Дисертації з теми "CDK17"
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Dust, Sofia [Verfasser]. "Biochemical characterization, regulation, and inhibition of human transcription kinases CDK12 and CDK13 and human cell cycle-related kinase CDK14 / Sofia Dust." Bonn : Universitäts- und Landesbibliothek Bonn, 2019. http://d-nb.info/1223538028/34.
Повний текст джерелаLianga, Noel. "Cdk1 Regulates Anaphase Onset." Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31860.
Повний текст джерелаChun, Stella Soyoung. "Identification and validation of CDK13 interacting proteins." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/43130.
Повний текст джерелаMoreira, Juliana. "Expressão e purificação da quinase dependente de ciclina 13 humana em sistema bacteriano." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/75/75133/tde-28082014-135313/.
Повний текст джерелаThe cyclin-dependent kinases are proteins that can be classified by their function in the cell cycle or transcriptional control. They are activated in particular steps of the cell cycle depending on their phosphorylation degree, cyclin binding and inhibitory proteins. They act phosphorylating other proteins involved in the cell cycle and transcriptional control, influencing in their activities, ensuring that each step of the cell cycle occur in an ordered sequence. The CDK13 is one of the cyclin-dependent kinases family member, it can bind to L or K cyclins, regulates the alternative splicing and interact with HIV Tat protein, acting as a possible restriction factor, its overexpression decreases the production of some viral proteins, and suppresses the virus production. The DNA corresponding to CDK13 is replicated in cancer cells, mainly of hepatic and colon rectal types; therefore it is a target for inhibitors for cancer therapy. In order to contribute for the studies of this protein, the goal of the project is to express it using methods of recombinant DNA technology. The DNA sequence corresponding to CDK13 was amplified by polymerase chain reaction, after its purification, it was inserted to pCR-Blunt vector and cloned into E. coli DH5α competent cells. However, the DNA wasn\'t released by the BamHI and NdeI restriction enzymes. The Rosetta(DE3) cells transformed with a synthetic plasmid pET28a::CDK13 and grown in auto-induction media expressed the CDK13. After cell lysis and purification by Ni2+ affinity colum, the protein was identified by Western Blot. However, the Rosetta(DE3) cells transformed with the modified synthetic plasmid (that comprehends the DNA region which expresses the binding pocket region) induced in LB media, expressed the CDK13. Yet, it wasn\'t possible to purify the protein in the Ni2+ affinity column.
Krämer, Thomas. "Gastrointestinale Stromatumoren (GIST) : CD117-Expression und klinischer Verlauf /." Würzburg, 2007. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253020.
Повний текст джерелаDixon-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.
Повний текст джерелаBondke, Alexander. "Design and synthesis of selective CDK7 inhibitors." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/43965.
Повний текст джерелаKamkar, Fatemeh. "Pftaire1 (Cyclin Dependent Kinase14): Role and Function in Axonal Outgrowth During the development of the CNS." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32860.
Повний текст джерелаDubbury, Sara Jane. "Cdk12 regulates DNA repair Genes by suppressing intronic polyadenylation." Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/115596.
Повний текст джерелаThis electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis. Vita.
Includes bibliographical references.
During transcription, cyclin-dependent kinases (CDKs) dynamically phosphorylate the C-terminal domain (CTD) of RNA Polymerase II (RNAPII) to recruit factors that coordinate transcription and mRNA biogenesis. Cdk12 phosphorylates Serine 2 (Ser2) of the RNAPII CTD, a modification associated with the regulation of transcription elongation, splicing, and cleavage/polyadenylation. Unlike other transcriptional CDKs that regulate most expressed genes, Cdk12 depletion abrogates the expression of homologous recombination (HR) genes relatively specifically, suppressing the HR DNA damage repair pathway and sensitizing cells to genotoxic stresses that cause replication fork collapse, such as Parp1 inhibitors. The proposed role for Cdk12 in regulating HR is clinically significant for two reasons. First, Cdk12 loss-of-function mutations populate high-grade serous ovarian carcinoma and castration-resistant prostate tumors raising the possibility that Cdk12 mutational status may predict the effectiveness of chemotherapeutics that target HR-deficient tumors. Second, readily available small molecule inhibitors of Cdk12 induce sensitization of HR-competent tumors to Parp1 inhibitors in vivo raising the possibility that inhibitors against Cdk12 could be used as chemotherapeutics. Despite this growing clinical interest, the mechanism behind Cdk12's regulation of HR genes remains unknown. Here we show that Cdk12 suppresses intronic polyadenylation (IPA) and that this mechanism explains the exquisite sensitivity of HR genes to Cdk12 loss. We find that Cdk12 globally enhances transcription elongation rate to kinetically suppress IPA events. Many HR genes harbor multiple IPA sites per gene, and the cumulative effect of these sites accounts for the increased sensitivity of HR genes to Cdk12. Finally, we find evidence that Cdk12 LOF mutations and deletions cause upregulation of IPA sites in HR genes in human tumors. Our results define the mechanism by which Cdk12 regulates transcription, mRNA biogenesis, and the HR pathway. This work clarifies the biological function of CDK12 and underscores its potential both as a chemotherapeutic target and as a tumor biomarker.
by Sara Jane Dubbury.
Ph. D.
Maino, Marcelo Marafon. "Expressão imunoistoquímica de CD117 no carcinoma epidermóide de esôfago." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2008. http://hdl.handle.net/10183/53132.
Повний текст джерелаAim: To investigate the CD117 expression in specimens of patients with squamous cell carcinoma of the esophagus (SCCE). Methods: A pilot study was performed for CD177 immunoreactivity, using a monoclonal antibody against CD117 (DAKO), on 27 esophageal squamous cell carcinoma specimens from patients who underwent surgical resection at the Hospital de Clínicas de Porto Alegre University Hospital, Faculty of Medicine, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil. As a control group, specimens of esophageal mucosa obtained from 10 healthy subjects were also studied. Results: Twenty-one (78%) males and six (12%) females with median (sd) age of 58 (8) years, ranging from 36 to 77 years. Most of the patients were of TNM stage IIb or III and mean overall survival was 21 (2 to 72) months. Cytoplasmic membrane CD117 immunoreactivity was demonstrated in only 4 (15%) out of 27 tumors and in none of the controls (0%). Conclusions: These results suggest that the decreased expression of CD117 may be due to lack of control of the cell cycle in SCCE. Additional studies are needed to better define the role of the CD117 in such tumors.
Büntemeyer, Tjark-Ole [Verfasser]. "Funktionelle Charakterisierung von CDK11 im Nierenzellkarzinom / Tjark-Ole Büntemeyer." Mainz : Universitätsbibliothek Mainz, 2020. http://d-nb.info/1214326390/34.
Повний текст джерелаMeschini, Elisa. "Purine-based dual inhibitors of CDK2 and CDK7." Thesis, University of Newcastle Upon Tyne, 2011. http://hdl.handle.net/10443/1363.
Повний текст джерелаChan, Wai-man Vivian. "Functional characterization of liver intestine-cadherin (CDH17) in hepatocellular carcinoma." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B37424671.
Повний текст джерелаChan, Wai-man Vivian, and 陳慧雯. "Functional characterization of liver intestine-cadherin (CDH17) in hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B38891116.
Повний текст джерелаAldridge, Roland Christopher Lochore. "Investigating the influence of CDK11 in developmental and cancer phenotypes." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31527.
Повний текст джерелаSantos, Níkolas Paparidis Ferreira dos. "Obtenção das quinases dependentes de ciclinas CDK9 e CDK11 humanas utilizando um sistema bacteriano de expressão (E. coli)." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/75/75133/tde-16062015-091524/.
Повний текст джерелаCDK9 and CDK11 are members of the subfamily of transcriptional CDKs and therefore play central roles in the control of the dynamic activity of messenger RNA synthesis and processing by RNA polymerase II. Because of their ability to individually modulate the activity of RNAP II transcription complexes, these kinases are of great importance for the regulation of gene expression in eukaryotic cells. Several cases of deregulation of the transcriptional CDKs have been linked to important human diseases, including various types of cancer and also AIDS (due to the essential role of CDK9 in HIV replication). The objective of this work is to obtain human CDK9 and CDK11 heterologously expressed in Escherichia coli, seeking improved methods to produce these enzymes in quantity and purity suitable for structural studies. A bacterial system offers many practical advantages to protein production, such as technical simplicity, low costs, high levels of expression and high purification yield. However, it has always been an experimental challenge to obtain active human kinases from E. coli, because of the problems commonly associated with heterologous expression. The results presented here demonstrate the possibility of obtaining the enzymatically active human CDK9 by in vitro refolding of the protein expressed as bacterial inclusion bodies, after its solubilization and purification under denaturing conditions. Human CDK11, on the other hand, could only be obtained in a shortened form consisting just of its kinase domain, due to the strong inhibition that an N-terminal stretch exerts on the protein\'s own expression. Therefore, this work provides examples of how it is possible to overcome some of the common adversities of heterologous expression in order to obtain active human CDKs through the bacterial system.
Zeng, Fanli. "Novel Modes of Regulation of Cyclin Dependent Kinase Cdk1." Doctoral thesis, Universitat Autònoma de Barcelona, 2014. http://hdl.handle.net/10803/133357.
Повний текст джерелаCyclin dependent kinases are drive cell division cycle progression in eukaryotic cells. In the model eukaryotic organism Saccharomyces cerevisiae (budding yeast) a single Cyclin Dependent Kinase, Cdk1, is essential and sufficient to drive the cell cycle. Alternately bound to G1, S and G2/M phase cyclins, Cdk1 regulates cell cycle transcriptional programs, chromosome replication and segregation, spindle dynamics, polarized cell growth, morphogenesis, etc. Misregulated CDK activity induces unscheduled proliferation as well as genomic instability. Given its essential function in cell cycle progression, Cdk1 is tightly regulated by binding partners (cyclins, Cks1 and Cyclin dependent Kinase Inhibitors -CKIs) and post-translational modifications. However, many details on Cdk1 regulation remain unknown, such as how G1 or mitotic CDK activities are inhibited in response to challenging conditions. When the cell cycle progression is challenged by genotoxic stress such as DNA replication stress or DNA damage, a surveillance mechanism, the S phase checkpoint is activated to protect the integrity of the genome. In the budding yeast the S phase checkpoint is mediated by the Mec1 kinase (ATR/ATM in humans) and its downstream effector kinase Rad53 (Chk2 in humans). To explore whether the effector kinase Rad53 regulates Cdk1 in response to genotoxic stress, we have been exploring two main avenues: (1) Cdk1 phosphorylation by the S phase checkpoint effector kinase Rad53 and (2) Rad53 dependent regulation of Cdk1 associated factors. With respect to the first question, taking advantage of a Rad53 in vitro kinase assay, we show that recombinant Cdk1 is directly phosphorylated by Rad53. We also proteomically identified two sites of Cdk1 (Ser46, Ser258) phosphorylated by Rad53 in vitro. Cells carrying the non-phosphorylatable Cdk1 allele (Cdk1-2A) display a wee phenotype, compatible with increased/unrestrained CDK activity. Cells carrying the phosphomimetic Cdk1 allele (Cdk1-2E) are elongated and larger in size than wild type cells. Moreover, we also assign and quantify the different phosphorylation forms of Cdk1 in vivo using Phos-tag electrophoresis technology. With respect to the second question, we have proteomically identified proteins associated with Cdk1 in the presence of replication stress in a Rad53 dependent manner. The product of the unknown function gene YPL014W, which we name Cip1 (for Cdk1 Interacting Protein 1), with the highest score, is further studied. Our data shows that Cip1 is a cell cycle regulated protein. In addition, the abundance of Cip1 increases in a Rad53 dependent manner upon DNA replication stress. Overexpression of Cip1 blocks cells in G1 and stabilizes the S-phase-Cdk1 inhibitor Sic1 in vivo. Moreover, Cip1 specifically interacts with G1 phase Cln2-Cdk1 but not with S phase Clb5-Cdk1 or M phase Clb2-Cdk1. Cip1 inhibits Cln2-CDK activity both in vivo and in vitro. Our finding suggests that Cip1 may be a novel CKI of G1 phase CDK activity.
Chen, Jian 1969. "Regulation of CAK activity of Cdk7 in Drosophila melanogaster." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82842.
Повний текст джерелаWoodbury, Erika L. "Regulation of spindle stability by Cdk1 and the APC." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2007. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3261256.
Повний текст джерелаZhu, Rui, and 朱睿. "Liver-intestine cadherin (CDH17) in hepatocellular carcinoma: molecular analysis and clinicalimplications." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43703793.
Повний текст джерелаRafael, Tiago João Reuter Hirst de Sousa. "Proliferação de mastócitos em felinos. Imunomarcação para CD117 e MMP-9." Master's thesis, Universidade Técnica de Lisboa. Faculdade de Medicina Veterinária, 2011. http://hdl.handle.net/10400.5/3607.
Повний текст джерелаExistem, no gato, várias formas de proliferação anormal de mastócitos na pele e noutros tecidos. Embora em alguns casos se trate indubitavelmente de neoplasias, outros há que podem corresponder a reacções de hipersensibilidade. Opostamente ao cão, não há um sistema de classificação nos felinos que permita prever a evolução clínica, embora, normalmente, se tratem de processos benignos. No presente estudo, procurou-se caracterizar vários casos de mastocitoma cutâneo, extracutâneo, mastocitose cutânea e sistémica, para alguns parâmetros epidemiológicos, clínicos e histiopatológicos, comparando estes dados com o que foi observado anteriormente noutros estudos. Recorreu-se a métodos de imunohistoquímica para a proteína de membrana ckit (CD117) e para a metaloproteinase MMP-9 de modo a definir a sua utilidade como indicadores de prognóstico, à semelhança do que foi feito para o cão. Verificaram-se poucas diferenças entre esta amostra e estudos recentes e concluiu-se que o padrão de expressão da marcação para c-kit pode realmente ser indicativo do comportamento biológico destes tumores. Quanto à marcação para a MMP-9 não foi possível tirar idênticas conclusões.
ABSTRACT - FELINE MAST CELL PROLIFERATION. CD117 AND MMP-9 IMMUNOSTAINING - In the cat there are different forms of abnormal mast cell proliferation in the skin and other tissues. Even though some may undoubtedly be viewed as neoplasia, there are others that might as well be considered a mere hypersensitivity reaction. Contrarily to the dog, there is no classification system that helps to predict the outcome of these lesions, even thought they are normally benign. In the present study, some epidemiologic, clinical and histopathologic parameters were characterized for cases of mast cell tumors of the skin, non cutaneous mast cell tumors, systemic mastocytosis and cutaneous mastocytosis, comparing this data to what has been observed in previous studies. Immunohistochemistry methods were also used to identify the membrane protein c-kit and MMP-9 in order to estimate their usefulness as prognostic tools in the same way they are used in dogs. Few differences were seen between this data and recent studies. It was concluded that the expression pattern of c-kit may indeed be linked to the biologic behavior of these tumors. As for the immunostaining of MMP-9, it was not possible to achieve such conclusions.
Heusse, Emmanuelle. "Expression de TAL1 et de CD117 dans les leucémies aigües myéloi͏̈des." Paris 5, 1999. http://www.theses.fr/1999PA05P166.
Повний текст джерелаLink, Patrick. "THE ROLE OF THE MECHANICAL ENVIRONMENT ON CD117+ ENDOTHELIAL CELL ANGIOGENESIS." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5970.
Повний текст джерелаSoni, Deena. "Studies on regulation of mitotic transition by cyclin B1/CDK1." Connect to text online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1099070698.
Повний текст джерела[School of Medicine] Department of Environmental Health Sciences. Includes bibliographical references. Available online via OhioLINK's ETD Center.
Lamas, Cíntia Betite. "Clonagem, expressão e purificação da quinase dependente de ciclina 10 (CDK10) humana." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/75/75133/tde-02022015-112005/.
Повний текст джерелаCyclin-dependent kinases (CDKs) comprise a family of proteins that can be subdivided into two major groups based on their functional role in cell cycle and / or transcriptional control. Over 30 human CDKs have been identifies. CDK10 is a cyclin-dependent kinase protein that belongs to the cdc2-related kinases group. CDK10 is essential in phase G2 / M of the cell cycle, possibly in the progress of this phase, monitoring the complete DNA replication and allowing the cells to pass through this restriction point. This protein is an important determinant of resistance to endocrine therapy for breast cancer. Therefore, it is a potential target for the development of inhibitors, since it is present in cancerous cells. The study of the structure and function of CDK10 must be performed after its cloning, expression and purification. cDNA of CDK10 was amplified by polymerase chain reaction (PCR) and then the product was applied into agarose gel for analysis and purification The cloning vector was obtained, which was cloned into competent cells and sequenced. The obtaining of the recombinant plasmid for expression was due to the insertion of DNA into expression vectors pET28a(+) and pET23a(+) (Novagen). The protein was expressed in competent cells and analyzed by electrophoresis on polyacrylamide gel. Then, the obtained protein was purified by nickel affinity column and ATP affinity column. With the optimization of the results obtained, it will be possible, in the future, to biochemically characterize CDK10 and elucidate its secondary and tertiary structures. The study of CDK10 will contribute to the understanding of its structure-function relationship and its relationship with oncogenes and tumor suppressors, and the structural study for the development of low molecular weight chemical inhibitors that can specifically inhibit CDK10. The structural studies will contribute to the development of chemical inhibitors of low molecular weight that may this and other CDKs.
Zhu, Rui. "Liver-intestine cadherin (CDH17) in hepatocellular carcinoma molecular analysis and clinical implications /." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43703793.
Повний текст джерелаY, Hu Nie Kdam Siriwan Grisurapong. "Cultural factors in male adolescent alcohol use among ede ethnic minority in central highland Vietnam /." Abstract, 2008. http://mulinet3.li.mahidol.ac.th/thesis/2551/cd417/4938061.pdf.
Повний текст джерелаTAGLIALATELA, ANGELO. "CDK12 IS A NOVEL ONCOGENE WITH CLINICAL AND PATHOGENETIC RELEVANCE IN BREAST CANCER." Doctoral thesis, Università degli Studi di Milano, 2013. http://hdl.handle.net/2434/219124.
Повний текст джерелаRen, Ping. "Control of cytokinesis by the mitotic cyclin dependent kinase M-Cdk1." Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/458616.
Повний текст джерелаCytokinesis is the final regulated process in the eukaryotic mitotic cell division cycle. Cells enter cytokinesis once that chromosome segregation is satisfactorily completed. During cytokinesis cells physically separate, giving place to two daughter cells. Defects in the control of cytokinesis result in aneuploidies and genomic instability. A key controller of cytokinesis is the mitotic Cdk1 (M-Cdk1) activity. Our project derives from the observed correlation between the onset of cytokinesis and the termination of M-Cdk1 activity. Complementary to such observation, expression of a hyperstable allele of the mitotic cyclin Clb2, blocks cytokinesis. Thus, the very same activity that pushes cells into mitosis and promotes mitotic entry and anaphase, blocks the occurrence of premature cytokinesis. These observations suggest that one or more proteins, essential to trigger cytokinesis, are inhibited by M-Cdk1 phosphorylation. The identity of such critical M-Cdk1 substrate/s is unknown. Therefore, the goal of this thesis is to gain insight on how M-Cdk1 prevents premature cytokinesis during anaphase in the model eukaryotic organism Saccharomyces cerevisiae. The thesis work reveals that the Mitotic Exit Network is unexpectedly partially activated in the presence of prevailing high M-Cdk1 activity, and drives the release of the Cdc14 phosphatase to the cytoplasm under such conditions.
Soni, Deena V. "Studies on the regulation of mitotic transition by cyclin B1/Cdk1." Case Western Reserve University School of Graduate Studies / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=case1099070698.
Повний текст джерелаMartin, Ina Verena. "Analysis of the structure and function of the S.pombe DNA ligase I protein Cdc17." Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/11101.
Повний текст джерелаPetretti, Clotilde. "Contrôle de la mitose par phosphorylation : une nouvelle fonction pour la protéine kinase CDK11." Rennes 1, 2006. http://www.theses.fr/2006REN1S137.
Повний текст джерелаKroll, Sebastian Herbert Benjamin. "Towards the synthesis of selective CDK7 inhibitors as potential anti-cancer drugs." Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/11657.
Повний текст джерелаKorsisaari, Nina. "Functional analysis of Cdk7-interacting proteins Mat1 and Hint in model organisms." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/mat/bioti/vk/korsisaari/.
Повний текст джерелаGamero, Angel Mauricio Castro. "Efeitos da Inibição Transcricional de Survivina e Cdk1 através do Ácido Tetra-O-Metil Nordihidroguaiarético em Células de Glioblastoma." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/17/17135/tde-29082013-140405/.
Повний текст джерелаGlioblastoma (GBM), one of the most human malignant neoplasia, responds poorly to current treatment modalities, being temozolomide (TMZ) the most used drug in its treatment. TetraO-methyl Nordihydroguaiaretic Acid (M4N) is a global transcriptional repressor of genes dependents of Sp1 transcription factor, such as Survivin and Cdk1. In this study was evaluated the gene expression of Survivin, their spliced-variants and Cdk1 in GBM samples and cell lines. Moreover, it was investigated the effects of M4N combined or not with TMZ and/or radiation on primary cultures and cell lines of GBM. qRT-PCR assays were performed to determine the Survivin-spliced variants and Cdk1 gene mRNA expression in GBM tumor samples and cell lines. Cell proliferation was measured by XTT assay and cell cycle and apoptosis were determined by flow cytometry. Drug combination analyzes using different schedules of administration (simultaneous and sequential) were performed based in ChouTalalay method on GBM cell lines and primary cultures. For clonogenic survival, it was used the doses of 2, 4, and 6 Gy of gamma radiation. All Survivin-spliced variants and Cdk1 gene were expressed in GBM samples (n=16) and cell lines (n=6), except the Survivin-2B variant that was only expressed in GBM cell lines. M4N treatment down regulated the expression of Cdk1, Survivin and Survivin-Ex3 variant, while the Survivin-2B variant was up-regulated. M4N decreased the cell proliferation separately and synergistically with TMZ, moreover it enhanced the radiation effects, mainly when associated with TMZ. M4N also induced apoptotic cell death, decreased mitotic index and arrested the cell cycle mainly in G2/M phase. Our results suggest a potential clinical application of M4N in combination with TMZ and radiation in GB treatment.
Bernis, Cyril. "Caractérisation de nouveaux mécanismes de régulation de la kinase mitotique Cdk1-cycline B." Montpellier 2, 2007. http://www.theses.fr/2007MON20246.
Повний текст джерелаEl, Dika Mohammed. "Régulation de la phase M du cycle cellulaire par CDK1, PP2A et CDC6." Thesis, Rennes 1, 2013. http://www.theses.fr/2013REN1S068.
Повний текст джерелаThe aim of this thesis is to understand better the regulation of the M-phase of the cell cycle. Experiments were done in cell-free extracts of Xenopus laevis one-cell embryos. Firstly, we show that the timing of the M-phase entry is precisely determined by a balance between the activity of CDK1 kinase and okadaic acid sensitive phosphatase, mainly PP2A. Secondly, we show the role of CDC6 protein in regulation of the entry into the first embryonic M-phase. CDC6 inhibits CDK1 and through this action regulates the dynamic of this kinase upon M-phase entry and during M-phase progression. This mechanism discovered during my PhD allows controlling precisely the timing of embryonic cleavage. This control plays a key role in coordinating the cell cycle regulating machinery and the development program of the embryo
Ji, Jun-Yuan. "Functions of Cdk1-cyclin B in regulating the early embryonic mitoses in Drosophila /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/5124.
Повний текст джерелаŠupák, Marek. "Příprava myších monoklonálních protilátek proti cyklin-dependentní kináze 13." Master's thesis, Vysoké učení technické v Brně. Fakulta chemická, 2019. http://www.nusl.cz/ntk/nusl-401868.
Повний текст джерелаCHIAVETTA, Roberta. "Study of the combined effects of CDK1 inhibitors and senolytic drugs for the clearance of aneuploid-senescent cells." Doctoral thesis, Università degli Studi di Palermo, 2022. http://hdl.handle.net/10447/533837.
Повний текст джерелаDávila, André Vieira Peixoto. "Caracterização do gene CDK10 putativo e análise de sua possível atuação nos endociclos de Rhynchosciara americana." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/87/87131/tde-13092011-164136/.
Повний текст джерелаRhynchosciara americana is studied since the 50s decade when gene amplifications was discovered in some regions of its polytene chromosomes. The phenomena of amplification and the formation of these giant chromosomes happens through the endocycles, regulated by an activity oscillation of the complex CyclinE/CDK2. It is known that, in the salivary glands of our model, during it is development, there is the occurrence of these polytene chromosomes, formed since the beginning of the larval life. It was sequenced a message of CDK10, a cyclin depended kinase that shows no participation with the endocycles, as described at the literature. This transcript was fully sequenced by 5\'RACE experiments. Its genomic sequence was partially determined. The relative expression pattern was determined for ovaries, salivary glands and fat body. The CDK10 protein was observed by western blot experiments in the salivary glands. Its cellular location was determined at the ovaries. Results suggest the existence of two isoforms of the RaCDK10 gene at the tissues analyzed.
Simonovic, Sinisa [Verfasser]. "The role of cyclin-dependent kinase 18 (CDK18) in clear cell renal cell carcinoma / Sinisa Simonovic." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2021. http://d-nb.info/1234984814/34.
Повний текст джерелаBonnet, Christine. "Un motif sur la cycline B nécessaire à l'activation de CDK1 chez la levure ?" Paris 6, 2002. http://www.theses.fr/2002PA066509.
Повний текст джерелаChoi, Sung Hugh. "The Role of Dynamic Cdk1 Phosphorylation in Chromosome Segregation in Schizosaccharomyces pombe: A Dissertation." eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/453.
Повний текст джерелаSouza, João Ricardo Malheiros de. "Injeção intracitoplasmática de espermatozoide: métodos de ativação oocitária e desestabilização da membrana espermática." Universidade Federal de Santa Maria, 2017. http://repositorio.ufsm.br/handle/1/11701.
Повний текст джерелаDevelopment of bovine embryos produced by intracytoplasmic sperm injection (ICSI) is low compared to fertilized embryos. Deficient oocyte activation, inappropriate sperm capacitation, and lack of sperm decondensation are thought to be the main constrains affecting ICSI success in cattle. In the present study, activation compounds were tested to establish an effective protocol for activation of bovine oocytes, and then used for oocyte activation after ICSI. The activation approach consisted of exposing in vitro matured oocytes to Ionomycin (ION) following by a specific CDK1 inhibitor (RO-3306), a specific PKC activator (OAG) or both RO+OAG. In the first experiment, the rate of activation (pronuclear (PN) formation), cleavage, development to the blastocyst stage, and number of cells per blastocyst were evaluated after oocyte treatment. The PN rates were higher (P≤0.01) in the groups activated with ION+RO (48.5 %) and ION+RO+OAG (65.6 %) compared to ION (12.3 %) and ION+OAG (9.2 %). There was no significant effect between the RO concentrations tested (5, 7.5 and 10 μM) on oocyte activation. The PN rate was significantly higher (P≤0.01) when oocytes were exposed to RO for 240 min (84.6 %) compared to 60 (53.6 %) and 120 min (60.0 %). However, there was no difference between groups when treatment with RO started at 0, 30 or 60 min after on ION exposure. Cleavage rate was higher in ION+RO (70.2 %) and ION+RO+OAG (62.4 %) groups compared to ION (11.8 %) and ION+OAG (22.8 %). Blastocyst rate was also higher in the ION+RO+OAG (24.1 %) group, but not statistically different between ION+RO (19.7 %) and ION+OAG (9.5 %) groups. There was no development to the blastocyst stage after treatment with ION alone. The average cell number in blastocysts was not statistically different among treatments. In the second experiment, the effect of activation with ION+RO (10 μM for 240 min) was tested after ICSI using control (ICSI-Cont) or treated by electroporation (ICSI-El) sperm. Most oocytes presented a well-developed female PN (66.4%). Male PN formation was higher (P≤0.05) in the ICSI-El (33.3%) compared to the ICSI-Cont (9.4%) group. In conclusion, this study revealed that the specific inhibition of CDK1 after ION treatment is an effective approach to activate bovine oocytes. Male pronuclear formation after ICSI is increased by sperm electroporation, but is lower than female pronuclear formation. This indicates that deficient sperm decondensation and male PN formation rather than deficient oocyte activation is likely the main problem to develop an effective protocol for bovine ICSI.
O desenvolvimento de embriões bovinos produzidos por injeção intracitoplasmática de espermatozóides (ICSI) é baixo em relação aos embriões fertilizados. Deficiência na ativação de oócitos, capacitação inadequada de espermatozóides e falta de descondensação de espermatozóides são os principais transtornos que afetam o sucesso de ICSI em bovinos. No presente trabalho, foram testados métodos de ativação com o intuito de estabelecer um protocolo efetivo para a ativação de oócitos bovinos após a ICSI. Para isso, um inibidor específico de CDK1 (RO-3306) e um ativador específico de PKC (OAG) foram utilizados após a incubação com Ionomicina (ION) para avaliar a retomada da meiose em oócitos bovinos. Além disso, a incubação em meio Fert durante 6 h e a eletroporação (El) de espermatozoides previamente a ICSI foram testadas para verificar o efeito sobre a descondensação do espermatozoide e formação do pró-núcleo (PN) masculino. Inicialmente oócitos bovinos foram incubados, com diferentes concentrações e períodos de exposição aos tratamentos. Foram avaliados conforme a taxa de ativação oocitária (formação de PN), clivagem, desenvolvimento a blastocisto e número de células nos embriões que se desenvolveram a blastocisto. As taxas de PN foram maiores (P≤0,01) nos grupos ativados com ION+RO (48,5 %) e ION+RO+OAG (65,6 %) comparado com ION (12,3 %) e ION+OAG (9,2 %). Não houve efeito significativo entre as concentrações 5,0, 7,5 e 10,0 μM de RO sobre a taxa de ativação. A taxa de ativação foi significativamente maior (P≤0,01) em oócitos tratados com RO por 240 min (84,6 %) comparado a 60 (53,6 %) e 120 min (60,0%). No entanto, não houve diferença significativa na taxa de ativação quando o tratamento com RO foi iniciado a 0, 30 ou 60 minutos após a incubação com ION. A taxa de clivagem foi inferior nos grupos ION (11,8 %) e ION+OAG (22,8 %) comparada aos grupos ION+RO (70,2 %) e ION+RO+OAG (62,4 %). A taxa de blastocistos também foi maior no grupo ION+RO+OAG (24,1 %), mas não houve diferença estatística entre os grupos ION+RO (19,7 %) e ION+OAG (9,5 %). Não houve desenvolvimento a blastocisto quando os oócitos foram tratados somente com ION. Não foi detectada diferença estatística entre os tratamentos sobre o número médio de células por blastocistos. No segundo experimento, espermatozoides não tratados (ICSI-Cont) ou tratados por electroporação (ICSI-El) foram microinjetados em oócitos, os quais foram ativados com ION+RO por 240 min e fixados cerca de 15 h após a injeção para determinar a taxa de formação de PNs masculino e feminino (2PN). A maioria dos oócitos apresentaram o PN feminino bem desenvolvido (66,4 %). A formação de 2PN (masculino e feminino) foi maior no grupo ICSI-El (33,3 %) comparado ao grupo ICSI-Cont (9,4 %). Em conclusão, esse estudo demonstrou que a inibição específica da CDK1 após o tratamento com ION promove a ativação de oócitos bovinos. O tratamento de espermatozoides com eletroporação melhora a formação do PN masculino após ICSI, mas a taxa é inferior a formação do PN feminino. Esses resultados indicam que a deficiente descondensação do espermatozoide é o principal limitante para estabelecer um protocolo eficaz para ICSI em bovinos.
Piard, Juliette. "Déficience intellectuelle : identification de nouveaux gènes par une approche multicentrique." Thesis, Bourgogne Franche-Comté, 2018. http://www.theses.fr/2018UBFCE005.
Повний текст джерелаIntellectual disability (ID) impacts 1 to 3% of the general population with an excess of affected males. This condition is characterized by an extreme clinical and genetic heterogeneity making the deciphering of its causes more complex. The technological revolution that took place in the study of the genome over the last two decades has provided a useful tool for identification of new genetic entities. This is particularly true for chromosomal micro-array analysis since early 2000s and for next generation sequencing since 2011. We took advantage of this by identifying the molecular basis of three singular conditions. We applied a structured methodology and created a network of collaborations to define or confirm these new ID syndromes. 1. Whole exome sequencing alongside with array-CGH 2.Identification of a candidate gene sequence alteration in the index case and other affected patients of the family 3.Constitution and study of a replication cohort 4.Biochemical studies and/or animal models in order to support the assumption of causalityBased on this research strategy, we were able to complete the following projects : Discovery of a syndromic form of autosomal recessive ID associated with cervical spine defects due to bi-allelic CDK10 mutations. Identification of an ATAD1-related profound and lethal autosomal recessive encephalopathy with stiffness and distal arthrogryposis. Characterization of a FRMPD4-related X-linked non-syndromic ID
Carrieri, Francesca Anna. "Molecular and biochemical characterisation of phosphorylation-dependent NICD1 turnover : novel roles for CDK1 and CDK2." Thesis, University of Dundee, 2018. https://discovery.dundee.ac.uk/en/studentTheses/ff090523-366c-4fd7-a4f7-964e5bc2b285.
Повний текст джерелаMartens, Adam Arai. "Caracterização do gene CDK7 e análise de sua possível atuação nos endociclos de Rhynchosciara americana." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-26072012-142501/.
Повний текст джерелаCDKs are proteins responsible for activation and progression of cell cycle and also work on the activation and elongation of transcription. Among them, CDK7 acts in both functions, phosphorylating cell cycle CDKs and as a part of general transcription factor TFIIH as its catalytic subunit. From an EST library of salivary gland, constructed with mRNAs present during the period when the beginning of the last polyteny replicative cycle occurs, it was found only few messages directly related to cell cycle, corresponding to 3.11% of the ESTs. Among them, it was found Cdc2-like and Cdk7; therefore, it was performed the characterisation of Cdk7 gene and the analysis of its role during the larval development of Rhynchosciara americana. Cdk7 gene presents 4 exons, more than in vertebrates. Complete mRNA sequence was obtained via RACE, presenting 1230 bases and an 1020 bases ORF. Expression profiles were determined by RT-PCR and Western blots. Posttranslational modifications were analysed by 2D immunoblots. Its mRNA and protein expression profiles presented variations during cell cycle and between the studied tissues; immunoblots showed the presence of one phosphorylation and possible modifications on the side chain of some amino acids. The study of proteins related to cell cycle in this model is important for a better understanding of uncommon cell cycles in different insect tissues.
Leclerc, Vincent. "Caracterisation fonctionnelle de deux couples cdk-cycline, cdk7-cych et cdk8-cycc, chez la drosophile." Nice, 1999. http://www.theses.fr/1999NICE5330.
Повний текст джерелаDate, Dipali A. "Regulation and Post-translational modifications of Borealin." University of Toledo / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1279127511.
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