Relevant bibliographies by topics / Aurora Kinase A

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Academic literature on the topic 'Aurora Kinase A'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 January 2023

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Journal articles on the topic "Aurora Kinase A"

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Kim, Hyo Jin, and Jongchan Kim. "OTUD6A Is an Aurora Kinase A-Specific Deubiquitinase." International Journal of Molecular Sciences 22, no. 4 (February 16, 2021): 1936. http://dx.doi.org/10.3390/ijms22041936.

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Aurora kinases are serine/threonine kinases required for cell proliferation and are overexpressed in many human cancers. Targeting Aurora kinases has been a therapeutic strategy in cancer treatment. Here, we attempted to identify a deubiquitinase (DUB) that regulates Aurora kinase A (Aurora-A) protein stability and/or kinase activity as a potential cancer therapeutic target. Through pull-down assays with the human DUB library, we identified OTUD6A as an Aurora-A-specific DUB. OTUD6A interacts with Aurora-A through OTU and kinase domains, respectively, and deubiquitinates Aurora-A. Notably, OTUD6A promotes the protein half-life of Aurora-A and activates Aurora-A by increasing phosphorylation at threonine 288 of Aurora-A. From qPCR screening, we identified and validated that the cancer gene CKS2 encoding Cyclin-dependent kinases regulatory subunit 2 is the most upregulated cell cycle regulator when OTUD6A is overexpressed. The results suggest that OTUD6A may serve as a therapeutic target in human cancers.
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Qi, Guangying, Jing Liu, Sisi Mi, Takaaki Tsunematsu, Shengjian Jin, Wenhua Shao, Tian Liu, Naozumi Ishimaru, Bo Tang, and Yasusei Kudo. "Aurora Kinase Inhibitors in Head and Neck Cancer." Current Topics in Medicinal Chemistry 18, no. 3 (May 14, 2018): 199–213. http://dx.doi.org/10.2174/1568026618666180112163741.

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Aurora kinases are a group of serine/threonine kinases responsible for the regulation of mitosis. In recent years, with the increase in Aurora kinase-related research, the important role of Aurora kinases in tumorigenesis has been gradually recognized. Aurora kinases have been regarded as a new target for cancer therapy, resulting in the development of Aurora kinase inhibitors. The study and application of these small-molecule inhibitors, especially in combination with chemotherapy drugs, represent a new direction in cancer treatment. This paper reviews studies on Aurora kinases from recent years, including studies of their biological function, their relationship with tumor progression, and their inhibitors.
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Shi, Yijiang, Tony Reiman, Weiqun Li, Christopher Maxwell, Linda Pilarski, Rick Feldman, and Alan Lichtenstein. "Targeting Aurora Kinases as Therapy in Multiple Myeloma." Blood 108, no. 11 (November 16, 2006): 3484. http://dx.doi.org/10.1182/blood.v108.11.3484.3484.

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Abstract The aurora kinases A and B are critical for facilitating cell cycle transit from G2 through to cytokinesis. As important regulators of the mitotic event, they are being tested as potential targets in cancer therapy. Multiple myeloma (MM) is a B cell malignancy characterized by progressive genetic instability, suggesting a disruption of cell cycle checkpoints has occurred that normally arrest cells at G2M or within mitosis when injury to the mitotic machinery occurs. Since these deficient checkpoints would prevent cell cycle arrest and potential repair and may render MM cells susceptible to apoptotic death in mitosis, we tested the anti-myeloma effecy of two separate agents that inhibit aurora kinases. Both agents induced cytoreduction of MM cell lines and primary myeloma samples at nM concentrations while normal peripheral blood lymphocytes and CLL cells were not affected. MM cells were not protected by IL-6 or activating mutations of RAS. Anti-myeloma effects were characterized by induction of tetraploidy followed by apoptosis. The myeloma apoptotic effect correlated well with the inhibition of aurora kinase activity as shown by reduction of histone 3B phosphorylation (substrate of auroras). Furthermore, stable ectopic over-expression of aurora kinase A significantly protected MM cells against aurora inhibitors but had no effect on apoptosis induced by velcade. As expression of the centrosomal protein RHAMM in MM cells may contribute to genetic instability, we tested effects of RHAMM over-expression on the sensitivity to aurora inhibitors. Although RHAMM over-expression in transfected MM cells was very modest, it significantly enhanced sensitivity to apoptosis induced by aurora kinase inhibitors. These results suggest the potential for aurora kinase inhibitors in multiple myeloma especially in patients where RHAMM is over-expressed.
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Hochegger, Helfrid, Nadia Hégarat, and Jose B. Pereira-Leal. "Aurora at the pole and equator: overlapping functions of Aurora kinases in the mitotic spindle." Open Biology 3, no. 3 (March 2013): 120185. http://dx.doi.org/10.1098/rsob.120185.

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The correct assembly and timely disassembly of the mitotic spindle is crucial for the propagation of the genome during cell division. Aurora kinases play a central role in orchestrating bipolar spindle establishment, chromosome alignment and segregation. In most eukaryotes, ranging from amoebas to humans, Aurora activity appears to be required both at the spindle pole and the kinetochore, and these activities are often split between two different Aurora paralogues, termed Aurora A and B. Polar and equatorial functions of Aurora kinases have generally been considered separately, with Aurora A being mostly involved in centrosome dynamics, whereas Aurora B coordinates kinetochore attachment and cytokinesis. However, double inactivation of both Aurora A and B results in a dramatic synergy that abolishes chromosome segregation. This suggests that these two activities jointly coordinate mitotic progression. Accordingly, recent evidence suggests that Aurora A and B work together in both spindle assembly in metaphase and disassembly in anaphase. Here, we provide an outlook on these shared functions of the Auroras, discuss the evolution of this family of mitotic kinases and speculate why Aurora kinase activity may be required at both ends of the spindle microtubules.
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Pflug, Alexander, Taianá Maia de Oliveira, Dirk Bossemeyer, and Richard A. Engh. "Mutants of protein kinase A that mimic the ATP-binding site of Aurora kinase." Biochemical Journal 440, no. 1 (October 27, 2011): 85–93. http://dx.doi.org/10.1042/bj20110592.

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We describe in the present paper mutations of the catalytic subunit α of PKA (protein kinase A) that introduce amino acid side chains into the ATP-binding site and progressively transform the pocket to mimic that of Aurora protein kinases. The resultant PKA variants are enzymatically active and exhibit high affinity for ATP site inhibitors that are specific for Aurora kinases. These features make the Aurora-chimaeric PKA a valuable tool for structure-based drug discovery tasks. Analysis of crystal structures of the chimaera reveal the roles for individual amino acid residues in the binding of a variety of inhibitors, offering key insights into selectivity mechanisms. Furthermore, the high affinity for Aurora kinase-specific inhibitors, combined with the favourable crystallizability properties of PKA, allow rapid determination of inhibitor complex structures at an atomic resolution. We demonstrate the utility of the Aurora-chimaeric PKA by measuring binding kinetics for three Aurora kinase-specific inhibitors, and present the X-ray structures of the chimaeric enzyme in complex with VX-680 (MK-0457) and JNJ-7706621 [Aurora kinase/CDK (cyclin-dependent kinase) inhibitor].
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Deretic, Jovana, Alastair Kerr, and Julie P. I. Welburn. "A rapid computational approach identifies SPICE1 as an Aurora kinase substrate." Molecular Biology of the Cell 30, no. 3 (February 2019): 312–23. http://dx.doi.org/10.1091/mbc.e18-08-0495.

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Aurora kinases play a major role in mitosis by regulating diverse substrates. Defining their critical downstream targets is important in understanding Aurora kinase function. Here we have developed an unbiased computational approach to identify new Aurora kinase substrates based on phosphorylation site clustering, protein localization, protein structure, and species conservation. We validate the microtubule-associated proteins Clasp2, Elys, tubulin tyrosine ligase-like polyglutamylase residues 330–624 and spindle and centriole associated protein 1, residues 549–855 (SPICE1), as Aurora A and B kinases substrates in vitro. We also demonstrate that SPICE1 localization is regulated by Aurora kinases during mitosis. In the absence of Aurora kinase activity, SPICE1 remains at centrioles but does not target to the spindle. Similarly, a nonphosphorylatable SPICE1 mutant no longer localizes to the spindle. Finally, we show that misregulating SPICE1 phosphorylation results in abnormal centriole number, spindle multipolarity, and chromosome alignment defects. Overall, our work indicates that temporal and spatial Aurora kinase–mediated regulation of SPICE1 is important for correct chromosome segregation. In addition, our work provides a database-search tool that enables rapid identification of Aurora kinase substrates.
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Dvořák Tomaštíková, Eva, Twan Rutten, Petr Dvořák, Alisa Tugai, Klara Ptošková, Beáta Petrovská, Daniel van Damme, Andreas Houben, Jaroslav Doležel, and Dmitri Demidov. "Functional Divergence of Microtubule-Associated TPX2 Family Members in Arabidopsis thaliana." International Journal of Molecular Sciences 21, no. 6 (March 22, 2020): 2183. http://dx.doi.org/10.3390/ijms21062183.

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TPX2 (Targeting Protein for Xklp2) is an evolutionary conserved microtubule-associated protein important for microtubule nucleation and mitotic spindle assembly. The protein was described as an activator of the mitotic kinase Aurora A in humans and the Arabidopsis AURORA1 (AUR1) kinase. In contrast to animal genomes that encode only one TPX2 gene, higher plant genomes encode a family with several TPX2-LIKE gene members (TPXL). TPXL genes of Arabidopsis can be divided into two groups. Group A proteins (TPXL2, 3, 4, and 8) contain Aurora binding and TPX2_importin domains, while group B proteins (TPXL1, 5, 6, and 7) harbor an Xklp2 domain. Canonical TPX2 contains all the above-mentioned domains. We confirmed using in vitro kinase assays that the group A proteins contain a functional Aurora kinase binding domain. Transient expression of Arabidopsis TPX2-like proteins in Nicotiana benthamiana revealed preferential localization to microtubules and nuclei. Co-expression of AUR1 together with TPX2-like proteins changed the localization of AUR1, indicating that these proteins serve as targeting factors for Aurora kinases. Taken together, we visualize the various localizations of the TPX2-LIKE family in Arabidopsis as a proxy to their functional divergence and provide evidence of their role in the targeted regulation of AUR1 kinase activity.
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Li, Hui, Qian Chen, Markus Kaller, Wolfgang Nellen, Ralph Gräf, and Arturo De Lozanne. "Dictyostelium Aurora Kinase Has Properties of both Aurora A and Aurora B Kinases." Eukaryotic Cell 7, no. 5 (March 7, 2008): 894–905. http://dx.doi.org/10.1128/ec.00422-07.

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ABSTRACT Aurora kinases are highly conserved proteins with important roles in mitosis. Metazoans contain two kinases, Aurora A and B, which contribute distinct functions at the spindle poles and the equatorial region respectively. It is not currently known whether the specialized functions of the two kinases arose after their duplication in animal cells or were already present in their ancestral kinase. We show that Dictyostelium discoideum contains a single Aurora kinase, DdAurora, that displays characteristics of both Aurora A and B. Like Aurora A, DdAurora has an extended N-terminal domain with an A-box sequence and localizes at the spindle poles during early mitosis. Like Aurora B, DdAurora binds to its partner DdINCENP and localizes on centromeres at metaphase, the central spindle during anaphase, and the cleavage furrow at the end of cytokinesis. DdAurora also has several unusual properties. DdAurora remains associated with centromeres in anaphase, and this association does not require an interaction with DdINCENP. DdAurora then localizes at the cleavage furrow, but only at the end of cytokinesis. This localization is dependent on DdINCENP and the motor proteins Kif12 and myosin II. Thus, DdAurora may represent the ancestral kinase that gave rise to the different Aurora kinases in animals and also those in other organisms.
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Shin, Soon, Youngshim Lee, Beom Kim, Junho Lee, Seunghyun Ahn, Dongsoo Koh, Yoongho Lim, and Young Lee. "Inhibitory Effect of Synthetic Flavone Derivatives on Pan-Aurora Kinases: Induction of G2/M Cell-Cycle Arrest and Apoptosis in HCT116 Human Colon Cancer Cells." International Journal of Molecular Sciences 19, no. 12 (December 17, 2018): 4086. http://dx.doi.org/10.3390/ijms19124086.

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Members of the aurora kinase family are Ser/Thr kinases involved in regulating mitosis. Multiple promising clinical trials to target aurora kinases are in development. To discover flavones showing growth inhibitory effects on cancer cells, 36 flavone derivatives were prepared, and their cytotoxicity was measured using a long-term clonogenic survival assay. Their half-maximal growth inhibitory effects against HCT116 human colon cancer cells were observed at the sub-micromolar level. Pharmacophores were derived based on three-dimensional quantitative structure–activity calculations. Because plant-derived flavones inhibit aurora kinase B, we selected 5-methoxy-2-(2-methoxynaphthalen-1-yl)-4H-chromen-4-one (derivative 31), which showed the best half-maximal cell growth inhibitory effect, and tested whether it can inhibit aurora kinases in HCT116 colon cancer cells. We found that derivative 31 inhibited the phosphorylation of aurora kinases A, aurora kinases B and aurora kinases C, suggesting that derivative 31 is a potential pan-aurora kinase inhibitor. The results of our analysis of the binding modes between derivative 31 and aurora A and aurora B kinases using in-silico docking were consistent with the pharmacophores proposed in this study.
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Chen, Ya-Ping, Hui-Ju Lin, Kung-Chao Chang, Jiann-Shiuh Chen, Ming-Ying Tsai, Liang-Yi Hung, and Tsai-Yun Chen. "Targeting Aurora Kinases in Acute Lymphoblastic Leukemia." Blood 120, no. 21 (November 16, 2012): 4907. http://dx.doi.org/10.1182/blood.v120.21.4907.4907.

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Abstract Abstract 4907 Introduction: Despite improved treatment outcome in acute lymphoblastic leukemia (ALL), drug resistance and disease recurrence remain major obstacles in specific subgroups. Thus, there is an urgent need to identify new targets for therapy. Several studies showed that Aurora kinases were therapeutic targets in cancer therapy, including solid tumors and hematological malignancies. Here we describe preclinical testing of Aurora kinase inhibitors in ALL and the molecular mechanism of different drug activity. Materials and methods: Quantitative RT-PCR and Western blot were used to assess the expressions of Aurora kinases and their activators in ALL. RT-PCR was used to detect the expression of MDR-1. To test activity against Aurora kinases, different ALL cell lines were treated with various concentrations of Aurora kinase inhibitors “VE-465 and VX-680”. The effects of Aurora kinase inhibitors on the cell cycle were evaluated by flow cytometry. Gene expression profiling was performed to identify the candidate targets which regulate the different drug sensitivity. Transient knockdown and overexpression of candidate genes in ALL cell lines were also employed in this study. Results: Nine ALL cell lines treated with Aurora kinase inhibitors (VE-465 and VX-680) exhibited different drug sensitivity. Five ALL cell lines were sensitive to drug treatment with IC50 around 10–40 nM, including MLL-AF4-positive and BCR-ABL-positive cell lines. However, RPMI-8402 was one of the three cell lines which were resistant to VE-465 and VX-680 with IC50 more than 10 μM. Among these sensitive ALL cell lines, treatment of Aurora kinase inhibitors resulted in an increased G2/M and sub-G1 populations. In contrast, drug-resistant ALL cell lines showed increased polyploidy status after exposure to Aurora kinase inhibitors. The different treatment efficacy was not related to the expression of Aurora kinases, their activators or MDR-1. In order to elucidate the molecular mechanism to regulate the different drug sensitivity, microarray study was performed. It showed that treatment of Aurora kinase inhibitors resulted in differential expressions of genes (75 up-regulated and 90 down-regulated genes) and CDKN1Awas one of the potential molecules which regulated the treatment diversity. RT-PCR and Western blot confirmed the cDNA microarray data: CDKN1A was up-regulated after treatment with Aurora kinase inhibitors in the drug-sensitive cell lines, but no change in the level of CDKN1A in the drug-resistance cell lines. Knockdown of CDKN1A in drug-sensitive cell lines impaired the treatment activity. Over-expression of CDKN1A in drug-resistant cell lines increased the anti-leukemia effect of Aurora kinase inhibitors. Conclusion: These data suggest that treatment with Aurora kinase inhibitors may be a novel and effective therapy in specific subgroups of ALL, including MLL-AF4-positive ALL. These data show that status of Aurora kinases, their activators or MDR-1 does not correlate with the drug susceptibility in ALL cell lines. The susceptibility to Aurora kinase inhibitors in ALL depends on the activation status of CDKN1A. Disclosures: No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "Aurora Kinase A"

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Lioutas, Antonio 1980. "Aurora A kinase function during anaphase." Doctoral thesis, Universitat Pompeu Fabra, 2012. http://hdl.handle.net/10803/97290.

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Aurora A (AurA) is an important mitotic kinase mainly studied for its involvement in cell cycle progression, centrosome maturation, mitotic spindle pole organization and bipolar spindle formation. It localizes to duplicated centrosomes and spindle microtubules (MTs) during mitosis where it regulates various factors participating in metaphase spindle formation. AurA is degraded late in mitosis suggesting that it might also have a function in anaphase. In this study we focused in understanding AurA function during anaphase in two different experimental systems. First, we kept AurA active in cycled Xenopus egg extracts and found that MTs maintained their mitotic organization longer throughout mitotic exit. We also observed chromosome segregation defects and problematic nuclear envelope formation. These observations indicate that AurA activity needs to be down-regulated for the transition from metaphase back to interphase. To get insights into the role of AurA during metaphase-anaphase transition we initially asked whether its kinase activity is still necessary for the maintenance of the metaphase spindle. We saw that the inhibition of AurA kinase activity in metaphase resulted to a collapse of the established metaphase spindle in HeLa cells. Indicating that AurA activity is necessary for the metaphase spindle maintenance. Then, we looked whether AurA kinase activity is still necessary during anaphase. We inhibited AurA at the onset of anaphase in Hela cells and found that anaphase spindles were smaller. We also observed that the MT structure responsible for anaphase spindle elongation, the central spindle, was defectively assembled and organized. Moreover, in cells where AurA was inhibited segregation of chromosomes was defective. These results indicate that AurA kinase activity is necessary for anaphase spindle elongation, central spindle assembly and organization and chromosome segregation. To understand further how AurA regulates anaphase spindle formation we looked known AurA substrates. We depleted TACC3, a known AurA substrate involved in MT formation earlier in mitosis and observed that TACC3 depletion phenocopied AurA inhibition. This indicates that TACC3 has a function in MT organization and chromosome segregation during anaphase and this function could possibly be regulated by AurA. In this study we have demonstrated that AurA activity is essential for metaphase spindle maintenance. We also found that during anaphase when AurA is either maintained active or inhibited MT organization is greatly affected and chromosome segregation is defective. Suggesting that AurA activity needs to be tightly controlled during anaphase for a correct completion of mitosis.
Aurora A (AurA) es una quinasa mitótica importante que se ha estudiado principalmente en su papel durante la progresión del ciclo celular, la maduración del centrosoma, la organización y la formación del polo y del huso mitótico. Durante la mitosis, AurA se localiza en los centrosomas duplicados y en los microtúbulos (MTs) del huso y se ha observado que regula varios factores que participan en la formación del huso mitótico. AurA se degrada al final de la mitosis indicando que pueda tener una función durante la anafase. En este estudio nos hemos centrado en la comprensión de la función de AurA durante la anafase en dos sistemas experimentales diferentes. En primer lugar, utilizando extractos de huevos de Xenopus hemos mantenido AurA activa durante la transición de metafase a anafase y hemos visto que los MTs del huso mitótico mantienen su organización durante más tiempo. También hemos observado que cuando AurA se mantiene activa existen defectos en la segregación cromosómica y la formación de la membrana nuclear. Esto indica que la actividad de AurA tiene un papel regulador sobre los MTs y la chromatina durante la transición de la metafase a la interfase. Para entender cual es la función de AurA durante la transición de metafase a anafase primero hemos estudiado si la actividad de la quinasa es necesaria para el mantenimiento del huso mitótico. Hemos visto que la inhibición de la actividad quinasa AurA resultó en el colapso del huso durante la metafase en células HeLa. Esto indica que la actividad de AurA es necesaria para el mantenimiento del huso mitótico de metafase. A continuación hemos analizamos si la actividad quinasa de AurA sigue siendo necesaria para la anafase. Para ello hemos inhibido AurA en células Hela al inicio de la anafase. En estas condiciones los husos de la anafase son más pequeños y la estructura de los MTs responsable del alargamiento del huso mitótico durante la anafase, el huso central, se organiza defectuosamente. Además, se encontraron errores durante la segregación de los cromosomas. Estos resultados indican que la actividad quinasa de AurA es necesaria para el alargamiento del huso durante la anafase y la organización y segregación cromosómica. Para entender el mecanismo de la función de AurA durante la anafase hemos estudiado a sustratos de AurA. Al estudiar TACC3 , un sustrato conocido de AurA que participa en la formación de MTs en las fase iniciales de la mitosis hemos encontrado que su eliminación de células HeLa produce el mismo fenotipo que la inhibición de AurA. Esto indica que TACC3 tiene una función en la organización de MT y la segregación de cromosomas durante la anafase y que esta función podría estar regulada por la quinasa AurA. En este estudio hemos demostrado que la actividad quinasa de AurA es esencial para el mantenimiento del huso mitótico. También hemos encontrado que durante la anafase cuando la quinasa AurA se mantiene activa o se inhibe la organización de los MTs del huso mitótico se ve muy afectada y los cromosomas se segregan defectuosamente. Por tanto los resultados de este estudio indican que la actividad quinasa de AurA está estrechamente controlada durante la anafase para el correcto cumplimiento de la mitosis.
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Dittmann, Linda [Verfasser]. "Expressionsanalyse von Aurora-Kinase A, Aurora-Kinase B, Repp 86, Cyclin-Dependent-Kinase 1 und Cyclin-Dependent-Kinase 2 bei Mamma- und Ovarialkarzinomen / Linda Dittmann." Kiel : Universitätsbibliothek Kiel, 2014. http://d-nb.info/1062536061/34.

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Douglas, M. E. "Regulation of cytokinesis by aurora B kinase." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598609.

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In the first part of this thesis, I identify 14-3-3 protein as an interaction partner of an Aurora-phosphorylated region of MKLP1, the kinesin component of centralspindlin. I show that MKLP1 contains a highly conserved amino acid motif that encompasses a known Aurora B phosphorylation site, S708, and binds 14-3-3 when phosphorylated at a conserved serine, S710. Aurora-mediated phosphorylation of S708 inhibits binding of 14-3-3 to MKLP1. Given that S708-phosphorylated MKLP1 (which cannot bind 14-3-3) becomes highly enriched at the central spindle during anaphase, whereas S710-phosphorylated MKLP1 (which can bind 14-3-3) does not, these results suggest that Aurora B regulates centralspindlin by controlling the binding and release of 14-3-3 at different subcellular structures during cell division. Finally, I investigate whether regulated binding of MKLP1 to 14-3-3 is required for centralspindlin function and cytokinesis. I show that the sole function of Aurora-mediated S708 phosphorylation is the removal of 14-3-3 that is bound to MKLP1, and that this is required for stable binding of MKLP1 to the central spindle. 14-3-3 is necessary and sufficient to prevent the assembly of centralspindlin into higher order multimers that are known to be required for centralspindlin to bind and bundle microtubules. Collectively, these findings show that Aurora B regulates cytokinesis by releasing MKLP1 from 14-3-3 protein, enabling centralspindlin to assemble into higher order multimers that bind and bundle microtubules into the central spindle.
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Khan, Jabbar. "Relationship between aurora kinase-C and cancer." Rennes 1, 2011. http://www.theses.fr/2011REN1S082.

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Aurora kinases belong to a conserved family of serine/threonine kinases key regulators of cell cycle progression. Aurora-A and Aurora-B are expressed in somatic cells and involved mainly in mitosis while Aurora-C is expressed during spermatogenesis and oogenesis and is involved in meiosis. Aurora-C is hardly detectable in normal somatic cells. However all three kinases are overexpressed in many cancer lines. Aurora-A possesses an oncogenic activity while Aurora-B does not. Here we investigated whether Aurora-C possesses such an oncogenic activity. We report that overexpression of Aurora-C induces abnormal cell division resulting in centrosome amplification and multinucleation in both transiently transfected cells and in stable cell lines. Only stable NIH3T3 cell clones overexpressing active Aurora-C formed foci of colonies when grown on soft agar, indicating that a gain of Aurora-C activity is sufficient to transform cells. Furthermore, we reported that NIH-3T3 stable cell lines overexpressing Aurora-C induced tumour formation when injected into nude mice, demonstrating the oncogenic activity of enzymatically active Aurora kinase C. Interestingly enough tumour aggressiveness was positively correlated with the rate of kinase activity, making Aurora-C a potential anti-cancer therapeutic target
Les kinases Aurora appartiennent à une famille très conservée de sérine/thréonine kinases. Ces kinases sont des régulateurs clés de la progression dans le cycle cellulaire. Aurora-A et Aurora-B sont exprimées dans les cellules somatiques et sont impliquées principalement en mitose. Aurora-C, en revanche, est exprimée au cours de la spermatogenèse et de l’oogenèse et est impliquée en méiose. Aurora-C est à peine détectable dans les cellules somatiques normales. Ces trois kinases cependant sont surexprimées dans de nombreuses lignées issues de cellules cancéreuses. Aurora-A est un oncogène alors que Aurora-B ne l’est pas. Dans ce travail, nous cherchons à déterminer si Aurora-C présente aussi une activité oncogénique. Nous rapportons que la surexpression d’Aurora-C induit une division cellulaire anormale résultant en une amplification des centrosomes et une multinucléation à la fois dans les cellules transfectées transitoirement et dans les lignées stables surexprimant Aurora-C. Seuls les clones stables de cellules NIH3T3 surexprimant Aurora-C active sont capable de former des colonies en agar mou, indiquant qu’un gain d’activité d’Aurora-C est suffisant pour transformer des cellules. De plus, nous rapportons que les clones stables de cellules NIH3T3 surexprimant Aurora-C active sont capable d’induire une formation de tumeur quand ces cellules sont injectées dans des souris immuno-compromises, démontrant l’activité oncogénique d’Aurora-C enzymatiquement active. Finalement, nous trouvons que l’aggressivité des tumeurs est positivement corrélée au taux d’activité kinase d’Aurora-C. Nos travaux posent Aurora-C en tant que bonne cible potentielle thérapeutique pour le traitement de cancers
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Hoang, Thi My Nhung. "Survivine et Aurora B kinase, deux cibles potentielles des drogues anti-mitotiques ; identification d’une nouvelle classe d’inhibiteurs des aurora kinases." Grenoble 1, 2008. http://www.theses.fr/2008GRE10007.

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Le complexe passager joue un rôle clé en mitose: contrôlant à la fois la ségrégation des chromosomes, la tension du fuseau, l'entrée en anaphase et la cytodirèse. Le complexe est composé de quatre protéines: INCENP, la kinase B, Survivine et Boréaline. Sachant que la protéine Survivine est phosphorylée par Aurora B et qu'elle a un role p sein du complexe, nous avons étudié un mutant mimant sa phosphorylation: Survivine TlI7E. La phosphoryla Survivine est nécessaire à la transition Métaphase! Anaphase. Le mutant Survivine TIl 7E est faiblement centromères en métaphase et agit comme un dominant négatif de la cytodirèse, empêchant la séparation de cellules filles. Lors de la recherche d'inhibiteurs des Aurora kinases, nous avons identifié une nouvelle classe de molécu inhibent la phosphorylation de l'histone H3 et le point de contrôle du fuseau. Ces molécules prévienr prolifération des cellules tumorales. Ces composés sont des outils intéressants pour étudier la fonction du COI passager et représentent un nouveau motif moléculaire pour le développement de drogues anti-cancéreuses. Survivine et Aurora B kinase dont l'expression est restreinte à la mitose sont deux cibles pour de nouvelles thérapies anti-mitotiques
The chromosomal passenger complex (CPe) plays a key role in mitosis : controlling both chromosome segre spindle tension, anaphase onset and cytokinesis. The complex is composed offour proteins : INCENP, Aurora B 1 Survivin and Borealin. Taking into account that Survivin is phosphorylated by Aurora Band has a pivotaI role complex, we have studied the phosphomimetic mutant SurvivinTl 17E. Survivin phosphorylation is requir anaphase onset and the phospho-mutant is poorly linked to centromere. Moreover it exhibits a dominant 11( function in cytokinesis, preventing abscission. Ln a search for Aurora kinase inhibitors we have identified a new class of Aurora B kinase inhibitors that pl Histone H3 phosphorylation, impairs mitotic spindle checkpoint. Moreover these molecules prevent tum! proliferation. These inhibitors are interesting too]s for understanding CPC function and represent a new lead development of anti-cancer drugs. Survivin and Aurora B kinase, which are expressed exclusively in mitosis, are thus two druggable targets for ne\ mitotic therapies
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Diallo, Alghassimou. "Identification d’une nouvelle fonction de la protéine kinase Aurora-A." Thesis, Rennes 1, 2013. http://www.theses.fr/2013REN1S111/document.

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Les protéines kinases « Aurora » sont des régulatrices clés du cycle cellulaire. Alors que l'activité de Aurora-A est requise en début de la mitose, Aurora-B et -C sont nécessaires pour la fin de mitose. Toute perturbation de leur activité peut conduire au processus de tumorisation. Plus spécifiquement, Aurora-A se comporte à la fois comme oncogène et suppresseur de tumeur. Par conséquent, la connaissance du rôle de Aurora-A durant cycle cellulaire est essentielle. Toutefois, peu d'études ont exploré, jusque là, le rôle de Aurora-A dans les phases tardives de la mitose. En fait, l'inhibition de Aurora-A conduit à l'arrêt du cycle rendant impossible de voir ce qui se passe au delà de la transition métaphase/anaphase. Néanmoins, en combinant le couple génétique chimique et inhibiteur spécifique, j'ai pu identifier une nouvelle fonction de la kinase Aurora-A liée au checkpoint (SAC). En effet, mes résultats montrent que l'inhibition de l'activité de Aurora-A induit un défaut de congression et une chute de l'index mitotique. Ce résultat paradoxal suggère un défaut du SAC. J'ai donc pu montré que cette inhibition outrepassait le SAC en perturbant la localisation aux kinétochores de Mad2 et BubR1. Cependant, ma tentative pour sauver le phénotype du SAC par le mutant S19D-P150Glued n'a pas réussi malgré que le mutant S19AP150Glued se soit comporté comme un vrai dominant négatif. Enfin, j'ai pu montré que l'activité de Aurora-A est requise pour maintenir le SAC actif durant la prométaphase
Protein kinases "Aurora " are the key regulators of the cell cycle. While the activity of Aurora-A is required at the beginning of mitosis, Aurora-B and -C are required for the end of mitosis. Any disruption of their activity can lead to process tumorisation. Specifically, Aurora-A acts as both oncogene and tumor suppressor. Therefore, knowledge of the role of Aurora-A is essential for cell cycle. However, few studies have explored so far, the role of Aurora-A in the late stages of mitosis. In fact, inhibition of Aurora-A leads to cell cycle arrest making it impossible to see what happens beyond the transition metaphase / anaphase. However, by combining chemical genetics couple and specific inhibitor, I have identified a new function of Aurora-A kinase -related checkpoint (SAC). Indeed, my results show that inhibition of the activity of Aurora-A induces a congression defect and the mitotic index decrease. This paradoxical result suggests a defect in the SAC. So I have shown that this inhibition was beyond the SAC disrupting kinetochore localization of Mad2 and BubR1. However, my attempt to rescue the phenotype of the SAC by the S19D-P150Glued mutant failed despite the fact that S19A-P150Glued mutant behaved like a true negative dominant. Finally, I have shown that the activity of Aurora-A is required to maintain the active SAC during prometaphase
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Kotwaliwale, Chitra V. "Regulation and functions of the Ipl1/aurora protein kinase /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/5081.

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Noujaim, Michael. "The role of microtubules in Aurora-B's kinase activity." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=107846.

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Cell division is the process by which a single cell divides into two daughter cells. Each of these two daughter cells must inherit one complete copy of the genome. If not, cancer or cell-death occurs. Not surprisingly, then, life has evolved mechanisms for ensuring that cell division is error-free. The mechanisms, broadly termed "checkpoints," prevent cell division from occurring if mistakes arise or if each daughter cell were not to inherit one copy of the genome. A major molecule involved in regulating the cell division checkpoint is called Aurora-B. Aurora-B can be thought of as a police officer--Aurora-B stops the cell division process whenever mistakes arise and corrects them before allowing cell division to continue. Unfortunately, if Aurora-B itself becomes faulty or error-prone, the police officer is off-duty, and a greater number of errors occur during cell division. For this reason, Aurora-B is commonly found to be aberrant in tumor cells. Consequently, Aurora-B has recently emerged as a main target for a vast range of novel anti-cancer drugs. In order to divide the genome properly, the cell builds a special mechanical scaffold, reminiscent of the scaffolds at construction sites, called the mitotic spindle. The building blocks of this scaffold are called microtubules. Microtubules are also a target of anti-cancer therapies. Aurora-B interacts with these microtubules in order to perform its role properly. Although significant, this interaction remains elusive for the most part. Here we provide experimental evidence for the importance of these interactions at the spindle midzone during anaphase. Using in vitro kinase assays we show that microtubules sequester Aurora-B's activity to ensure the efficiency with which crucial microtubule-associated substrates are phosphorylated at the spindle midzone. Thus, allowing the unhindered progression of anaphase and the completion of cytokinesis.
La division cellulaire est le processus par lequel une cellule se divise en deux cellules filles. Chacune de ces cellules filles doivent hériter d'une copie complète du génome. Sinon, cela mène à la mort cellulaire ou au cancer. Ainsi, il n'est pas surprenant que la vie a fait évoluer des mécanismes pour s'assurer que la division cellulaire est dénuée d'erreurs. Ces mécanismes, appelés « points de contrôle », empêchent la division cellulaire de se produire si des erreurs apparaissent ou si chaque cellule fille n'a pas hérité d'une copie complète du génome. Une molécule exerçant un rôle majeur dans la régulation du point de contrôle du cycle cellulaire est appelée Aurora-B. Son rôle est en quelque sorte analogue à celui d'un officier de police – Aurora-B arrête la division cellulaire dès que des erreurs surviennent et les corrige avant de permettre à la division cellulaire de continuer. Malheureusement, si Aurora-B devient défectueux ou sujet à des erreurs, l'officier de police est hors-service, alors un plus grand nombre d'erreurs peuvent survenir pendant la division cellulaire. Pour cette raison, Aurora-B est fréquemment identifié comme étant aberrant dans les cellules tumorales. Conséquemment, Aurora-B a récemment émergé en tant que cible principale pour une vaste gamme de nouveaux médicaments anti-cancer. Afin de diviser le génome correctement, la cellule construit un échafaudage mécanique spécial, qui rappelle les échafaudages retrouvés dans les chantiers de construction, qu'on appelle le fuseau mitotique. Les morceaux constituant cet échafaudage sont appelés microtubules. Les microtubules sont aussi une cible de certaines thérapies anti-cancer. Aurora-B interagit avec ces microtubules afin d'exécuter son rôle correctement. Malgré le caractère significatif de cette interaction, elle demeure nébuleuse en bonne partie. Nous fournissons donc ici des preuves expérimentales de l'importance de ces interactions dans la zone médiane du fuseau pendant l'anaphase. En utilisant des essais kinase in vitro, nous montrons que les microtubules séquestrent l'activité d'Aurora-B afin d'assurer l'efficacité avec laquelle les substrats associés aux microtubules sont phosphorylés dans la zone médiane du fuseau. Ainsi, cela permet une progression sans entrave de l'anaphase et la fin de la cytocinèse.
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Janecek, Matej. "Inhibiting the interactions between Aurora kinase A and TPX2." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708828.

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He, Lili. "Molecular Mechanism of Aurora-A Kinase in Human Oncogenesis." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002582.

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Books on the topic "Aurora Kinase A"

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Gabriella, Matta, Romero Graciela trl, and Iboix Estudi, eds. Aurora: La fiesta perfecta. México, D.F: Planeta Mexicana, 2012.

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Gonçalves, Serafim João Carlos, and Carvalho, José Adriano Moreira de Freitas, eds. A aurora da quinta monarquia (1604-1605). Porto: Edições Afrontamento, 2011.

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Martin, Marie-Madeleine. Les Français, auront-ils un roi espagnol. 2nd ed. Paris: F.-X. de Guibert, 2000.

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Pérez de Castro, Ignacio, Mar Carmena, Claude Prigent, and David M. Glover, eds. Aurora Kinases: Classical Mitotic Roles, Non-canonical Functions and Translational Views. Frontiers Media SA, 2017. http://dx.doi.org/10.3389/978-2-88945-257-6.

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Twain, Mark. Las Aventuras De Tom Sawyer / the Adventures of Tom Sawyer (Clasicos Auriga). Fernandez USA Pub Co, 1994.

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Book chapters on the topic "Aurora Kinase A"

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Li, Sara Antonia, Luke K. T. Lam, Nayaz Ahmed, Adrianne E. Hontz, and Jonathan J. Li. "Estrogen-Induced Breast Oncogenesis: Modulation by an Aurora Kinase Inhibitor." In Hormonal Carcinogenesis V, 213–20. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-69080-3_20.

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Heron, Nicola. "From Discovery to Clinic: Aurora Kinase Inhibitors as Novel Treatments for Cancer." In Protein Kinases as Drug Targets, 195–228. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527633470.ch7.

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Kelly, Kevin R., Ciara L. Freeman, and Francis J. Giles. "The Clinical Development of Aurora Kinase Inhibitors in Acute Myeloid Leukemia." In Targeted Therapy of Acute Myeloid Leukemia, 391–407. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1393-0_20.

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Yang, Kuo-Tai, Yi-Nan Lin, Shu-Kuei Li, and Tang K. Tang. "Studying the Roles of Aurora-C Kinase During Meiosis in Mouse Oocytes." In Methods in Molecular Biology, 189–202. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-191-2_13.

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Sen, Subrata, Hiroshi Katayama, and Kaori Sasai. "Functional Significance of Aurora Kinase A in Centrosome Amplification and Genomic Instability." In Hormonal Carcinogenesis V, 99–108. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-69080-3_9.

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Gontarewicz, Artur, and Tim H. Brümmendorf. "Danusertib (formerly PHA-739358) – A Novel Combined Pan-Aurora Kinases and Third Generation Bcr-Abl Tyrosine Kinase Inhibitor." In Recent Results in Cancer Research, 199–214. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-01222-8_14.

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Reboutier, David, and Claude Prigent. "Aurora Kinases." In Encyclopedia of Signaling Molecules, 483–91. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_81.

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He, Lili, and Jin Q. Cheng. "Aurora Kinases." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_465-2.

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Reboutier, David, and Claude Prigent. "Aurora Kinases." In Encyclopedia of Signaling Molecules, 1–9. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_81-1.

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Sen, Subrata, and Hiroshi Katayama. "Aurora Kinases." In Targeted Therapy of Acute Myeloid Leukemia, 371–89. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1393-0_19.

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Conference papers on the topic "Aurora Kinase A"

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Petersen, William C., Jingbo Liu, and Tobey J. MacDonald. "Abstract 2485: Combined Src and aurora kinase inhibition in medulloblastoma." 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.am2012-2485.

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Noguchi, Kohji, Kazuhiro Katayama, and Yoshikazu Sugimoto. "Abstract B62: AKT3 expression modulates chemosensitivity to aurora kinase inhibitors." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-b62.

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Marinak, Kristina, Anna Kiseleva, Yuriy Loskutov, Matthew Smolkin, and Elena Pugacheva. "Abstract 4863: Aurora-A kinase: a nuclear driver of metastasis." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4863.

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Patel, Disha, Nicolaus Gordon, Katsuyuki Shirai, Arnab Chakravarti, and Kamalakannan Palanichamy. "Abstract 2478: Silencing Aurora Kinase A radio-sensitizes glioma cells." 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.am2011-2478.

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Kollareddy, Madhusudhan, Daniella Zheleva, Petr Dzubak, and Marian Hajduch. "Abstract 633: Tumor cell resistance mechanisms to aurora kinase inhibitors." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-633.

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Kozyreva, Varvara K., Sarah L. McLaughlin, Laura Kelley, and Elena N. Pugacheva. "Abstract B61: HEF1-dependent Aurora A kinase phosphorylation activates HDAC6." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-b61.

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Sinha, A., S. Yoo, T. Sato, R. Kong, A. Patel, H. Watanabe, A. Borczuk, J. Zhu, and C. A. Powell. "Aurora Kinase: Master Regulator of Invasiveness in Early Stage Lung Adenocarcinoma." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2534.

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Mukherjee, Sucheta, Carolyn Tu, and Clay Gustafson. "Abstract 5818: Disrupting the Aurora kinase A interactome in pediatric cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5818.

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Sinha, Abhilasha, Seungyeul Yoo, Hideo Watanabe, Jun Zhu, and Charles A. Powell. "Abstract 814: Aurora kinase: A target modulating invasiveness of lung adenocarcinoma." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-814.

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Toughiri, Raheleh, Achuth Padmanabhan, Xiang Li, and Charles Bieberich. "Abstract 1619: Discovering a new physiological substrate of Aurora-A kinase." 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.am2011-1619.

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Reports on the topic "Aurora Kinase A"

1

Kotwaliwale, Chitra, and Sue Biggins. Regulation and Function of the Ipl1/Aurora Kinase. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada432454.

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Buvelot, Stephanie, and Sue Biggins. Regulation and Functions of the Ipll/Aurora Kinase. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada416064.

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