Dissertations / Theses on the topic 'Polo kinases/Cdc5'
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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.
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 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 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 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 textMASSARI, LUCIA FRANCESCA. "Complete resolution of sister chromatid intertwines requires the Polo-like kinase Cdc5 and the phosphatase Cdc14 in budding yeast." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/556680.
Full textArgunhan, 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 textArnold, Lea [Verfasser], and Wolfgang [Akademischer Betreuer] Seufert. "Studien zur Regulation und Funktion der Polo-Kinase Cdc5 im Zellteilungszyklus der Hefe Saccharomyces cerevisiae / Lea Arnold. Betreuer: Wolfgang Seufert." Regensburg : Universitätsbibliothek Regensburg, 2013. http://d-nb.info/1047236869/34.
Full textFINARDI, ALICE. "THE POLO-LIKE KINASE CDC5 AND THE CDK-COUNTERACTING PHOSPHATASE CDC14 PLAY DISTINCT ROLES IN THE RESOLUTION OF DNA LINKAGES IN MITOSIS." Doctoral thesis, Università degli Studi di Milano, 2022. http://hdl.handle.net/2434/906786.
Full textDonnianni, R. A. "Elevated levels of the polo kinase Cdc5 overridethe Mec1/ATR checkpoint in budding yeast by acting at different steps of the signaling pathway." Doctoral thesis, Università degli Studi di Milano, 2009. http://hdl.handle.net/2434/158403.
Full textMartino, 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
Daoud, Amani. "Création de mutants cdc5 en vue de l’identification des substrats de PLK/Cdc5 lors de la réponse d’adaptation aux dommages à l’ADN." Thèse, 2016. http://hdl.handle.net/1866/16240.
Full text"Suppression of the DNA damage checkpoint by the Saccharomyces cerevisiae polo-like kinase, CDC5, to promote adaptation." UNIVERSITY OF CALIFORNIA, SAN FRANCISCO, 2009. http://pqdtopen.proquest.com/#viewpdf?dispub=3352477.
Full textRatsima, Hery Damien. "Contribution de l’activité des domaines polo-box et kinase de la Polo-like kinase Cdc5 dans ses fonctions de régulation mitotique et dans le maintien de la stabilité du génome." Thèse, 2015. http://hdl.handle.net/1866/18531.
Full textNeutzner, Melanie [Verfasser]. "Regulatoren des Zellteilungszyklus der Hefe Saccharomyces cerevisiae : die Polo-Kinase Cdc5 und der Ubiquitinierungsfaktor Hct1 / vorgelegt von Melanie Neutzner." 2003. http://d-nb.info/96787839X/34.
Full textMarkant, Shirley Loretta. "Regulation of Cerebellar Development and Tumorigenesis by CXCR4 and by Aurora and Polo-Like Kinases." Diss., 2013. http://hdl.handle.net/10161/7104.
Full textDuring development, the precise regulation of the processes of proliferation, migration, and differentiation is required to establish proper organ structure and function and to prevent the deregulation that can lead to disease, such as cancer. Improved understanding of the signals that regulate these processes is therefore necessary to both gain insight into the mechanisms by which organ development proceeds and to identify strategies for treating the consequences of deregulation of these processes. In the cerebellum, some of the factors that regulate these processes have been identified but remain incompletely understood. Our studies have focused on the signals that regulate the migration of cerebellar granule neuron progenitors (GNPs) and the contribution of the SDF-1/CXCR4 signaling axis to postnatal cerebellar development. Using conditional knockout mice to delete CXCR4 specifically in GNPs, we show that loss of CXCR4 results in premature migration of a subset of GNPs throughout postnatal development that are capable of proliferation and survival outside of their normal mitogenic niche. Loss of CXCR4 also causes a reduction in the activity of the Sonic hedgehog (SHH) pathway (the primary mitogen for GNPs) but does not affect GNP proliferation, differentiation, or capacity for tumor formation. Our data suggest that while other factors likely contribute, SDF-1/CXCR4 signaling is necessary for proper migration of GNPs throughout cerebellar development.
In addition to understanding the signals that regulate normal development, the identification of vulnerabilities of established tumors is also necessary to improve cancer treatment. One strategy to improve treatment involves targeting the cells that are critical for maintaining tumor growth, known as tumor-propagating cells (TPCs). In the context of the cerebellar tumor medulloblastoma (MB), we have previously identified a population of TPCs in tumors from patched mutant mice that express the cell surface carbohydrate antigen CD15/SSEA-1. Here, we employed multiple approaches in an effort to target these cells, including a biochemical approach to identify molecules that carry the CD15 carbohydrate epitope as well as an immunotoxin approach to specifically target CD15-expressing cells. Unfortunately, these strategies were ultimately unsuccessful, but an alternative approach that recognized a vulnerability of CD15+ cells was identified. We show that CD15+ cells express elevated levels of genes associated with the G2/M phases of the cell cycle, progress more rapidly through the cell cycle than CD15- cells, and contain an increased proportion of cells in G2/M. Exposure of tumor cells to inhibitors of Aurora and Polo-like kinases, key regulators of G2/M, induces cell cycle arrest, apoptosis and enhanced sensitivity to conventional chemotherapy, and treatment of tumor-bearing mice with these agents significantly inhibits tumor progression. Importantly, cells from human patient-derived MB xenografts are also sensitive to Aurora and Polo-like kinase inhibitors. Our findings suggest that targeting G2/M regulators may represent a novel approach for the treatment of human MB.
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