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1

Sen, Onur. "Phospho-regulation of the spindle assembly checkpoint." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/15873.

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Mitosis is a highly regulated process by which a cell duplicates and distributes its chromosomal DNA into two identical daughter cells equally. Equal distribution of the chromosomes is crucial for accurate propagation of genetic information. This is essential for maintaining viability and preventing genomic instability that can potentially lead to cancer. In order to avoid unequal distribution of chromosomes, cells employ a surveillance mechanism called the spindle assembly checkpoint (SAC). The SAC is an inhibitory signalling network, which delays segregation of chromosomes, until they have s
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2

Hewitt, Laura. "Using a novel small molecule inhibitor to investigate the role of Mps1 kinase activity." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/using-a-novel-small-molecule-inhibitor-to-investigate-the-role-of-mps1-kinase-activity(fcacfefc-90d9-4e92-9af4-a57897737329).html.

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During mitosis, accurate chromosome segregation is essential: gain or loss of genetic information can be detrimental to cell viability, or promote tumourigenesis. The mitotic checkpoint (also known as the spindle assembly checkpoint or SAC) ensures accurate chromosome segregation by delaying cell cycle progression until accuracy can be guaranteed. Mps1 is a protein kinase that is crucial for mitotic checkpoint signalling and also for proper chromosome alignment at metaphase. However, the precise role of Mps1’s catalytic activity is still unclear. Here, I present AZ3146, a novel small molecule
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3

Tipton, Aaron R. "How to Assemble a Functional Mitotic Checkpoint Complex." University of Toledo / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1341597834.

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4

Cotsiki, Marina. "Identification of novel protein interactors of the SV40 large T antigen using the yeast two hybrid system." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268375.

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5

Sze, Man-fong. "Characterization of mitotic checkpoint proteins, MAD1 and MAD2, in hepatocellular carcinoma." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36841286.

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6

Leontiou, Ioanna. "'SynCheck' : new tools for dissecting Bub1 checkpoint functions." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/33246.

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The accurate segregation of DNA during cell division is essential for the viability of future cellular generations. Genetic material is packaged in the form of chromosomes during cell division, and chromosomes are segregated equally into two daughter cells. Chromosome mis-distribution leads to genetic disorders (e.g. Down's syndrome), aneuploidy and cancer. The spindle checkpoint ensures proper chromosome segregation by monitoring kinetochore-microtubule interactions. Upon checkpoint activation, unattached kinetochores recruit checkpoint proteins that combine to form a diffusible inhibitor (th
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7

Jaffrey, Ross G. "Genomic instability in cancer : the role of the mitotic spindle checkpoint gene hBUB1." Thesis, University of Aberdeen, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400744.

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In this study, a number of human cancer cell lines were characterised for their genomic instability phenotypes: using a panel of centromeric probes utilising the fluorescence <i>in situ</i> hybridisation (FISH) technique to detect CIN, and a microsatellite assay using radioactive PCR labelling to detect MIN.  This characterisation allowed comparison of hBUB1 expression data, and assessed the differences between phenotypic cell line groups for <i>hBUB1</i> mutations and polymorphisms.  Having demonstrated the potential of radioactive-microsatellite PCR to display changes between drug sensitive
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8

Sze, Man-fong, and 施敏芳. "Characterization of mitotic checkpoint proteins, MAD1 and MAD2, in hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B38438550.

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9

LaBelle, Jenna J. "Characterizing BUBR1 interactions with MAD2 and p31comet during the Mitotic Checkpoint." University of Toledo / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1533237730601357.

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10

Li, Deyu. "Spatial and temporal regulation of mitotic progression by the spindle checkpoint in Drosophila melanogaster." Thesis, University of Newcastle Upon Tyne, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491836.

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The spindle assembly checkpoint is a cell-cycle surveillance system which ensures the mother cell equally and faithfully separates its replicated DNA contents into two daughter cells before the onset of anaphase. Mad2, BubRl and Cdc20 (Fzy in Drosophila melanogaster) are all kinetochore proteins which dynamically turnover on and off the mitotic kinetochores. It is believed that these proteins are forming a diffusible kinetochore anaphase inhibitory signal for spindle checkpoint function, inhibiting APC/C activity in order to delay the metaphase-anaphase transition (Musacchio and Salmon, 2007).
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11

Lock, Rowena Lesley. "Investigation into how mitotic spindle checkpoint function is compromised by Sv40 large T antigen." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1444978/.

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The viral oncoprotein Simian virus 40 large T antigen (LT) efficiently immortalises primary rodent cells and occasionally transforms them to tumourigenicity. It has long been known that LT can cause genomic instability and induce aneuploidy, and that it disrupts the mitotic spindle checkpoint, involved in monitoring the segregation of sister chromatids. LT has recently been shown to interact with the spindle checkpoint protein Bubl. This thesis describes research into the effects of LT on spindle checkpoint function and examines the possibility that interaction of LT with Bubl is responsible.
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12

Orr, Bernard Nunes de Almeida. "The role of Mad2 and BudR1 in the spindle assembly checkpoint and mitotic progression." Tese, Instituto de Ciências Biomédicas Abel Salazar, 2009. http://hdl.handle.net/10216/50174.

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13

Orr, Bernard Nunes de Almeida. "The role of Mad2 and BudR1 in the spindle assembly checkpoint and mitotic progression." Doctoral thesis, Instituto de Ciências Biomédicas Abel Salazar, 2009. http://hdl.handle.net/10216/50174.

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14

Nannas, Natalie Jo. "Investigation of Force, Kinetochores, and Tension in the Saccharomyces Cerevisiae Mitotic Spindle." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11047.

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Cells must faithfully segregate their chromosomes at division; errors in this process causes cells to inherit an incorrect number of chromosomes, a hallmark of birth defects and cancer. The machinery required to segregate chromosomes is called the spindle, a bipolar array of microtubules that attach to chromosomes through the kinetochore. Replicated chromosomes contain two sister chromatids whose kinetochores must attach to microtubules from opposite poles to ensure correct inheritance of chromosomes. The spindle checkpoint monitors the attachment to the spindle and prevents cell division unt
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15

Stucke, Volker Matthias. "Human Mps1 kinase is required for the mitotic spindle checkpoint, but not for centrosome duplication." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968551076.

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16

Putnam, Charles Wellington. "Integration of G2/M checkpoint, spindle assembly checkpoint,and Ran cycle regulators in the Saccharomyces cerevisiae DNA damage mitotic arrest response." Diss., The University of Arizona, 2004. http://hdl.handle.net/10150/280738.

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It is axiomatic that genomic stability is dependent upon regulatory pathways, termed checkpoints, which sense perturbations of cell cycle execution including damage to chromosomal DNA. In Saccharomyces cerevisiae, the principal DNA damage checkpoint is at G2/M. Heretofore, this and other checkpoints, such as the spindle assembly checkpoint, which is also operative at the metaphase/anaphase transition, have been viewed as essentially linear pathways, responding to a specific type of damage, signaling via sui generis proteins, and targeting a limited number of effectors for arrest. In a 1999 rep
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17

STUABACH, AMY ELIZABETH. "THE REGULATION OF BubR1 EXPRESSION BY p53: A ROLE FOR p53 IN THE MITOTIC SPINDLE CHECKPOINT AND CHROMOSOME INSTABILITY." University of Cincinnati / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1100831777.

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18

Pinsky, Benjamin Alan. "Characterization of the Ipl1/Aurora protein kinase in chromosome segregation and the spindle checkpoint /." Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/5028.

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19

Horikoshi, Yasunori. "Analyses of the Substrate-Selective Ubiquitination of Mitotic Regulators and its Involvement in Silencing the Spindle Assembly Checkpoint." 京都大学 (Kyoto University), 2013. http://hdl.handle.net/2433/179379.

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20

Kim, Haein. "Temporal Coordination Of Mitotic Chromosome Alignment And Segregation: Structural And Functional Studies Of Kif18a." ScholarWorks @ UVM, 2018. https://scholarworks.uvm.edu/graddis/930.

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Chromosome alignment is highly conserved in all eukaryotic cell divisions. Microtubule (MT) -based forces generated by the mitotic spindle are integral for proper chromosome alignment and equal chromosome segregation. The kinetochore is a multi-subunit protein complex that assembles on centromeric regions of chromosomes. Kinetochores tether chromosomes to MTs (K fibers) that emanate from opposite poles, in a process called biorientation. This linkage translates K fiber dynamics into chromosome movements during alignment and segregation. Stable, high-affinity kinetochore attachments promote spi
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21

Staubach, Amy. "The regulation of BubR1 expression by p53 a role for p53 in the mitotic spindle checkpoint and chromosome instability /." Cincinnati, Ohio : University of Cincinnati, 2004. http://www.ohiolink.edu/etd/view.cgi?acc%5Fnum=ucin1100831777.

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22

Li, Tong. "Analyse quantitative et multi-paramétrique de la mitose afin de comprendre la ségrégation des chromosomes." Thesis, Toulouse 3, 2019. http://www.theses.fr/2019TOU30265.

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La mitose est un processus cellulaire robuste, mais les mécanismes qui contrôlent la fidélité de la mitose restent une question importante en Biologie. La compréhension des processus conduisant à des défauts mitotiques sont essentiels pour déchiffrer les mécanismes moléculaires conduisant à la tumorigenèse, à la trisomie ou encore aux maladies génétiques. Une ségrégation chromosomique fidèle repose sur la coopération de nombreuses protéines tout au long du cycle cellulaire. De ce fait, l'utilisation d'approches quantitatives sophistiquées s'est avérée nécessaire pour l'étude de la robustesse d
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23

Wiedemuth, Ralf. "Untersuchungen zur Funktion des Inhibitor der Apoptose Proteins Survivin in der chromosomalen Stabilität und „DNA Damage Response“ von Tumorzellen." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-97250.

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Das nur 16,5 kDa große Survivin ist ein bifunktionales Protein, welches eine bedeutende Rolle in zwei wichtigen zellulären Prozessen spielt, der Apoptose und der Mitose. Aufgrund seiner BIR Domäne wird es zu den Inhibitor der Apoptose Proteine (IAP) gezählt. Diese Gruppe an Proteinen interferiert negativ mit der Aktivierung der Caspasen und wirkt somit einer Induktion der Apoptose entgegen. Neben seiner anti-apoptotischen Funktion besitzt das Survivin zudem eine essentielle Rolle bei der Segregation der Chromosomen und während der Zytokinese. In der Mitose bildet Survivin mit Borealin, INCENP
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24

Restall, Ian J. "Inducing Cellular Senescence in Cancer." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23691.

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Cellular senescence is a permanent cell cycle arrest that is induced as a response to cellular stress. Replicative senescence is a well-described mechanism that limits the replicative capacity of cells and must be overcome by cancer cells. Oncogene-induced senescence (OIS) is a form of premature senescence and a potent tumor suppressor mechanism. OIS is induced in normal cells as a result of deregulated oncogene or tumor suppressor gene expression. An exciting area of research is the identification of novel targets that induce senescence in cancer cells as a therapeutic approach. In this study
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25

He, Enuo. "Stochastic modelling of the cell cycle." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:04185cde-85af-4e24-8d06-94b865771cf1.

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Precise regulation of cell cycle events by the Cdk-control network is essential for cell proliferation and the perpetuation of life. The unidirectionality of cell cycle progression is governed by several critical irreversible transitions: the G1-to-S transition, the G2-to-M transition, and the M-to-G1 transition. Recent experimental and theoretical evidence has pulled into question the consensus view that irreversible protein degradation causes the irreversibility of those transitions. A new view has started to emerge, which explains the irreversibility of cell cycle transitions as a consequen
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26

On, Kin Fan. "The role of MAD2L1BP in the silencing of the spindle-assembly checkpoint and the DNA damage checkpoint /." View abstract or full-text, 2009. http://library.ust.hk/cgi/db/thesis.pl?BICH%202009%20ON.

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27

Lara, González Pablo. "Investigating how the Spindle Assembly Checkpoint inhibits the onset of anaphase." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/investigating-how-the-spindle-assembly-checkpoint-inhibits-the-onset-of-anaphase(91d10d3a-9fc9-4395-9a18-d29969d604f8).html.

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The Spindle Assembly Checkpoint (SAC) delays the onset of anaphase in response to unattached kinetochores. The mechanism by which the SAC works is by inhibiting the activity of the Anaphase-promoting complex/cyclosome (APC/C), a large E3 ubiquitin ligase that targets several anaphase inhibitors for proteasome-mediated degradation, including securin and cyclin B. When the SAC is satisfied, the APC/C becomes active and this allows progression through the cell cycle. Work from the last decade identified the mitotic checkpoint complex (MCC) as the main transducer of the SAC. The MCC is composed of
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28

Roca, Marianne. "The spindle assembly checkpoint in Phallusia mammillata embryos." Electronic Thesis or Diss., Sorbonne université, 2019. http://www.theses.fr/2019SORUS500.

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Le point de contrôle du fuseau mitotique (Spindle Assembly Checkpoint : SAC) retarde l’anaphase jusqu’à ce que tous les chromosomes soient attachés correctement aux microtubules. Le SAC permet ainsi d’éviter des erreurs de ségrégation des chromosomes aboutissant à des cellules filles aneuploïdes (i.e. avec un nombre anormal de chromosomes). L’aneuploïdie, délétère pour les cellules, peut entrainer des problèmes de développement et est observée dans les cancers. Cependant, chez certaines espèces, le SAC n’est pas efficace au cours de la phase précoce du développement embryonnaire. J’ai mis en é
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29

Arnst, Christopher Edward. "TRIP13 AAA-ATPase Promotes Spindle Assembly Checkpoint Activation through Coordinating with MAD1 at Unattached Kinetochores." University of Toledo / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1560867340515027.

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30

Dreier, Megan Renee. "The Regulation of Sororin by Phosphorylation." University of Toledo / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1333736093.

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31

Edgerton, Heather Dawn. "Functions of Gamma-tubulin in the Spindle Assembly Checkpoint and APC/C Regulation in Aspergillus nidulans." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1374159200.

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32

Mossaid, Ikram. "The nuclear pore protein Nup153: Dissecting its role in nuclear envelope and nuclear pore complex architecture and its interaction with the spindle assembly checkpoint protein Mad1." Doctoral thesis, Universite Libre de Bruxelles, 2016. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/234375.

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Nuclear pore complexes (NPCs) are embedded in the nuclear envelope (NE) and composed of proteins called nucleoporins. NPCs as such control the bidirectional traffic of proteins and RNAs between the nucleus and the cytoplasm in eukaryotic cells whereas individual nucleoporins were found to be implicated in other cellular processes such as, cell division, kinetochore assembly, gene expression and cell migration. A prime example for nucleoporin functional versatility can be seen in Nup153. Nup153 is since its discovery known to be a central player in nucleocytoplasmic transport, but additionally
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33

Pommier, Roxane. "Identification des fonctions oncosuppressives de TIF1γ (Transcriptional Intermediary Factor 1 γ)". Thesis, Lyon 1, 2014. http://www.theses.fr/2014LYO10356/document.

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TIF1γ est une protéine nucléaire de 1127 acides aminés possédant deux activités : une activité d'E3-ubiquitine ligase et des fonctions de régulateur transcriptionnel. TIF1γ exerce majoritairement ses fonctions dans les processus de développement embryonnaire et de différenciation cellulaire, notamment via son implication dans la voie de signalisation du TGFβ. Le rôle anti-tumoral de TIF1γ a été mis en évidence dans plusieurs modèles murins et son expression est diminuée dans de nombreuses tumeurs humaines de diverses origines tissulaires. Néanmoins, les mécanismes moléculaires et cellulaires p
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34

Brioudes, Estelle. "RSK2 et Greatwall, deux AGC kinases actrices de la mitose." Thesis, Montpellier 2, 2010. http://www.theses.fr/2010MON20251/document.

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La mitose est une phase importante du cycle cellulaire. Les mécanismes de surveillance s'assurent de l'ordre et de l'exécution correcte des événements du cycle cellulaire dont les erreurs peuvent conduire à l'aneuploïdie. Pendant la mitose, la séparation des chromatides sœurs est régulée par le point de contrôle du fuseau mitotique qui s'assure que tous les chromosomes sont correctement alignés sur la plaque métaphasique. L'entrée et la sortie de mitose sont régulées par l'activation et l'inactivation du complexe cycline B/Cdk1. Cette fine régulation fait intervenir de nombreuses kinases et ph
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35

Davidas, Axelle. "Dissection des fonctions mitotiques de la kinase Aurora B par CALI (Chromophore-Assisted Light Inactivation)." Phd thesis, Université de Grenoble, 2012. http://tel.archives-ouvertes.fr/tel-00903744.

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La kinase Aurora B appartient au complexe des protéines passagères. Ce complexe est impliqué dans la régulation de la condensation, constriction et ségrégation des chromosomes, ainsi que dans la cytokinèse. Son rôle est donc crucial pour prévenir la formation de cellules cancéreuses. Cependant, l'étude de la fonction précise d'Aurora B dans chacune des phases de la mitose est limitée par la durée de celle-ci, et par le manque de spécificité des inhibiteurs existants. Nous avons donc développé une stratégie basée sur la photo-inactivation de la kinase par le chromophore Killer-Red, fusionné à l
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36

Tzeng, Mi-Chi, and 曾秘麒. "Degradation of mitotic spindle checkpoint protein Mad3." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/99389453182387390395.

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碩士<br>國立陽明大學<br>生化暨分子生物研究所<br>95<br>The mitotic spindle checkpoint arrests cells at the metaphase-to-anaphase transiton until all chromosomes have properly attached to the mitotic spindle. The mitotic spindle checkpoint ensures accurate chromosome segregation during mitosis. Defects in the checkpoint reduce the accuracy of chromosome segregation and may cause genomic instability that is associated with cancer progression. Six mitotic spindle checkpoint proteins have been identified in the budding yeast Saccharomyces cerevisiae, including Mps1, Mad1, Mad2, Mad3, Bub1, and Bub3. The spi
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37

Huang, Yi-Fu, and 黃億富. "The role of the spindle checkpoint kinase TTK/hMps1 in p53-dependent post mitotic checkpoint." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/85551645550687937889.

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博士<br>國立清華大學<br>分子與細胞生物研究所<br>97<br>Upon prolonged arrest in mitosis, cells undergo adaptation and exit mitosis without cell division. These tetraploid cells are arrested in the subsequent G1 phase in a spindle checkpoint and p53-dependent manner. p53 has long been known to be activated by spindle poison such as nocodazole and taxol, although the underlying mechanism is still unclear. In this study, evidence was presented which demonstrated that stabilization and activation of p53 by spindle disruption required the spindle checkpoint kinase TTK/hMps1. Down regulation of TTK/hMPS1 diminishes p5
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Enzor, Rikki S. "The Fanconi anemia signaling network regulates the mitotic spindle assembly checkpoint." Thesis, 2014. http://hdl.handle.net/1805/5904.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>Fanconi anemia (FA) is a heterogenous genetic syndrome characterized by progressive bone marrow failure, aneuploidy, and cancer predisposition. It is incompletely understood why FA-deficient cells develop gross aneuploidy leading to cancer. Since the mitotic spindle assembly checkpoint (SAC) prevents aneuploidy by ensuring proper chromosome segregation during mitosis, we hypothesized that the FA signaling network regulates the mitotic SAC. A genome-wide RNAi screen and studies in primary cells were performed to systematically evaluat
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Vogel, Celia [Verfasser]. "The role of the mitotic spindle checkpoint in chemotherapy-induced apoptosis / vorgelegt von Celia Vogel." 2009. http://d-nb.info/993807062/34.

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40

Stucke, Volker Matthias [Verfasser]. "Human Mps1 kinase is required for the mitotic spindle checkpoint, but not for centrosome duplication / vorgelegt von Volker Matthias Stucke." 2003. http://d-nb.info/968551076/34.

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Van, Zijl Magdalena Catherina. "In vitro effects of 2-methoxyestradiol, an endogenous estrogen, on MCF-12A and MCF-7 cell cycle progression." Diss., 2006. http://hdl.handle.net/2263/26594.

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2-Methoxyestradiol (2ME) is an endogenous estrogen metabolite with antiproliferative and antiangiogenic properties. 2ME also plays an active role in the induction of apoptosis, especially in cancerous cells. These properties have been confirmed by various in vitro and in vivo studies and render 2ME a potential antitumor agent. The mechanism of action of 2ME, however, is not yet fully elucidated and it is believed that multiple mechanisms are involved that may be dependent on cell type. The aim of this study was to investigate the differential effects of 2ME on cell growth, morphology and spind
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42

Matchett, K. B., S. McFarlane, S. E. Hamilton, et al. "Ran GTPase in Nuclear Envelope Formation and Cancer Metastasis." 2014. http://hdl.handle.net/10454/10861.

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No<br>Ran is a small ras-related GTPase that controls the nucleocytoplasmic exchange of macromolecules across the nuclear envelope. It binds to chromatin early during nuclear formation and has important roles during the eukaryotic cell cycle, where it regulates mitotic spindle assembly, nuclear envelope formation and cell cycle checkpoint control. Like other GTPases, Ran relies on the cycling between GTP-bound and GDP-bound conformations to interact with effector proteins and regulate these processes. In nucleocytoplasmic transport, Ran shuttles across the nuclear envelope through nuclear pore
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43

Wiedemuth, Ralf. "Untersuchungen zur Funktion des Inhibitor der Apoptose Proteins Survivin in der chromosomalen Stabilität und „DNA Damage Response“ von Tumorzellen." Doctoral thesis, 2012. https://tud.qucosa.de/id/qucosa%3A26156.

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Das nur 16,5 kDa große Survivin ist ein bifunktionales Protein, welches eine bedeutende Rolle in zwei wichtigen zellulären Prozessen spielt, der Apoptose und der Mitose. Aufgrund seiner BIR Domäne wird es zu den Inhibitor der Apoptose Proteine (IAP) gezählt. Diese Gruppe an Proteinen interferiert negativ mit der Aktivierung der Caspasen und wirkt somit einer Induktion der Apoptose entgegen. Neben seiner anti-apoptotischen Funktion besitzt das Survivin zudem eine essentielle Rolle bei der Segregation der Chromosomen und während der Zytokinese. In der Mitose bildet Survivin mit Borealin, INCENP
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44

Foss, Kristen. "Regulation of the DNA Damage Response and Spindle Checkpoint Signaling Pathways." Diss., 2015. http://hdl.handle.net/10161/11342.

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<p>The ultimate goal of any living cell is to pass on a complete, unaltered copy of its DNA to its daughter cell. The DNA damage response (DDR) and spindle checkpoint are two essential signaling pathways that make it possible for a cell to achieve this goal. The DDR protects genetic integrity by sensing errors in the DNA sequence and activating signaling pathways to arrest the cell cycle and repair the DNA. The spindle checkpoint protects chromosomal integrity by preventing the separation of chromosomes during mitosis until all chromosomes are correctly attached to the mitotic spindle. Proper
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45

Windecker, Hanna [Verfasser]. "Spindle assembly checkpoint-independent functions of Bub1 and Bub3 in fission yeast mitosis / vorgelegt von Hanna Windecker." 2010. http://d-nb.info/1009635247/34.

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46

Diogo, Vânia Sofia dos Reis. "Checkpoint mitótico como alvo terapêutico para sensibilizar células cancerígenas a agentes antimitóticos." Master's thesis, 2015. http://hdl.handle.net/10400.1/8636.

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Dissertação de Mestrado, Oncobiologia – Mecanismos Moleculares do Cancro, Departamento de Ciências Biomédicas e Medicina, Universidade do Algarve, 2015<br>Muitos cancros são tratados com agentes antimitóticos, como o taxol. Estes agentes param as células em mitose ao danificarem os microtúbulos, ativando o checkpoint mitótico (SAC), mecanismo que controla a correta segregação dos cromossomas durante a mitose. Contudo, células resistentes conseguem contornar esses danos e prosseguir com a mitose, emergindo assim o SAC como potencial alvo terapêutico no tratamento do cancro. Desta forma surgiu o
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Vázquez, de Castro Diez Cayetana. "Causes and consequences of chromosome segregation errors in the mouse preimplantation embryo." Thesis, 2018. http://hdl.handle.net/1866/21198.

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Abstract:
La division cellulaire est un processus biologique universel nécessaire à la reproduction, au développement, à la survie cellulaire ainsi qu’à la réparation des tissus. Une ségrégation chromosomique exacte pendant la mitose est essentielle pour une répartition égale des chromosomes répliqués entre les cellules filles. Des erreurs dans la ségrégation des chromosomes mènent à une condition appelée aneuploïdie, définie par un nombre inadéquat de chromosomes dans une cellule. L’aneuploïdie est associée à une altération de la santé cellulaire, la tumorigénèse, des malformations congénitales et l'in
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