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"Auroras"
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The aurora kinases in cell cycle and leukemia
The Aurora kinases, which include Aurora A (AURKA), Aurora B (AURKB) and Aurora C (AURKC), are serine/threonine kinases required for the control of mitosis (AURKA and AURKB) and meiosis (AURKC). Since their discovery nearly 20 years ago, Aurora kinases have been studied extensively in cell and cancer biology. Several early studies found that Aurora kinases are amplified and overexpressed at the transcript and protein level in various malignancies, including several types of leukemia. These discoveries and others provided a rationale for the development of small-molecule inhibitors of Aurora kinases as leukemia therapies. The first generation of Aurora kinase inhibitors did not fare well in clinical trials, owing to poor efficacy and high toxicity. However, the creation of second-generation, highly selective Aurora kinase inhibitors has increased the enthusiasm for targeting these proteins in leukemia. This review will describe the functions of each Aurora kinase, summarize their involvement in leukemia and discuss inhibitor development and efficacy in leukemia clinical trials.
Journal Article
Les Observateurs d'aurores Boréales D'Europe
Souvent observées simultanément depuis différents observatoires d'Europe, les aurores boréales font une réapparition spectaculaire au début du XVIIIe siècle, mobilisant et fédérant une large communauté d'astronomes à l'échelle européenne.Cet ouvrage présente quelques-uns parmi les plus remarquables de ces observateurs dans le contexte humain, institutionnel et philosophique dans lequel ils ont évolué. Il décrit la façon dont ils se sont constitués en réseau en vue d'établir un catalogue le plus exhaustif possible des observations réalisées, permettant l'établissement d'un système raisonné de l'aurore boréale, suivant la méthode expérimentale héritée du siècle précédent.Les observateurs d'aurores boréales d'Europe constitue un voyage rétrospectif à travers le monde savant des Lumières, offrant au lecteur de multiples occasions de rencontre, dans des contextes et suivant des angles variés, avec ces pionniers de la science aurorale, et lui dévoilant par la même occasion le fourmillement d'idées et d'échanges qu'a constitué le développement de la science expérimentale au cours de cette époque charnière de l'évolution de la pensée scientifique.
eBook
Arctic white
\"A young girl looks around her home in the arctic and sees only white, white, white. But one day her grandfather takes her out on a journey across the tundra. And at the end of their cold walk, the dark opens up to show the Northern Lights dancing across the sky--blue, green, and purple.\"-- Provided by publisher.
Book
Allosteric modulation of a human protein kinase with monobodies
Despite being the subject of intense effort and scrutiny, kinases have proven to be consistently challenging targets in inhibitor drug design. A key obstacle has been promiscuity and consequent adverse effects of drugs targeting the ATP binding site. Here we introduce an approach to controlling kinase activity by using monobodies that bind to the highly specific regulatory allosteric pocket of the oncoprotein Aurora A (AurA) kinase, thereby offering the potential for more specific kinase modulators. Strikingly, we identify a series of highly specific monobodies acting either as strong kinase inhibitors or activators via differential recognition of structural motifs in the allosteric pocket. X-ray crystal structures comparing AurA bound to activating vs inhibiting monobodies reveal the atomistic mechanism underlying allosteric modulation. The results reveal 3 major advantages of targeting allosteric vs orthosteric sites: extreme selectivity, ability to inhibit as well as activate, and avoidance of competing with ATP that is present at high concentrations in the cells. We envision that exploiting allosteric networks for inhibition or activation will provide a general, powerful pathway toward rational drug design.
Journal Article
The right track
While traveling to Troll Valley to celebrate the Crystal Ceremony, Anna, Elsa, and their friends help a young troll named Little Rock.
Book
Feedback control of chromosome separation by a midzone Aurora B gradient
Accurate chromosome segregation during mitosis requires the physical separation of sister chromatids before nuclear envelope reassembly (NER). However, how these two processes are coordinated remains unknown. Here, we identified a conserved feedback control mechanism that delays chromosome decondensation and NER in response to incomplete chromosome separation during anaphase. A midzone-associated Aurora B gradient was found to monitor chromosome position along the division axis and to prevent premature chromosome decondensation by retaining Condensin I. PP1/PP2A phosphatases counteracted this gradient and promoted chromosome decondensation and NER. Thus, an Aurora B gradient appears to mediate a surveillance mechanism that prevents chromosome decondensation and NER until effective separation of sister chromatids is achieved. This allows the correction and reintegration of lagging chromosomes in the main nuclei before completion of NER.
Journal Article
The night sky : a Frozen discovery book
\"Anna, Elsa, and friends explore the night sky. Engaging nonfiction text presents the northern lights, the solar system, eclipses, and more\"--Provided by publisher.
Book
Proteomic profiling identifies upregulation of aurora kinases causing resistance to taxane-type chemotherapy in triple negative breast cancer
Nowadays, chemotherapy and immunotherapy remain the major treatment strategies for Triple-Negative Breast Cancer (TNBC). Identifying biomarkers to pre-select and subclassify TNBC patients with distinct chemotherapy responses is essential. In the current study, we performed an unbiased Reverse Phase Protein Array (RPPA) on TNBC cells treated with chemotherapy compounds and found a leading significant increase of phosphor-AURKA/B/C, AURKA, AURKB, and PLK1, which fall into the mitotic kinase group. The increase of AURKA and AURKB protein was majorly due to a post-transcription level regulation, and Paclitaxel treatment induced Aurora Kinases protein phosphorylation on AURKA(T288)/AURKB(T232) sites and their protein stability. In our UAB TNBC cohort, the expression of AURKA and AURKB was significantly higher in TNBC tumors compared to normal adjacent tissues, and AURKB was found to be highly expressed in African American TNBC patients compared to European Americans. Moreover, Aurora Kinases overexpression in TNBC cells renders resistance to Paclitaxel treatment and attenuates the apoptosis effect triggered by chemotherapy treatment, suggesting Aurora Kinases could mediate the chemo-resistance in TNBC. Hence, a combination of Aurora kinase inhibitors or PROTAC degrader and taxane-type chemotherapy significantly enhanced the chemotherapy effect. In summary, we revealed that Aurora Kinases upregulation after treatment with chemotherapy could confer chemotherapy resistance to TNBC cells, and AURKB could serve as preselection markers for stratifying patients’ response to neoadjuvant chemotherapy.
Journal Article