Academic literature on the topic 'Polo kinases'
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Journal articles on the topic "Polo kinases"
Archambault, Vincent, and Mar Carmena. "Polo-like kinase-activating kinases." Cell Cycle 11, no. 8 (April 15, 2012): 1490–95. http://dx.doi.org/10.4161/cc.19724.
Full textvon Schubert, Conrad, and Erich A. Nigg. "Polo-like kinases." Current Biology 23, no. 6 (March 2013): R225—R227. http://dx.doi.org/10.1016/j.cub.2013.01.066.
Full textLee, Kyung S., Tallessyn Z. Grenfell, Frederic R. Yarm, and Raymond L. Erikson. "Mutation of the polo-box disrupts localization and mitotic functions of the mammalian polo kinase Plk." Proceedings of the National Academy of Sciences 95, no. 16 (August 4, 1998): 9301–6. http://dx.doi.org/10.1073/pnas.95.16.9301.
Full textCarmena, Mar, Miguel Ortiz Lombardia, Hiromi Ogawa, and William C. Earnshaw. "Polo kinase regulates the localization and activity of the chromosomal passenger complex in meiosis and mitosis in Drosophila melanogaster." Open Biology 4, no. 11 (November 2014): 140162. http://dx.doi.org/10.1098/rsob.140162.
Full textGaruti, L., M. Roberti, and G. Bottegoni. "Polo-Like Kinases Inhibitors." Current Medicinal Chemistry 19, no. 23 (July 1, 2012): 3937–48. http://dx.doi.org/10.2174/092986712802002455.
Full textSong, Sukgil, Tallessyn Z. Grenfell, Susan Garfield, Raymond L. Erikson, and Kyung S. Lee. "Essential Function of the Polo Box of Cdc5 in Subcellular Localization and Induction of Cytokinetic Structures." Molecular and Cellular Biology 20, no. 1 (January 1, 2000): 286–98. http://dx.doi.org/10.1128/mcb.20.1.286-298.2000.
Full textDai, Wei. "Polo-like kinases, an introduction." Oncogene 24, no. 2 (January 2005): 214–16. http://dx.doi.org/10.1038/sj.onc.1208270.
Full textEckerdt, Frank, Juping Yuan, and Klaus Strebhardt. "Polo-like kinases and oncogenesis." Oncogene 24, no. 2 (January 2005): 267–76. http://dx.doi.org/10.1038/sj.onc.1208273.
Full textBerg, Tobias, Gesine Bug, Oliver G. Ottmann, and Klaus Strebhardt. "Polo-like kinases in AML." Expert Opinion on Investigational Drugs 21, no. 8 (June 6, 2012): 1069–74. http://dx.doi.org/10.1517/13543784.2012.691163.
Full textHagan, Iain M. "The spindle pole body plays a key role in controlling mitotic commitment in the fission yeast Schizosaccharomyces pombe." Biochemical Society Transactions 36, no. 5 (September 19, 2008): 1097–101. http://dx.doi.org/10.1042/bst0361097.
Full textDissertations / Theses on the topic "Polo kinases"
Michel, Daniel R. "Cytoskeletal Architecture and Cell Motility Remain Unperturbed in Mouse Embryonic Fibroblasts from Plk3 Knockout Mice." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1446546516.
Full textPrimot, Aline. "Etude de la régulation de deux protéines kinases : : GSK-3 et polo." Rennes 1, 2001. http://hal.upmc.fr/tel-01117984.
Full textRandall, Catherine Leah. "Genetic dissection of polo-like kinase 1's functions in human cell division /." Access full-text from WCMC, 2009. http://proquest.umi.com/pqdweb?did=1692357351&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.
Full textLong, Thavy. "Caractérisation structurale et régulation de l'activité de deux Polo-like kinases de Schistosoma mansoni : SmPlk1 et SmSak." Lille 2, 2010. http://www.theses.fr/2010LIL2S007.
Full textSchistosomiasis is the most important helminthic infection in term of morbidity and mortality in many developing countries and represents the second parasitic disease to malaria. The evidence for praziquantel (PZQ) resistance, the only drug currently used to treat the disease, led the World Health Organization (WHO) to consider as a priority the finding of novel therapeutic targets. Egg production is responsible for disease transmission by complex trematodes parasites but also for the pathology of schistosomiasis. My PhD work contributes to a better understanding of the complex mechanisms that regulate schistosome reproduction. One particularity of schistosomes is that the sexual development of females requires a permanent contact with the male, allowing a level of fecundity exceptionally high. Therefore, the molecular mechanisms implied in this hyperfecundity are obvious targets for the control of schistosomiasis. Polo kinases are serine/threonine kinases, belonging to the Polo-like kinase family (Plks) whose members are conserved from yeast to mammals. During last years, human Plks have been extensively studied and considered as major targets for cancer because of their dramatic overexpression in proliferating cells and many tumors. In silico researches have led us to the characterization in S. Mansoni, SmPlk1, homologous to human Plk1. SmPlk1 was abundantly transcribed in parasite stages containing germinal cells expected to undergo frequent cell divisions, and particularly in the reproductive organs of adult worms suggesting a potential role of SmPlk1 in division processes. We have shown that SmPlk1 induced resumption of meiosis in oocytes of Xenopus. Moreover, the specific Plk1- inhibitor BI 2536 used in clinical trials, induces morphological aberrations in reproductive organs and inhibits oogenesis and spermatogenesis in paired worms, indicating a role of SmPlk1 in gamete multiplication and differentiation in S. Mansoni parasites and so the possibility that this kinase could be a novel potential target for schistosomiasis treatment. In parallel to this work, we recently identified a second Plk in S. Mansoni, SmSak different for its structure and its functions, and notably its role in the centriole duplication. Moreover, we identified a potential activator of Plk, SmSLK (S. Mansoni Ste-20 like kinase) able to activate specifically SmPlk1 in particular conditions. Indeed, two original mechanisms, one dependent on caspases and the other one dependent on antisense RNA, could regulate the kinase activity of SmSLK and therefore, the activity of SmPlk1
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 textDahmene, Manel. "Caractérisation de la voie de dégradation de l'α-synucléine catalysée par la Polo-Like Kinase 2." Master's thesis, Université Laval, 2018. http://hdl.handle.net/20.500.11794/28320.
Full textParkinson's disease is a chronic neurological disease characterized by the progressive degeneration of the dopaminergic neurons of the substantia nigra pars compacta. A second neuropathological feature of this disease is the accumulation of intracellular aggregates called Lewy bodies. These aggregates are formed by a pre-synaptic protein, α-synuclein (α-syn). This pathological accumulation interferes with the vital metabolic pathways of neurons such as synaptic transmission and mitochondrial activity, leading to cell death. Consequently, promoting the elimination of the toxic forms, reducing the expression of the native form and decreasing the probability of aggregate formation could be a therapeutic strategy of interest for the treatment of Parkinson's disease and other related disorders. Recently, we have described a novel α-syn degradation pathway that is catalyzed by the enzymatic activity of Polo-like kinase 2 (PLK2). However, the cellular mechanism and the identity of the molecules involved are still unknown. So, my work has focused on studying this pathway and its various steps that lead to remove the toxic effect of α-syn. In this thesis we show that, in addition to PLK2, PLK3, another member of the PLK family, is able to phosphorylate α-syn at S129 and induce its elimination. In addition, we declare that this action requires a physical interaction between the 2 proteins (α-syn and PLK2) involving the N-terminal domain and that a poly-ubiquitination step is essential for the autophagic degradation of the α-syn and PLK2 complex. This effect of PLK2 is also observed on mutated forms of α-syn such as α-syn A30P, α-syn A53T and is more pronounced in the case of the α-syn E46K mutant. The characterization of this elimination pathway offers new opportunities for the development of treatments that allow, in a specific and selective manner, the degradation of α-syn and thus the reduction of its toxic forms.
Pearson, John Robert. "Metazoan polo-like kinases : their conservation and function during the specialised cell cycles of oogenesis and early embryogenesis." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620065.
Full textBrassac, Thierry. "Analyse fonctionnelle de la kinase "Polo-like" lors de l'entrée et de la sortie de phase M des ovocytes de Xénope." Montpellier 2, 2000. http://www.theses.fr/2000MON20056.
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 textRenner, Annelies. "Mise au point de tests "preuve de principe" pour l'étude des inhibiteurs de la Plk1 et caractérisation de la Plk1 en tant que cible dans le traitement des leucémies aigües myéloïdes." Toulouse 3, 2008. http://thesesups.ups-tlse.fr/430/.
Full textPolo-like kinase 1, a major regulator of mitosis, is found overexpressed in many cancers and its overexpression correlates with a bad prognosis. Experimentally, the constitutive expression of Plk1 induces transformation of NIH3T3 cells and confer them the ability to initiate new tumours in athymic mice. In addition, Plk1 depletion in cancer cells induces apoptosis, suggesting that Plk1 may be a new pharmacological target in anticancer therapies. The first aim of my thesis was to generate molecular and cellular tools in order to characterize the activity of Plk1 inhibitors, evaluate the implication of Plk1 in different steps of cell division and to find new partners Plk1. We generated inducible cell lines allowing the expression of wild type and mutants' forms (inactivated, overactivated) of Plk1, and the analysis of their impact on growth, proliferation, cell cycle and also on known substrates of Plk1. As expected, the higher the activity of Plk1 is, the best its impact on these biological processes. We have tested on these inducible cell lines several inhibitors of Plk1, and developed an assay allowing a rapid and highly efficient evaluation of the effect of these inhibitors on the Plk1 pathway. The Luminex methodology was used on cell extracts in order to assess the activity of Plk1 on its downstream effectors. This methodology appears to be very efficient to analyse the effects of putative Plk1 inhibitors in cellulo. The second aim of my thesis was to analyse the status and role of Plk1 in a malignant hemopathy, Acute Myeloid Leukemia (AML). AML is a clonal hemopathy characterized by a block in differentiation and by an uncontrolled proliferation of immature leukemic cells. Molecular mechanisms involved in the dysregulation of cell cycle in AML are still poorly understood. We have characterized the expression and the role of Plk1 in AML cell lines and primary cells and analysed the consequences of a specific Plk1 inhibition in this pathology. .
Books on the topic "Polo kinases"
Ullrich, Andrea. Expression der Polo-Like-Kinase 1 und 3 Im Magenkarzinom. Südwestdeutscher Verlag für Hochschulschriften AG & Company KG, 2013.
Find full textBook chapters on the topic "Polo kinases"
Berry, Lynne D., Roy M. Golsteyn, Heidi A. Lane, Kirsten E. Mundt, Lionel Arnaud, and Erich A. Nigg. "The family of polo-like kinases." In Progress in Cell Cycle Research, 107–14. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5873-6_11.
Full textSharma, Nitin, Rajni Vaid, Kamal Dev, and Anuradha Sourirajan. "Polo-Like Kinase (PLK)." In Encyclopedia of Signaling Molecules, 4100–4106. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101760.
Full textSharma, Nitin, Rajni Vaid, Kamal Dev, and Anuradha Sourirajan. "Polo-like Kinase (PLK)." In Encyclopedia of Signaling Molecules, 1–7. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6438-9_101760-1.
Full textWäsch, R., J. Hasskarl, D. Schnerch, and M. Lübbert. "BI_2536 - Targeting the Mitotic Kinase Polo-Like Kinase 1 (Plk1)." In Recent Results in Cancer Research, 215–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-01222-8_15.
Full textReindl, Wolfgang, Klaus Strebhardt, and Thorsten Berg. "A Fluorescence Polarization Assay for the Discovery of Inhibitors of the Polo-Box Domain of Polo-Like Kinase 1." In Methods in Molecular Biology, 69–81. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-337-0_5.
Full textMarcisauskas, R. P., D. J. Karalyte, O. F. Sudziuviene, and I. G. I. Pesliakas. "Use of Triazine Dyes in Purification of T4 Poly-Nucleotide Kinase." In Protein-Dye Interactions: Developments and Applications, 331–36. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-1107-9_33.
Full textYoshihara, Koichiro, Yasuharu Tanaka, Asako Itaya, Tomoya Kamiya, Takashi Hironaka, Takeyoshi Minaga, and Samuel S. Koide. "In Vitro Evidence for Poly(ADP-Ribosyl)ation of DNA Polymerase α-Primase and Phosphorylation of Poly(ADP-Ribose) Synthetase by Protein Kinase C." In ADP-Ribose Transfer Reactions, 39–46. New York, NY: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4615-8507-7_7.
Full textDurkacz, B. W., J. Lunec, H. Grindley, S. Griffin, O. Horne, and A. Simm. "Poly(ADP-ribose) polymerase inhibitors induce murine melanoma cell differentiation by a mechanism independent of alterations in cAMP levels and protein kinase A activity." In ADP-Ribosylation Reactions, 191–94. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4419-8718-1_32.
Full textDube, Divya. "Polo-like kinases: An antimitotic drug target for cancer therapy." In Protein Kinase Inhibitors, 457–77. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-91287-7.00002-8.
Full textLlamazares, Salud, and David M. Glover. "Polo." In The Protein Kinase FactsBook, 273–74. Elsevier, 1995. http://dx.doi.org/10.1016/b978-012324719-3/50084-4.
Full textConference papers on the topic "Polo kinases"
Wei, Iris, Vishal Kothari, Sunita Shankar, Shanker Kalyana-Sundaram, Catherine Grasso, Dan Robinson, Xuhong Cao, Diane Simeone, Arul Chinnaiyan, and Chandan Kumar-Sinha. "Abstract A17: Inhibiting polo-like kinases for the treatment of pancreatic cancer: Targeting kinase outliers for personalized therapy." In Abstracts: AACR Special Conference on Pancreatic Cancer: Progress and Challenges; June 18-21, 2012; Lake Tahoe, NV. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.panca2012-a17.
Full textWard, Alejandra, Gayathri Sivakumar, Caroline Hamm, Sindu Kanjeekal, and John W. Hudson. "Abstract LB-376: Deregulation of promoter methylation of the polo-like kinases in myelodysplastic syndromes (MDS) and other blood neoplasms." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-376.
Full textWard, Alejandra, and John W. Hudson. "Abstract LB-179: The effects of hypoxia and reactive oxygen species on the methylation status of the polo-like kinases." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-179.
Full textChapagai, Danda P., Merissa Baxter, Gurusankar Ramamoorthy, Campbell McInnes, and Michael Wyatt. "Abstract 4712: Selective polo-like kinase 1 PBD inhibitor." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4712.
Full textChapagai, Danda P., Merissa Baxter, Gurusankar Ramamoorthy, Campbell McInnes, and Michael Wyatt. "Abstract 4712: Selective polo-like kinase 1 PBD inhibitor." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4712.
Full textBaxter, Merissa, Sandra Craig, Campbell McInnes, and Michael D. Wyatt. "Abstract 2156: Targeting polo-like kinase 1 with novel inhibitors of the polo-box domain." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2156.
Full textPress, Michael F., Bin Xie, Simon Davenport, Yu Zhou, Neil O’Brien, Michael Palazzolo, Tak Mak, Joan Brugge, and Dennis J. Slamon. "Abstract 2736: Regulation of cytokinesis by polo-like kinase 4." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2736.
Full textChoi, Byeong Hyeok, Kyung S. Lee, and Wei Dai. "Abstract 2048: Phosphorylation and regulation of PTEN by Polo-like kinase 1." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2048.
Full textLi, Zhongkui, Zhe Chang, and Paul J. Chiao. "Abstract 2186: Function and regulation of Polo-like Kinase 3 in human pancreatic cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2186.
Full textLiu, X. Shawn, Bing Song, Bennett D. Elzey, Timothy L. Ratliff, Stephen F. Konieczny, Liang Cheng, and Xiaoqi Liu. "Abstract 233: Polo-like kinase 1 facilitates loss of Pten-induced prostate cancer formation." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-233.
Full textReports on the topic "Polo kinases"
Sessa, Guido, and Gregory Martin. A functional genomics approach to dissect resistance of tomato to bacterial spot disease. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695876.bard.
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