Dissertationen: „Cyclin-dependent kinases“

1

Kitsios, Georgios. „Characterization of Arabidopsis cyclin dependent kinases“. Thesis, University of East Anglia, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426634.

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2

Miller, Matthew P. Ph D. (Matthew Paul) Massachusetts Institute of Technology. „Meiotic regulation of cyclin-dependent kinases“. Thesis, Massachusetts Institute of Technology, 2013. http://hdl.handle.net/1721.1/79185.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2013.
Cataloged from PDF version of thesis.
Includes bibliographical references.
During meiosis, a single round of DNA replication is followed by two consecutive rounds of nuclear divisions called meiosis I and meiosis II. In meiosis I, homologous chromosomes segregate, while sister chromatids remain together. Determining how this unusual chromosome segregation behavior is established is central to understanding germ cell development. Here we show that preventing microtubule-kinetochore interactions during premeiotic S phase and prophase I is essential for establishing the meiosis I chromosome segregation pattern. Premature interactions of kinetochores with microtubules transform meiosis I into a mitosis-like division by disrupting two key meiosis I events: coorientation of sister kinetochores and protection of centromeric cohesin removal from chromosomes. Furthermore we find that restricting outer kinetochore assembly contributes to preventing premature engagement of microtubules with kinetochores. We propose that inhibition of microtubule-kinetochore interactions during premeiotic S phase and prophase I is central to establishing the unique meiosis I chromosome segregation pattern.
by Matthew P. Miller.
Ph.D.

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3

Gomes, Felipe Campelo. „Analysis of cyclin dependent kinases in Leishmania“. Thesis, University of Glasgow, 2007. http://theses.gla.ac.uk/32/.

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The results obtained from the experiments presented in this study aimed to further explore the role of cyclin dependent kinases and cyclins in the protozoan parasite Leishmania major. Cdks in kinetoplastids, CRKs, are the key regulators that allow cells to progress through different cell cycle phases and promote parasite proliferation during infection. In chapter 3 of this study, the results presented showed that L. major CYCA is capable of activating CRK3 in an in vitro kinase assay using histone H1 as substrate. The CRK3/CYCA active complex was then used to analyse the effect of the phosphorylation at the CRK3 activation threonine using a kinase activating kinase (yeast CAK or Civ-1). Phosphorylated CRK3 activity was compared to non-phosphorylated CRK3 and it was found that the phosphorylation promotes a 5-fold increase in kinase activity of the complex. The accessory protein Cks1 was assayed in vitro with the active CRK3/CYCA complex and it was shown that Cks1 might have an inhibitory effect when histone H1 substrate is used. The IC50 for two different kinase inhibitors (Flavopiridol and Indirubin) was determined for the in vitro CRK3/CYCA complex and compared with the values found for the in vivo purified CRK3. Similar values were obtained suggesting that the in vivo complex is indeed represented by the recombinant complex. In the following chapter 4, yeast Civ-1 purified from E. coli, was used to try to phosphorylate, in a similar manner, the activation of threonine/serine residues from other L. major CRKs. The kinases assessed were CRK1, CRK2, CRK4, CRK6 and CRK7. None of these were phosphorylated by Civ-1 suggesting that the only CRK under this type of regulation is CRK3. L. major CRK1-4 and CRK6-8 were tested in kinase assays by mixing under described conditions with L. major CYC9 and kinase activities towards three different substrates were assessed. L. major CYC9 was not able to activate the above kinases and the kinase subunit that interacts with this cyclin could not be identified. In chapter 5, the L. major CYCA was used to elucidate the characteristics of this cyclin in vivo. A gene disruption strategy aimed to replace the two genomic alleles of this protein gene by homologous recombination. Plasmids were developed with flanking regions of this gene placed in association with two different drug resistance genes, one for each of the allele’s disruption. These constructs were not able to produce the first allele knock out suggesting that not only this gene might be essential but the levels of expression may also be important. Tagging L. major CYCA was also attempted in vivo using two different strategies (i.e. two different tagging systems). The first tag employed was the TAP tag syste. Although drug resistant transfected cell lines were obtained, no tag detection could be observed by western blot using different tag-specific antibodies (α-protein-A and α-calmodulin antibodies). The second tag employed was HA, the 9-amino acid sequence YPYDVPDYA, derived from the human influenza hemagglutinin (HA) protein. Plasmids that contained C and N-terminal HA tagged L. major CYCA were used to transfect WT cells and cells extracts of resistant cell lines analysed by western blot. Both C and N-terminal HA tagged CYCA were detected by the α-HA antibody. Following the confirmation of the presence of the tagged CYCA in the cell extracts an affinity purification using an HA affinity matrix was attempted and the matrix binding material was used in in vitro kinase assays. The presence of kinase activity towards Histone H1 confirmed that CYCA was being succesfully immunoprecipitated in complex with a kinase partner. The identity of the co-eluted CRK could be confirmed using specific α-CRK3 antibody that detected CRK3 in the eluted material.

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4

Secombe, Julie. „Identification of novel G1 to S phase regulators in Drosophila /“. Title page, contents and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phs4448.pdf.

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5

Crack, Donna. „Analysis of the function of Drosophila cyclin E isoforms and identification of interactors“. Title page, table of contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09phc8837.pdf.

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"August 2002." Bibliography: p. 157-169. Analysis of the expression of Drosophilia cyclin EII through development show that it was present during larval development and oogenesis, implying a role for DmcycEII outside of early embyogenesis. Ectopic expression analyses using full-length DmcycE proteins as well as N- and C-terminal deletions of DmcycEI, revealed that DmcycEII and N-terminal deletions were able to drive all G1 cells within the morphogenetic furrow of the eye imaginal disc into S phase, while a C-terminal deletion of DmcycEI could not. These results show the DmcycEII is more potent than DmcycEI in driving cells into S phase and that the N-terminal region of DmcycEI contains a negative regulatory domean., suggesting that an inhibitor is present in the posterior morphogenetic furrow that binds to DmcycEI N-terminus and inhibits DmcycEI function. To identify the DmcycEI specific inhibitor, genetic interaction and yeast-2 hybrid screens were undertaken, and an enhancer CG7394, encoding a MAGUK homologue was identified for further study.

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6

Dixon-Clarke, Sarah. „Structure and inhibition of novel cyclin-dependent kinases“. Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:3c6955c9-469a-4f4b-9577-309ccb57b742.

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Protein phosphorylation by members of the cyclin-dependent kinase (CDK) family determines the cell cycle and regulates gene transcription. CDK12 and CDK16 are relatively poorly characterised family members containing atypical domain extensions and represent novel targets for structural studies, as well as cancer drug discovery. In this thesis, I developed protocols to express and purify the human CDK12 kinase domain in complex with its obligate partner, CycK. I solved three distinct crystal structures of the complex providing insights into the structural mechanisms determining CycK assembly and kinase activation. These structures revealed a C-terminal kinase extension that folded flexibly across the active site of CDK12 to potentially gate the binding of the substrate ATP. My structures also identified Cys1039 in the C-terminal extension as the binding site for the first selective covalent inhibitor of CDK12, which has enormous potential as a pharmacological probe to investigate the functions of CDK12 in the DNA damage response and cancer. I also identified rebastinib and dabrafenib as potent, clinically-relevant inhibitors of CDK16 and solved a co-crystal structure that defined the extended type II binding mode of rebastinib. Preliminary trials using these relatively non-selective compounds to inhibit CDK16 in melanoma and medulloblastoma cancer cell lines revealed rebastinib as the more efficacious drug causing loss of cell proliferation in the 1-2 micromolar range. Use of the co-crystal structure to design more selective derivatives would be advantageous to further explore the specific role of CDK16. Finally, I identified a D-type viral cyclin from Kaposi's sarcoma-associated herpesvirus that could bind to the CDK16 kinase domain and interfere with its functional complex with human CycY causing loss of CDK16 activity. These studies provide novel insights into the structural and regulatory mechanisms of two underexplored CDK family subgroups and establish new opportunities for cancer drug development.

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7

Sallam, Hatem. „Pharmacological and analytical studies of the cyclin dependent kinase inhibitors“. Stockholm, 2009. http://diss.kib.ki.se/2009/978-91-7409-706-1/.

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8

Alexiou, Konstantinos G. „Cyclin-dependent kinases and nuclear functions in Arabidopsis thaliana“. Thesis, University of East Anglia, 2011. https://ueaeprints.uea.ac.uk/34236/.

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9

Henderson, Andrew. „Isosteres of sulfonamide inhibitors of cyclin-dependent kinases (CDKs)“. Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.512187.

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10

Cheng, Kai. „Identification of Pctaire1 as a p35-interacting protein and a novel substrate for Cdk5 /“. View Abstract or Full-Text, 2003. http://library.ust.hk/cgi/db/thesis.pl?BICH%202003%20CHENG.

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Thesis (Ph. D.)--Hong Kong University of Science and Technology, 2003.
Includes bibliographical references (leaves 153-177). Also available in electronic version. Access restricted to campus users.

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11

Fung, Tsz Kan. „The functions and proteolysis of cyclin A and cyclin F during mitosis /“. View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?BICH%202006%20FUNG.

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12

Jämsä, Anne. „In vitro modelling of tau phosphorylating kinases: emphasis on Cdk5 /“. Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-400-6/.

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13

McIntyre, Neil A. „Synthesis of ring-constrained thiazolylpyrimidines : inhibitors of cyclin-dependent kinases /“. St Andrews, 2007. http://hdl.handle.net/10023/353.

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14

Sweeney, Claire. „Cell cycle regulators in the murine testis“. Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364276.

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15

McIntyre, Neil A. „Synthesis of ring-constrained thiazolylpyrimidines : inhibitors of cyclin-dependent kinases“. Thesis, University of St Andrews, 2006. http://hdl.handle.net/10023/353.

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One current approach in the treatment of cancer is the inhibition of cyclin dependent kinase (CDK) enzymes with small molecules. Here the discovery and development of 2-anilino-4-(thiazol-5-yl)pyrimidine CDK inhibitors is described, including details of the design and successful synthesis of novel ring-constrained thiazolylpyrimidines. The structure-activity relationship (SAR) trends exhibited by this constrained thiazolylpyrimidine family of CDK inhibitors are presented and compared with those from an unconstrained series of analogues. One significant finding from this aspect of the project was that ring-constrained thiazolylpyrimidines in general inhibit CDK2-cyclin E with greater potency than the corresponding unconstrained forms. Furthermore, an X-ray crystal structure of 2-methyl-N-[3-nitrophenyl]-4,5-dihydrothiazolo[4,5-h]quinazolin-8-amine, a representative from the constrained thiazolylpyrimidine series, in complex with CDK2-cyclin A is reported; confirming the binding mode within the CDK2 ATP binding pocket. A further assessment of SARs through the synthesis of control compounds and an extended study into the synthesis of N-substituted derivatives is described. The identification of CDK inhibitors that possess a strong selectivity profile across the CDK family is important. For example, the identification of highly CDK4-selective inhibitors should enable researchers to study the biological role of this important enzyme and to enable a block of cell division in the G1 phase. Here synthetic attempts to prepare a potentially CDK4 selective inhibitor compound, namely 5-methyl-N8-[4-(piperazin-1-yl)phenyl]thiazolo[4,5-h]quinazoline-2,8-diamine, are described. This approach was inspired by SAR data published on a structurally related inhibitor, 8-cyclopentyl-5-methyl-2-[4-(piperazin-1-yl)phenylamino]pyrido[2,3-d]pyrimidin-7(8H)-one.

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16

Ford, Jack Ragnar. „Cyclin dependent kinases and cell cycle control in Trypanosoma brucei“. Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312512.

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17

He, Lisheng. „Characterization of p35, a neuronal activator of Cdk5, as a novel microtubule-associated protein /“. View abstract or full-text, 2007. http://library.ust.hk/cgi/db/thesis.pl?BICH%202007%20HE.

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18

Yata, Keiko. „DNA damage signalling to cyclin dependent kinase inhibition“. Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670112.

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19

Chan, Lu Yan. „Functional characterization of cyclin L in caenorhabditis elegans“. HKBU Institutional Repository, 2018. https://repository.hkbu.edu.hk/etd_oa/517.

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It is well established that cyclin and cyclin-dependent kinase (CDK) form complex that plays a central role in driving cell cycle progression. The fundamental functions of CDK and cyclin are well conserved across eukaryotes. However, gene families encoding the two type of proteins are significantly expanded in multicellular organisms compared with single-cell species. Despite intensive studies on CDK and its associated cyclin in cultured cell lines, especially in cancer cell lines, the partnership between individual CDKs and cyclins remains elusive especially in vivo. Here I present our preliminary results on establishing the molecular function of a well-conserved cyclin L encoded by cyl-1 in C. elegans. Human cyclin L was demonstrated to form a complex with both CDK11 and CDK12, but its association with the latter remains controversial. Despite a possible function in both transcription and pre-mRNA splicing as suggested by in vitro studies or in yeast, the in vivo function of cyclin L has yet been established in any species. To study cyl-1's function in vivo, we generated multiple strains each expressing a chromosomally integrated single-copy transgenes consisting of CYL-1::GFP flanked by its native regulatory sequences using miniMos technique. The transgene demonstrates ubiquitous expression in nuclei across developmental stages and cell types with few exceptions, including maturing oocytes, in which gene activity is known to be shut down, consistent with its function in transcription and splicing. Co-immunoprecipitation followed by mass spectrometry reveals that CYL-1 interacts with both CDK-11 and CDK-12 along with some other uncharacterized factors. Functional validation of these interactions is underway.

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20

Wu, Qian. „Involvement of Cdk5/p35 in EphB2-dependent dendritic spine development /“. View abstract or full-text, 2008. http://library.ust.hk/cgi/db/thesis.pl?BICH%202008%20WUQ.

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21

Fu, Wing Yu. „The functional roles of cyclin-dependent kinase 5 in neural development /“. View Abstract or Full-Text, 2002. http://library.ust.hk/cgi/db/thesis.pl?BICH%202002%20FU.

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Thesis (Ph. D.)--Hong Kong University of Science and Technology, 2002.
Includes bibliographical references (leaves 154-172). Also available in electronic version. Access restricted to campus users.

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22

Marchetti, Francesco. „Structure-activity relationships for alkoxypirimidine inhibitors of cyclin-dependent kinases (CDK’s)“. Thesis, University of Newcastle Upon Tyne, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.556141.

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Cyclin-dependent kinases (CDKs) are a family of serine/threonine protein kinases that play a fundamental role in the regulation of eukaryotic cell-cycle progression, particularly at cell- cycle checkpoints. Cell-cycle alterations result in a loss of checkpoint function, which correlates with increased or aberrant CDK activity in human tumours. CDK inhibitors are therefore recognised to have potential therapeutic effects in the treatment of cancer and other proliferative diseases. This research project centres on the medicinal chemistry of a new class of CDK inhibitors, based on the 2,6-diamino-4-alkoxy- 5-nitrosopyrimidine pharmacophore (77). Previous studies, employing a structure-based inhibitor design approach, have resulted in the identification of 2-arylamino-06- alkylguanines exhibiting potent inhibitory activity against CDK2, and exemplified by NU6102 (31; IC50 = 5 nM). Structure-activity relationship studies revealed that the purine pharmacophore is not a prerequisite for CDK-inhibitory activity. Thus, comparable activity resides in the corresponding pyrimidines, where an intramolecular hydrogen bond between a 5-nitroso substituent and a 6-amino group confers a 'purine-mimetic' structure (164; CDK2/A, IC50 = 1 nM). Guided by results obtained previously for the corresponding 06-alkylguanines, systematic structural modifications have been made at the pyrimidine 2-, 4- and 5- positions, via the development and optimisation of efficient synthetic pathways Replacement of the 5-nitroso substituent of the parent inhibitors (77, 164) by groups that are more acceptable from a toxicological standpoint has been a prominent target of this work. Formyl, ketone and oxime functionalities have been successfully introduced at the pyrimidine 5-position, while different alkoxy and arylamino substituents were introduced at the pyrimidine 4-position and 2-position, respectively, to probe additional potential interactions within the ATP ribose-binding domain and CDK2 specificity pocket. The synthesis and structure-activity relationships for this new series of CDK inhibitors have been investigated, as exemplified by (220) (CDK2/A, IC50 = 49 nM), (239) (CDK2/A, IC50 = 7.4 nM) and (109) (CDK2/A, IC50 = 23.3 μM). These studies have resulted in the identification of novel compounds, such as (225), exhibiting improved potency against CDKs, with sub-nanomolar inhibitory activity versus CDK2/A (IC5o = 0.77 nM) and good cell growth inhibition properties (G150 = 0.57 μM).

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23

Sorrell, David Andrew. „CycD cyclins and cyclin-dependent kinases in tobacco BY-2 cells“. Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624421.

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24

Lindqvist, Arne. „Regulation of CDK dephosphorylation in mitotic entry /“. Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-362-0/.

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25

Li, Zheng. „The mechanisms of ethanol-induced damage to the developing cerebellum effects on the cerebellar granule cells /“. Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=3134.

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Thesis (Ph. D.)--West Virginia University, 2003.
Title from document title page. Document formatted into pages; contains vii, 146 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.

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26

Yu, Yan. „Functional investigation of the neuronal Cdk5 activator p35 in the regulation of actin dynamics /“. View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BICH%202005%20YUY.

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27

Chin, Wing Hong. „Identification of TrkB as a p35 interacting protein and a Cdk5 substrate /“. View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BICH%202005%20CHIN.

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28

Ng, Kung Yau. „ANKRA2 interacts with p35 and is a substrate for Cdk5/p35 /“. View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?BICH%202006%20NG.

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29

Hou, Zhibo. „Function and regulation of the neuronal Cdk5/p35 kinase in the control of protein translation /“. View abstract or full-text, 2007. http://library.ust.hk/cgi/db/thesis.pl?BICH%202007%20HOU.

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30

Kim, Sungwon. „Evaluation of the chicken cyclin-dependent kinase inhibitor 1B, p27(Kip1) in MDV-induced transformation“. Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 124 p, 2007. http://proquest.umi.com/pqdweb?did=1338885891&sid=13&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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31

Chow, Jeremy Pak Hong. „Inhibitory phosphorylation of cyclin-dependent kinases in normal cell cycle and checkpoints /“. View Abstract or Full-Text, 2003. http://library.ust.hk/cgi/db/thesis.pl?BICH%202003%20CHOW.

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Thesis (M. Phil.)--Hong Kong University of Science and Technology, 2003.
Includes bibliographical references (leaves 127-148). Also available in electronic version. Access restricted to campus users.

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32

Dante, Ricardo Augusto. „Characterization of cyclin-dependent kinases and their expression in developing maize endosperm“. Diss., Tucson, Arizona : University of Arizona, 2005. http://etd.library.arizona.edu/etd/GetFileServlet?file=file:///data1/pdf/etd/azu%5Fetd%5F1040%5F1%5Fm.pdf&type=application/pdf.

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33

Pratt, D. J. „On the inhibition of cyclin-dependent kinases : aspects of potency and selectivity“. Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418647.

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34

Puyol, Marta. „Cell cycle and cancer : the role of cyclin dependent kinases in tumourigenesis“. Thesis, Kingston University, 2009. http://eprints.kingston.ac.uk/20409/.

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Most human cancers carry mutations in cell cycle regulators that result in deregulated Cdk activity, which can either be amplification of the cyclins, elimination of the Cdk inhibitors or mutations in the Cdks. These modifications have a high prognostic value. Cdk2 activity has been shown to be upregulated in different kind of tumours (mammary and prostate carcinomas, and lymphomas) due to the mutation of its regulators, p27KiP1 and cyc/in E; and this alteration has a high prognostic value. Moreover, an insensible INK4 point mutation in Cdk4 has been described in human melanomas. To evaluate the importance of Cdks in neoplastic development, the loci encoding Cdk4, Cdk6 and Cdk2 were ablated to study the effect of Cdk deficiency in tumour development. To this end, the corresponding Cdk knock out mice were crossed with the K_Ras+/LSLG12V;RERertert strain that carries an endogenous K-Ras oncogene whose expression is dependent on Cre-mediated recombination. Postnatal expression of this oncogene leads to the development of lung adenomas and adenocarcinomas. Primary MEFs derived from K- Ras+ILSLG12V;RERrrtlert embryos lacking either Cdk4, Cdk6 or Cdk2 displayed decreased proliferation in culture and prevented the growth in low serum condition. However, no obvious differences were detected in immortal MEFs regardless of the missing Cdk.

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35

Hashemi, Jamileh. „Germline CDKN2A/ARF alterations in human melanoma /“. Stockholm : Karolinska institutet, 2002. http://diss.kib.ki.se/2002/91-7349-148-9.

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36

Larochelle, Stéphane. „Isolation and characterization of a cyclin-dependent kinase-activating kinase in Drosophila melanogaster“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0002/NQ44487.pdf.

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37

Tunnah, Paul Robert. „Crystallographic studies on control of cellular processes by phosphorylation“. Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365412.

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38

Noton, Elizabeth Anne. „The regulation of pre-replicative complex formation in the budding yeast cell cycle“. Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342284.

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39

Xu, Pei. „Cdk5 activity is required for BDNF-stimulated neuronal survival and synaptic plasticity /“. View abstract or full-text, 2008. http://library.ust.hk/cgi/db/thesis.pl?BICH%202008%20XU.

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40

Fong, Ka Wing. „Functional characterization of a novel protein, CDK5RAP2, in microtubule organization and regulation /“. View abstract or full-text, 2008. http://library.ust.hk/cgi/db/thesis.pl?BICH%202008%20FONG.

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41

Parry, David Alun. „Biochemical and functional analyses of p16INK4a, an inhibitor of cyclin D-dependent kinases“. Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243499.

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42

Grant, Sharon. „The design and synthesis of novel purine based inhibitors of cyclin-dependent kinases“. Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310023.

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43

Ma, Hoi Tang. „The functions of cyclin A in DNA re-replication and cell viability /“. View abstract or full-text, 2008. http://library.ust.hk/cgi/db/thesis.pl?BICH%202008%20MA.

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44

林秀華 und Sau-wah Selma Lin. „Modulation of cyclin expression by over-expression of the forkhead boxtranscription factor FoxM1“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31224817.

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45

唐思慧 und See-wai Cindy Tong. „Over-expression of the forkhead box transcription factor foxM1 activates expression of the cyclin-dependent kinase inhibitorp16INK4a“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31970795.

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46

Ching, Chi-yun Johannes, und 程子忻. „Transcriptional regulation of p16INK4a expression by the forkhead box transcription factor FOXM1“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29466192.

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47

Mak, Wing-yan Grace, und 麥詠恩. „Functional characterization of CDK5RAP3 in hepatocellular carcinoma and neuronal differentiation“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45151982.

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48

Wu, Yih-Yiing. „Response of skin to noxious stimuli : studies using in situ hybridisation“. Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263124.

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Tong, See-wai Cindy. „Over-expression of the forkhead box transcription factor foxM1 activates expression of the cyclin-dependent kinase inhibitor p16INK4a“. Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2517647x.

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Lo, Kin Yip. „Regulators of neurotrophin-mediated Trk signaling : SLAM-associated protein (SAP) and cyclin-dependent kinase 5 (Cdk5) /“. View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BICH%202005%20LO.

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Dissertationen zum Thema „Cyclin-dependent kinases“

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