK-3 humaine chez le parasite responsable du paludisme. PfGSK-3 est localisée au niveau de la membrane plasmique de l'érythrocyte et à l'intérieur du parasite. L'utilisation de PfGSK-3 comme cible devrait permettre la découverte d'inhibiteurs sélectifs dont les effets thérapeutiques potentiels seront évalués. Polo intervient à différents niveaux de la régulation cellulaire. Le clonage d'une partie de l'ADNc de Polo d'oursin (Plu1) a permis la synthèse d'anticorps spécifiques. L'immunoprécipitation de la protéine Plu1 au cours des premières divisions d'embryon d'oursin a révélé que Plu1 se lie à différentes protéines au cours du cycle dont l'identité reste à confirmer.

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Randall, 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.

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Long, 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.

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La schistosomiase est l'infection helminthique humaine la plus importante en termes de morbidité et de mortalité dans de nombreux pays. L'émergence récente de cas de résistances à la seule drogue efficace contre le schistosome, le praziquantel (PZQ) fait de cette maladie une priorité pour l'Organisation Mondiale de la Santé (OMS) de rechercher de nouvelles cibles thérapeutiques. La ponte massive des oeufs (jusqu'à 300 oeufs par jour par femelle) est responsable de la transmission de la maladie par des parasites complexes trématodes mais aussi de toute la pathologie de la schistosomiase. Mon travail de Doctorat vise avant tout à déchiffrer les mécanismes complexes de la reproduction des schistosomes et à élucider les voies de signalisation qui régulent cette hyperfécondité, dont les acteurs moléculaires peuvent être des cibles évidentes pour le contrôle de la schistosomiase. Les kinases Polo sont des membres conservés de la famille des Polo-like kinases (Plks) qui sont impliquées dans la progression du cycle cellulaire. Actuellement, les Plks humaines constituent une cible importante dans les traitements anticancéreux de par leur expression aberrante dans les tumeurs et signent d’ailleurs un mauvais pronostic. Sur la base de recherches in silico, nous avons caractérisé SmPlk1 (Schistosoma mansoni Plk1), homologue à la Plk1 humaine. SmPlk1 était principalement transcrit dans des stades de multiplication cellulaire intense et préférentiellement dans les organes reproducteurs des schistosomes adultes suggérant un rôle potentiel de SmPlk1 dans les processus de division. Nous avons montré que SmPlk1 possédait un rôle conservé dans la transition G2/M dans le modèle d’ovocyte de Xénope. L’inhibition dose-dépendante de l'ovogénèse et la spermatogénèse par le BI 2536, un inhibiteur spécifique des Plks, indiquait un rôle de SmPlk1 dans la multiplication et la différenciation des gamètes chez le parasite et suggérait que cette kinase pourrait être une nouvelle cible dans le traitement anti-schistosome. Parallèlement à ces travaux, une seconde Plk, SmSak, a été identifiée dont les résultats préliminaires ont montré une structure et des fonctions différentes de celles de SmPlk1 suggérant un rôle distinct de cette dernière. De plus, nous avons identifié un activateur potentiel de Plk, SmSLK (S. Mansoni Ste20-like kinase) capable d'activer spécifiquement SmPlk1 dans des conditions d'activation particulières dépendant de deux mécanismes originaux, l'un dépendant des caspases et l'autre dépendant d'ARN anti-sens
Schistosomiasis 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

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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.

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In budding yeast, progression through anaphase and exit from mitosis are controlled by the conserved protein phosphatase Cdc14. The activity of Cdc14 is regulated in space and time by changes in its subcellular localization. For most of the cell cycle up to metaphase, the phosphatase is sequestered in the nucleolus, by binding to a competitive inhibitor called Cfi1 (also known as Net1) (Shou et al., 1999; Straight et al., 1999; Visintin et al., 1999). During anaphase, Cdc14 is released from its inhibitor by the sequential activation of two signaling cascades, the Cdc Fourteen Early Anaphase Release (FEAR) network and the Mitotic Exit Network (MEN). Once released Cdc14 spreads throughout the nucleus and the cytoplasm, where it reaches its targets and promotes progression through and exit from mitosis (Pereira et al., 2002; Shou et al., 1999; Stegmeier et al., 2002; Visintin et al., 1999; Yoshida et al., 2002). Several in vivo and in vitro observations suggest that phosphorylation of Cdc14 and/or Cfi1 is responsible for the dissociation of Cdc14 from its inhibitor. Three kinases have been implicated in the process: the polo-like kinase Cdc5, the Clb2-Cdk complex and the MEN kinase Dbf2 (Azzam et al., 2004; Geymonat et al., 2003; Hu and Elledge, 2002; Hu et al., 2001; Mohl et al., 2009; Pereira et al., 2002; Queralt et al., 2006; Stegmeier et al., 2002; Visintin et al., 2003; Yoshida and Toh-e, 2002). The aim of my project was to assess the contribution of the above-mentioned kinases and to identify the molecular mechanisms by which these kinases mediate the release of Cdc14 from its inhibitor. By modulating the kinases of interest alone or in mutual combination we found that Cdc14 is released from the nucleolus by the combined activity of two kinases, Cdc5 always and either Clb-Cdks or Dbf2. Once active, Cdc14 triggers a negative feedback loop that, in the presence of stable levels of mitotic cyclins, generates periodic cycles of Cdc14 release and sequestration. Similar phenotypes have been described for yeast bud formation and centrosome duplication. A common theme emerges where events that must happen only once per cycle, although intrinsically capable of oscillations, are limited to one occurrence by their coupling with the cyclin-Cdk cell cycle engine.

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Dahmene, 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.

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La maladie de Parkinson est une maladie neurologique chronique caractérisée par la dégénérescence progressive des neurones dopaminergiques de la substance noire pars compacta. Une deuxième caractéristique neuropathologique de cette maladie est l’accumulation des agrégats intracellulaires appelés les corps de Lewy (CLs). Ces agrégats sont majoritairement formés par une protéine pré-synaptique, α-synucléine (α-syn). Cette accumulation pathologique interfère avec les voies métaboliques vitales des neurones telles que la transmission synaptique et l’activité mitochondriale, ce qui engendre la mort cellulaire. Par conséquence, éliminer les formes toxiques, diminuer l’expression de la forme native et réduire ainsi la probabilité de la formation d’agrégats pourrait être une stratégie thérapeutique d’intérêt pour le traitement de la maladie de Parkinson et d’autres désordres qui y sont reliés. Dans ce contexte, notre équipe a récemment décrit une nouvelle voie d’élimination de l’α-syn qui est catalysée par l’activité enzymatique de la kinase Polo-like kinase 2 (PLK2). Cependant, les mécanismes cellulaires ainsi que l’identité des molécules impliquées sont encore méconnus. Donc, mes travaux se sont concentrés sur l’étude de cette voie et ses différentes étapes qui mènent à enlever l’effet toxique de l’α-syn. Dans ce mémoire nous montrons que, en plus de la PLK2, la PLK3, un autre membre de la famille des PLKs, est capable de phosphoryler l’α-syn au niveau du résidu S129 et induire son élimination. En plus, nous déclarons que cette action exige une interaction physique entre les 2 protéines (α-syn et PLK2) impliquant le domaine N-terminal et qu’une étape de poly-ubiquitination est essentielle pour que ce complexe protéique se dirige vers la voie de dégradation autophagique. Cette action de la PLK2 est observée également sur des formes mutées de l’α-syn tels que α-syn A30P, α-syn A53T et d’une manière plus accentuée sur la forme mutante α-syn E46K. La caractérisation de cette voie d’élimination offre de nouvelles opportunités pour le développement des traitements qui favorisent, d’une façon spécifique et sélective, la dégradation de l’α-syn et par conséquent la réduction des formes toxiques de cette dernière.
Parkinson'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.

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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.

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Brassac, 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.

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L'entree en mitose est declenchee par l'activation du mpf (m-phase promoting factor ou cdc2/cyclineb). Ce complexe est maintenu inactif (pre-mpf) jusqu'en phase g2 du cycle cellulaire par deux phosphorylations inhibitrices, catalysees par les kinases wee1/myt1 chez les eucaryotes superieurs. Lors de l'entree en phase m, la phosphatase cdc25c produit la conversion du pre-mpf en mpf en dephosphorylant les residus threonine 14 et tyrosine 15 de cdc2. Le mpf active lui-meme cdc25c par phosphorylation (boucle de retrocontrole positif). La serine/threonine kinase polo-like de xenope (plx1) fut purifiee par sa capacite a activer cdc25c in vitro (a. Kumagai et al, 1996). L'objet de ce travail etait de preciser les roles de plx1 dans le cycle de division cellulaire des ovocytes de xenope. Nous avons montre que l'activation de plx1 est necessaire a la mise en place de la boucle d'amplification du mpf. Cette activation de plx1 est placee sous le controle positif (probablement indirect) des complexes cdc2/cyclineb. Les processus moleculaires d'activation de cdc2/cyclinea et plx1 sont en revanche independants. Nous avons egalement etudie la fonction de plx1 dans la regulation d'un autre substrat de cdc2/cyclineb : l'anaphase promoting complex (apc). Ce complexe multimerique est responsable de l'ubiquitinylation des cyclines mitotiques qui conduit a leur degradation par le proteasome en fin de mitose. In vitro, il fut prealablement montre que cdc2 et plx1 regulent positivement l'apc (s. Kotani et al, 1999). Nos experiences montrent que plx1 n'est ni necessaire, ni suffisant pour activer l'apc dans les extraits de xenope. En revanche, plx1 prolonge l'activation de l'apc en antagonisant une phosphatase sensible a la microcystine. En presence de microcystine, la fonction de plx1 n'est plus requise pour obtenir la degradation complete des cyclines. Plx1 peut etre considere comme une kinase agissant en synergie avec cdc2 dans la regulation de substrats tels que cdc25c et l'apc.

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Rawal, 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.

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The integrity of genomic DNA is continuously jeopardized through of environmental stresses such as UV light, ionizing radiations and various chemicals in addition to cellular byproducts such as reactive oxygen species. Furthermore, structural or chemical hindrances also affect the basic cellular processes (replication, transcription and translation) compromising genome stability. All the eukaryotic cells have thus evolved mechanisms to detect such genomic lesions and activate a surveillance mechanisms termed as checkpoint activation to arrest cell cycle, which in term provide time to repair the lesion using a suitable pathway to maintain genome stability. The resumption of cell cycle after the repair is also an important and finely regulated mechanisms. Indeed, resumption of cell cycle in case of faulty/un-repaired damage compromises genome integrity and may lead to cancer. In this thesis, I studied the role of Polo-kinase Cdc5 and DNA repair scaffold complex-Slx-Rtt107, specifically in response to one of the most deleterious lesion, DNA double strand break (DSB) in budding yeast Saccharomyces cerevisiae. The human counterpart Polo-like kinase 1 is overexpressed in many cancers, while Slx4/FANCP is one of the proteins involved in Fanconi anemia repair pathway. In first part, we characterized the role of phosphorylation of Threonine 238 in the activation loop of the Cdc5 kinase domain in unperturbed cell cycle and in response to repairable and unrepairable DSB. Using alanine/ aspartic acid mutagenesis and genetic approaches we delineated the requirement of T238 phosphorylation of Cdc5. Interestingly, we discovered that absence of T238 phosphorylation of Cdc5, even though doesn’t affect the normal cell cycle, affects kinase activity and leads to defect in checkpoint adaptation and recovery after one DSB. Importantly, we also found that cdc5-T238A cells also have altered genome stability, assessed by using multiple genetic approaches. In second part, we characterized the role of Slx4-Rtt107 complex in modulating the level of checkpoint signalling and initial processing of DSB. Indeed in the absence of functional Slx4-Rtt107 complex, we found slower processing of DSB and hyper-activated checkpoint signalling which is due to increased binding of checkpoint adaptor protein Rad9 at the lesion. Importantly, this hyper-activated checkpoint has consequent effect on cell cycle resumption and proliferation in response to various DNA damaging agents.

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Renner, 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/.

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La Polo-like kinase1 (Plk1) est un régulateur mitotique majeur, surexprimé dans différents cancers et souvent associé à un mauvais pronostic. D'un point de vue expérimental, l'expression constitutive de la Plk1 dans des cellules NIH 3T3 entraîne leur transformation et leurs confère la capacité à former des tumeurs chez des souris athymiques. De plus, la déplétion de Plk1 dans des cellules cancéreuses induit souvent leur apoptose. Plk1 est donc une cible potentielle très étudiée dans le cadre des thérapies anti-cancéreuses. L'un des objectifs de ma thèse a été de générer des outils moléculaires et cellulaires afin de mettre au point des tests "preuve de principe" rendant compte de l'activité d'inhibiteurs de Plk1. La construction de ces outils avait également pour objectif de mieux appréhender le rôle de Plk1 dans les différentes étapes de la division cellulaire, et de rechercher de nouveaux substrats et partenaires de cette kinase. Des lignées cellulaires inductibles permettant l'expression de la Plk1 sauvage et de différents mutants (inactifs, suractivés) ont été construites. L'effet de l'induction de ces diverses formes de Plk1 sur la prolifération, la répartition des cellules dans le cycle et les substrats de la kinase a été étudié. Comme attendu, plus la protéine est active, plus l'effet sur ces paramètres est marqué. Divers inhibiteurs de Plk1 ont été testés sur ces modèles cellulaires avec, in fine, la mise au point de tests permettant d'évaluer rapidement et à haut débit l'efficacité de molécules inhibitrices. La technologie Luminex a été notamment mise à profit pour doser Plk1 et certains de ses substrats (phosphorylés ou non), représentatifs de l'activité de la kinase, à partir de lysats cellulaires. Cette approche permet d'évaluer l'effet d'inhibiteurs potentiels de Plk1 in cellulo par une série de dosages réalisés simultanément à partir d'extraits cellulaires. Les Leucémies Aiguës Myéloïdes (LAM) sont des hémopathies clonales liées à la transformation maligne d'une cellule souche hématopoïétique qui présente un blocage de maturation et une prolifération anarchique. Les mécanismes moléculaires impliqués dans la dérégulation du cycle cellulaire dans cette pathologie sont encore mal connus. L'un des objectifs de cette étude a été de caractériser le statut et le rôle de la Plk1 dans la physiopathologie des LAM, afin d'évaluer l'intérêt d'un traitement spécifique ciblant cette kinase dans cette pathologie. .
Polo-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. .

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Books on the topic "Polo kinases"

1

Ullrich, Andrea. Expression der Polo-Like-Kinase 1 und 3 Im Magenkarzinom. Südwestdeutscher Verlag für Hochschulschriften AG & Company KG, 2013.

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Book chapters on the topic "Polo kinases"

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Berry, Lynne D., Roy M. Golsteyn, Heidi A. Lane, Kirsten E. Mundt, Lionel Arnaud, and Erich A. Nigg. "The family of polo-like kinases." In Progress in Cell Cycle Research, 107–14. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5873-6_11.

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Sharma, Nitin, Rajni Vaid, Kamal Dev, and Anuradha Sourirajan. "Polo-Like Kinase (PLK)." In Encyclopedia of Signaling Molecules, 4100–4106. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101760.

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Sharma, Nitin, Rajni Vaid, Kamal Dev, and Anuradha Sourirajan. "Polo-like Kinase (PLK)." In Encyclopedia of Signaling Molecules, 1–7. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6438-9_101760-1.

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Wäsch, R., J. Hasskarl, D. Schnerch, and M. Lübbert. "BI_2536 - Targeting the Mitotic Kinase Polo-Like Kinase 1 (Plk1)." In Recent Results in Cancer Research, 215–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-01222-8_15.

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Reindl, Wolfgang, Klaus Strebhardt, and Thorsten Berg. "A Fluorescence Polarization Assay for the Discovery of Inhibitors of the Polo-Box Domain of Polo-Like Kinase 1." In Methods in Molecular Biology, 69–81. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-337-0_5.

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Marcisauskas, R. P., D. J. Karalyte, O. F. Sudziuviene, and I. G. I. Pesliakas. "Use of Triazine Dyes in Purification of T4 Poly-Nucleotide Kinase." In Protein-Dye Interactions: Developments and Applications, 331–36. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-1107-9_33.

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Yoshihara, Koichiro, Yasuharu Tanaka, Asako Itaya, Tomoya Kamiya, Takashi Hironaka, Takeyoshi Minaga, and Samuel S. Koide. "In Vitro Evidence for Poly(ADP-Ribosyl)ation of DNA Polymerase α-Primase and Phosphorylation of Poly(ADP-Ribose) Synthetase by Protein Kinase C." In ADP-Ribose Transfer Reactions, 39–46. New York, NY: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4615-8507-7_7.

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Durkacz, B. W., J. Lunec, H. Grindley, S. Griffin, O. Horne, and A. Simm. "Poly(ADP-ribose) polymerase inhibitors induce murine melanoma cell differentiation by a mechanism independent of alterations in cAMP levels and protein kinase A activity." In ADP-Ribosylation Reactions, 191–94. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4419-8718-1_32.

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Dube, Divya. "Polo-like kinases: An antimitotic drug target for cancer therapy." In Protein Kinase Inhibitors, 457–77. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-91287-7.00002-8.

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Llamazares, Salud, and David M. Glover. "Polo." In The Protein Kinase FactsBook, 273–74. Elsevier, 1995. http://dx.doi.org/10.1016/b978-012324719-3/50084-4.

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Conference papers on the topic "Polo kinases"

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Wei, Iris, Vishal Kothari, Sunita Shankar, Shanker Kalyana-Sundaram, Catherine Grasso, Dan Robinson, Xuhong Cao, Diane Simeone, Arul Chinnaiyan, and Chandan Kumar-Sinha. "Abstract A17: Inhibiting polo-like kinases for the treatment of pancreatic cancer: Targeting kinase outliers for personalized therapy." In Abstracts: AACR Special Conference on Pancreatic Cancer: Progress and Challenges; June 18-21, 2012; Lake Tahoe, NV. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.panca2012-a17.

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Ward, Alejandra, Gayathri Sivakumar, Caroline Hamm, Sindu Kanjeekal, and John W. Hudson. "Abstract LB-376: Deregulation of promoter methylation of the polo-like kinases in myelodysplastic syndromes (MDS) and other blood neoplasms." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-376.

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Ward, Alejandra, and John W. Hudson. "Abstract LB-179: The effects of hypoxia and reactive oxygen species on the methylation status of the polo-like kinases." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-179.

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Chapagai, Danda P., Merissa Baxter, Gurusankar Ramamoorthy, Campbell McInnes, and Michael Wyatt. "Abstract 4712: Selective polo-like kinase 1 PBD inhibitor." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4712.

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Chapagai, Danda P., Merissa Baxter, Gurusankar Ramamoorthy, Campbell McInnes, and Michael Wyatt. "Abstract 4712: Selective polo-like kinase 1 PBD inhibitor." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4712.

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Baxter, Merissa, Sandra Craig, Campbell McInnes, and Michael D. Wyatt. "Abstract 2156: Targeting polo-like kinase 1 with novel inhibitors of the polo-box domain." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2156.

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Press, Michael F., Bin Xie, Simon Davenport, Yu Zhou, Neil O’Brien, Michael Palazzolo, Tak Mak, Joan Brugge, and Dennis J. Slamon. "Abstract 2736: Regulation of cytokinesis by polo-like kinase 4." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2736.

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Choi, Byeong Hyeok, Kyung S. Lee, and Wei Dai. "Abstract 2048: Phosphorylation and regulation of PTEN by Polo-like kinase 1." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2048.

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Li, Zhongkui, Zhe Chang, and Paul J. Chiao. "Abstract 2186: Function and regulation of Polo-like Kinase 3 in human pancreatic cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2186.

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Liu, X. Shawn, Bing Song, Bennett D. Elzey, Timothy L. Ratliff, Stephen F. Konieczny, Liang Cheng, and Xiaoqi Liu. "Abstract 233: Polo-like kinase 1 facilitates loss of Pten-induced prostate cancer formation." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-233.

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Reports on the topic "Polo kinases"

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Sessa, Guido, and Gregory Martin. A functional genomics approach to dissect resistance of tomato to bacterial spot disease. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695876.bard.

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The research problem. Bacterial spot disease in tomato is of great economic importance worldwide and it is particularly severe in warm and moist areas affecting yield and quality of tomato fruits. Causal agent of spot disease is the Gram-negative bacterium Xanthomonas campestris pv. vesicatoria (Xcv), which can be a contaminant on tomato seeds, or survive in plant debris and in association with certain weeds. Despite the economic significance of spot disease, plant protection against Xcvby cultural practices and chemical control have so far proven unsuccessful. In addition, breeding for resistance to bacterial spot in tomato has been undermined by the genetic complexity of the available sources of resistance and by the multiple races of the pathogen. Genetic resistance to specific Xcvraces have been identified in tomato lines that develop a hypersensitive response and additional defense responses upon bacterial challenge. Central goals of this research were: 1. To identify plant genes involved in signaling and defense responses that result in the onset of resistance. 2. To characterize molecular properties and mode of action of bacterial proteins, which function as avirulence or virulence factors during the interaction between Xcvand resistant or susceptible tomato plants, respectively. Our main achievements during this research program are in three major areas: 1. Identification of differentially expressed genes during the resistance response of tomato to Xcvrace T3. A combination of suppression subtractive hybridization and microarray analysis identified a large set of tomato genes that are induced or repressed during the response of resistant plants to avirulent XcvT3 bacteria. These genes were grouped in clusters based on coordinate expression kinetics, and classified into over 20 functional classes. Among them we identified genes that are directly modulated by expression of the type III effector protein AvrXv3 and genes that are induced also during the tomato resistance response to Pseudomonas syringae pv. tomato. 2. Characterization of molecular and biochemical properties of the tomato LeMPK3MAP kinase. A detailed molecular and biochemical analysis was performed for LeMPK3 MAP kinase, which was among the genes induced by XcvT3 in resistant tomato plants. LeMPK3 was induced at the mRNA level by different pathogens, elicitors, and wounding, but not by defense-related plant hormones. Moreover, an induction of LeMPK3 kinase activity was observed in resistant tomato plants upon Xcvinfection. LeMPK3 was biochemically defined as a dual-specificity MAP kinase, and extensively characterized in vitro in terms of kinase activity, sites and mechanism of autophosphorylation, divalent cation preference, Kₘand Vₘₐₓ values for ATP. 3. Characteriztion of molecular properties of the Xcveffector protein AvrRxv. The avirulence gene avrRxvis involved in the genetic interaction that determines tomato resistance to Xcvrace T1. We found that AvrRxv functions inside the plant cell, localizes to the cytoplasm, and is sufficient to confer avirulence to virulent Xcvstrains. In addition, we showed that the AvrRxv cysteine protease catalytic core is essential for host recognition. Finally, insights into cellular processes activated by AvrRxv expression in resistant plants were obtained by microarray analysis of 8,600 tomato genes. Scientific and agricultural significance: The findings of these activities depict a comprehensive and detailed picture of cellular processes taking place during the onset of tomato resistance to Xcv. In this research, a large pool of genes, which may be involved in the control and execution of plant defense responses, was identified and the stage is set for the dissection of signaling pathways specifically triggered by Xcv.

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