Rozprawy doktorskie na temat „Cell cycle progression”
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Santos, Carlo Steven. "Circadian Control of Cell Cycle Progression". Thesis, Virginia Tech, 2009. http://hdl.handle.net/10919/76987.
Pełny tekst źródłaMaster of Science
Joseph, Alton J. "Regulation of S6KL during cell cycle progression". Thesis, California State University, Long Beach, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=1527714.
Pełny tekst źródłamTOR (Mammalian Target ofRapamycin), PI3K (Phosphatidylinositol3-kinase) and MEK (Mitogen-activated protein kinase/ERK kinase) have been shown to be potent regulators ofS6Kl at G1 phase of the cell cycle. Research has been concentrated at the Gt phase to elucidate mTOR's role in cell growth and proliferation. Limited information is available on the activity ofmTOR, PI3K and ERKl/2 in cell cycle phases other than G1. Since we have observed that S6Kl is active in phases other than G1 our goal was to ascertain ifmTOR, PI3K or ERKl/2 have a role in regulating S6Kl during these cell cycle phases. Using cell cycle analysis and immunoblot analysis we have determined here that mTORand PI3K could play a role in regulating S6Kl at the G1/S transition iQ. the cell cycle but there is also indications that mTOR and PI3K are potentially involved in regulating S6Kl in the phases post-G1/S of the cell cycle, indicating a complex interaction between the kinases used to regulate S6Kl during the cell cycle. ERKl/2 is demonstrated to have limited involvement in the regulation of S6Kl during the cell cycle.
Fredlund, Jan O. "The role of polyanimes in cell cycle progression". Lund : Lund University Dept. of Animal Physiology, 1996. http://catalog.hathitrust.org/api/volumes/oclc/38100686.html.
Pełny tekst źródłaDelorme, Marilyne. "Downregulation of ATRX disrupts cell proliferation and cell cycle progression". Thesis, University of Ottawa (Canada), 2008. http://hdl.handle.net/10393/27627.
Pełny tekst źródłaStewart, Nancy G. "P53 control over cell cycle progression at G2". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ32022.pdf.
Pełny tekst źródłaRathbone, Christopher R. "Mechanisms regulating skeletal muscle satellite cell cycle progression". Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/5866.
Pełny tekst źródłaThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "December 2006" Includes bibliographical references.
Weber, Tom. "Optimal timing of phase resolved cell cycle progression". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2015. http://dx.doi.org/10.18452/17253.
Pełny tekst źródłaSelf-reproduction is one of the distinguishing marks of living organisms. The cell cycle is the underlying process by which self-reproduction is accomplished in single-celled organisms. In multi-cellular organisms, the cell cycle is in addition indispensable for other vital processes, including immune reactions. In this thesis a method is developed that allows to estimate the time it takes for a dividing cells to complete the CC phases. Knowledge of the CC phase durations allows to predict, for example, how fast a population of proliferating cells will grow in size, or how many new cells are born per hour in a given tissue. In Chapter 1 of this thesis, a cell cycle model with delays and variability in the completion times of each phase is developed. Analytical solutions are derived to describe a common experimental technique used for cell cycle analysis, namely pulse labeling with bromodeoxyuridine (BrdU). Comparison with data shows that the model reproduces closely measured cell cycle kinetics, however also reveals that some of the parameter values cannot be identified. This problem is addressed in Chapter 2. In a first approach, the framework of D-optimal experimental designs is employed, in order to choose optimal sampling schemes. In a second approach, the prevailing protocol with a single nucleoside is modified by adding a second nucleoside analog pulse. Both methods are tested and the results suggest that experimental design can significantly improve parameter estimation. In Chapter 3, the model is applied to the germinal center reaction. A substantial influx of cells into the dark zone of germinal centers is predicted. Moreover the wide-held view of rapid proliferation in germinal centers, appears, under this model, as an artifact of cell migration.
Poli, Alessandro <1985>. "New DAG-dependent mechanisms modulate cell cycle progression". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amsdottorato.unibo.it/6739/1/Tesi_Alessandro.Poli..pdf.
Pełny tekst źródłaPoli, Alessandro <1985>. "New DAG-dependent mechanisms modulate cell cycle progression". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amsdottorato.unibo.it/6739/.
Pełny tekst źródłaOuertani, A. "Determinants of cell cycle progression in human mammary epithelial MCF12 cells". Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1362848/.
Pełny tekst źródłaJurczyk, Agata. "Centrosomes in Cytokinesis, Cell Cycle Progression and Ciliogenesis: a Dissertation". eScholarship@UMMS, 2004. https://escholarship.umassmed.edu/gsbs_diss/73.
Pełny tekst źródłaPromwikorn, Waraporn. "Regulation of gene expression and cell cycle progression by cell shape". Thesis, University of Liverpool, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250316.
Pełny tekst źródłaSalinas, Daniel Cirera. "miR-33 regulates cell proliferation, cell cycle progression and liver regeneration". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2013. http://dx.doi.org/10.18452/16721.
Pełny tekst źródłaCholesterol metabolism is tightly regulated at the cellular level and is essential for cellular growth. Cellular imbalances of cholesterol and fatty acid metabolism lead to pathological processes, including atherosclerosis and metabolic syndrome. MicroRNAs (miRNAs), a class of noncoding RNAs, have emerged as critical regulators of gene expression acting predominantly at posttranscriptional level. Recent work from Fernández-Hernando´s group and others has shown that hsa-miR-33a and hsa-miR-33b, miRNAs located within intronic sequences of the sterol regulatory element-binding protein (SREBP-2 and SREBP-1) genes, respectively, regulate cholesterol metabolism in concert with their host genes. Similarly, miR-33 targets key enzymes involved in the regulation of fatty acid oxidation including CROT, CPT1A, HADHB, SIRT6 and AMPKα, likewise, IRS2, an essential component of the insulin- signaling pathway in the liver. This study shows that hsa-miR-33 family members not only regulate genes involved in cholesterol and fatty acid metabolism and insulin signaling, but in addition modulate the expression of genes involved in cell cycle regulation and cell proliferation. Thus, miR-33 inhibited the expression of CDK6 and CCND1, thereby reducing cell proliferation and cell cycle progression. Over-expression of miR-33 induced a significant G1 cell cycle arrest and most importantly, inhibition of miR-33 expression using 2’F/MOE-modified phosphorothioate backbone antisense oligonucleotides improved liver regeneration after partial hepatectomy (PH) in mice, suggesting an important role for miR-33 in regulating hepatocyte proliferation during liver regeneration. Altogether, these data establish that Srebf/miR-33 locus may co-operate to regulate cell proliferation, cell cycle progression and may also be relevant to human liver regeneration.
González, Rubio Christian. "Effects of aneuploidy on growth and cell cycle progression". Thesis, Massachusetts Institute of Technology, 2010. http://hdl.handle.net/1721.1/58291.
Pełny tekst źródłaCataloged from PDF version of thesis.
Includes bibliographical references.
In budding yeast, aneuploidy has a detrimental effect in cell growth and proliferation. The work presented here shows that most aneuploid yeast strains delay cell cycle entry by increasing the critical size for budding and by decreasing the rate of volume accumulation during the G 1 phase of the cell cycle. This increase in the critical size for budding is due to in a delay in CLN2 mRNA accumulation and can be suppressed by supplying cells with high levels of this cyclin. Deletion of the cell cycle entry inhibitor WHI5 only partially suppressed the GI delay of aneuploid cells. These two results combined point to the possibility that aneuploidy might be interfering through a parallel pathway with the activation of the transcription factors Swi4 and Swi6. The growth defect seen in aneuploid cells is not due to gross defects in the translational machinery or lack of nutrients. Instead, yeast cells respond to aneuploidy by altering the translational efficiency of a number of genes. The results presented here indicate that aneuploidy affects entry into the cell cycle in at least two ways. The condition elicits a growth defect during the G 1 phase of the cell cycle and increases the critical size for budding.
by Christian Gonzalez Rubio.
Ph.D.
Sun, Xiaoming. "Ki-67 Regulates Cell Cycle Progression and Heterochromatin Organization". eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/920.
Pełny tekst źródłaSun, Xiaoming. "Ki-67 Regulates Cell Cycle Progression and Heterochromatin Organization". eScholarship@UMMS, 2009. http://escholarship.umassmed.edu/gsbs_diss/920.
Pełny tekst źródłaOsnato, Anna. "Transcriptional networks variations during cell cycle progression in human embryonic stem cells". Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/276271.
Pełny tekst źródłaKittler, Ralf. "Functional genomic analysis of cell cycle progression in human tissue culture cells". Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2006. http://nbn-resolving.de/urn:nbn:de:swb:14-1161253856455-48321.
Pełny tekst źródłaArora, Mansi. "Dynamic chromatin associated ubiquitination with cell cycle progression in human cancer cells". The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1396182036.
Pełny tekst źródłaEscoté, Miró Xavier. "Control of cell cycle progression by the last MAPK Hog1". Doctoral thesis, Universitat Pompeu Fabra, 2005. http://hdl.handle.net/10803/7186.
Pełny tekst źródłaTait, Xavier Alastair Claude. "Investigation of human Pix protein regulation during cell cycle progression". Thesis, University of Leicester, 2012. http://hdl.handle.net/2381/10853.
Pełny tekst źródłaMartufi, Matteo. "Role of Cnot3 in gene regulation and cell cycle progression". Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/24778.
Pełny tekst źródłaLiao, Yongrong. "Role of novel ubiquitin-related factors in cell cycle progression". Thesis, Strasbourg, 2021. http://www.theses.fr/2021STRAJ060.
Pełny tekst źródłaUbiquitylation is a posttranslational modification which plays many important functions in cells. During my PhD study, I focused on two components of the ubiquitin system : the deubiquitinating enzyme (DUB) ubiquitin carboxyl-terminal esterase L3 (UCHL3) and the ubiquitin-binding domain (UBD) protein ubiquitin associated protein 2 like (UBAP2L, also known as NICE4). My studies showed that UCHL3 is necessary for maintaining proper nuclear shape of human cells and chromosome segregation. At the molecular level, UCHL3 physically interacts with and deubiquitylates Aurora B, thereby regulating its localization at the kinetochores and interaction with MCAK. In my second project, I identified a novel function of UBAP2L in the regulation of Fragile X mental retardation syndrome-related proteins (FXRPs) and in the nuclear pore complexes (NPCs) homeostasis, which surprisingly, is independent of UBAP2L ubiquitin-binding. Instead, I found that the arginines within the arginine–glycine–glycine (RGG) domain of UBAP2L are required for the interaction with FXRPs, and mediate the function on FXRPs and nucleoporins (Nups) in early G1 phase
Stern, Bodo. "Control of G1 progression in fission yeast". Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264166.
Pełny tekst źródłaHelton, Eric Scott. "A role for p63 in the regulation of cell cycle progression and cell death". Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. http://www.mhsl.uab.edu/dt/2007p/helton.pdf.
Pełny tekst źródłaWand, Nadina Ivanova. "Variant surface glycoprotein synthesis and cell cycle progression in Trypanosoma brucei". Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:01bbdf34-8cb3-4942-a14d-d6ba3a3e669d.
Pełny tekst źródłaStavropoulou, Vaia. "Role of tripeptidyl peptidase II in cell cycle regulation and tumor progression /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-851-7/.
Pełny tekst źródłaHabela, Christa Whelan. "Progression through the cell cycle is regulated by dynamic chloride dependent changes in cell volumes". Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009r/habela.pdf.
Pełny tekst źródłaTudan, Christopher Richard. "Mechanisms of fostriecin, AGM-1470 and taxol disruption of cell cycle progression and cell activation". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0003/NQ38991.pdf.
Pełny tekst źródłaSatyanarayana, Ande. "Impact of telomere shortening on cell cycle progression and induction of senescence". [S.l. : s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972263616.
Pełny tekst źródłaCheung, Man-sze, i 張敏思. "Investigating the role of FoxM1 in cell cycle progression by inducibleRNA interference". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B30396402.
Pełny tekst źródłaMAGISTRATI, ELISA. "FUNCTIONAL CHARACTERIZATION OF MYOSIN VI IN CENTROSOME BIOLOGY AND CELL CYCLE PROGRESSION". Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/609443.
Pełny tekst źródłaBlosser, Rachel J. "Effects of the anticonvulsant drug Dilantin on cell cycle progression in preimplantation mouse embryos". Virtual Press, 2003. http://liblink.bsu.edu/uhtbin/catkey/1273261.
Pełny tekst źródłaDepartment of Biology
Popov, Nikita. "Expression and activity of Myc network proteins during cell cycle progression and differentiation /". Sundbyberg, 2004. http://diss.kib.ki.se/2004/91-7349-856-4/.
Pełny tekst źródłaPeer, Zada Abdul Ali. "Signaling through CD44 affects cell cycle progression and c-Jun expression in acute myeloid leukemia cells". Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-28659.
Pełny tekst źródłaWatanabe, Naoki. "Hbp1 regulates the timing of neuronal differentiation during cortical development by controlling cell cycle progression". Kyoto University, 2015. http://hdl.handle.net/2433/200496.
Pełny tekst źródłaBUSTI, STEFANO. "Glucose and regulation of cell cycle in saccharomyces cerevisiae: analisys of mutans impaired in sugar uptake mechanisms". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2009. http://hdl.handle.net/10281/7482.
Pełny tekst źródłaSorensin, Troels Seyffart. "Characterisation of DP-1". Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243913.
Pełny tekst źródłaDavies, Rhian Jane. "Analysis of the Schizosaccharomyces pombe DNA structure dependent checkpoint gene rad26". Thesis, University of Sussex, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297959.
Pełny tekst źródłaBarr, Jennifer Yamaoka. "The Justy mutation disrupts the regulation of gene expression and cell cycle progression during B lymphopoiesis". Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/1542.
Pełny tekst źródłaRadeva, Galina. "Overexpression of the integrin-linked kinase (ILK) promotes anchorage-independent cell cycle progression". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0001/MQ45455.pdf.
Pełny tekst źródłaBöhm, Stefanie. "The Cdc48 Shp1 complex mediates cell cycle progression by positive regulation of Glc7". Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-154660.
Pełny tekst źródłaLinke, Christian [Verfasser]. "Identification of novel mechanisms controlling cell cycle progression in S. cerevisae / Christian Linke". Berlin : Freie Universität Berlin, 2013. http://d-nb.info/1036406555/34.
Pełny tekst źródłaZalli, Detina. "Regulation of the human Nek8/NPHP9 protein during cell cycle progression and ciliogenesis". Thesis, University of Leicester, 2012. http://hdl.handle.net/2381/10326.
Pełny tekst źródłaLeone, Marina [Verfasser], i Manfred [Akademischer Betreuer] Frasch. "The role of IQGAP3 in cell cycle progression / Marina Leone. Gutachter: Manfred Frasch". Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2015. http://d-nb.info/1079067639/34.
Pełny tekst źródłaMian, Shahid A. "Tissue transglutaminase and its relationship to cell cycle kinetics, apoptosis and tumour progression". Thesis, Nottingham Trent University, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360772.
Pełny tekst źródłaFülöp, Katalin. "Analysis of two plant protein complexes associated with transcription and cell cycle progression". Szegedi Tudományegyetem, 2005. http://www.theses.fr/2005PA112194.
Pełny tekst źródłaWernett, Pamela Joy. "The effects of Med12 variation upon cell cycle progression and differential gene expression". Diss., University of Iowa, 2011. https://ir.uiowa.edu/etd/2787.
Pełny tekst źródłaBoral, Debasish. "The Role of SOX2 in Colon Cancer Progression". OpenSIUC, 2014. https://opensiuc.lib.siu.edu/dissertations/911.
Pełny tekst źródłaDe, Nisco Nicole J. "Global analysis of the transcriptional regulation of Sinorhizobium meliloti cell cycle progression and study of cell cycle regulation during symbiosis with Medicago sativa". Thesis, Massachusetts Institute of Technology, 2013. http://hdl.handle.net/1721.1/83636.
Pełny tekst źródłaThis 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.
Includes bibliographical references.
The complex [alpha]-proteobacterial cell cycle regulatory network is essential not only for faithful replication and segregation of the genome, but also to coordinate unique cellular differentiation events that have evolved as adaptations to the different lifestyles of this diverse group of bacteria. The soil-dwelling [alpha]-proteobacterium, Sinorhizobium meliloti, not only has to accurately coordinate the replication of its tripartite genome, but also must undergo a dramatic cellular differentiation in order to form an effective symbiosis with the legume Medicago sativa. Preliminary analyses have indicated that plasticity in the S. meliloti cell cycle regulatory network may be essential to symbiosis, but cell cycle research in S. meliloti has been hindered largely by lack of a method to obtain synchronous populations of S. meliloti. In this thesis, I present the first method to generate synchronous cultures of S. meliloti. I performed microarray gene expression analysis on synchronous populations of S. meliloti to gain a global view of transcriptional regulation of cell cycle events. This represents the first work of this kind done in an [alpha]-proteobacterium besides Caulobacter crescentus, which is the current model for [alpha]-proteobacterial cell cycle studies. The importance of transcriptional regulation of cell cycle progression was first discovered in C. crescentus and the work presented in this thesis highlights the conservation of cell cycle regulated gene expression in S. meliloti. I identified 462 cell cycle regulated transcripts in S. meliloti, which included genes involved in vital cell processes such as cell division, flagella biogenesis, replication and segregation of its tripartite genome as well as several putative cell cycle regulators. I compared the set of genes with cell cycle regulated transcripts identified in my analysis with the set identified in C. crescentus to generate a core set of 128 conserved genes demonstrating cell cycle regulated gene expression in both species. To determine which of the S. meliloti genes with cell cycle regulated transcripts might be part of the CtrA and DnaA regulons in S. meiloti, I performed CtrA and DnaA binding motif analysis. To understand the evolutionary significance of these CtrA and DnaA binding motifs, I looked at conservation of these motifs in homologous genes from several related [alpha]-proteobacteria. The results indicated that the putative CtrA regulon might be more evolutionarily constrained than the putative DnaA regulon. Organisms more closely related to S. meliloti or with more similar lifestyles demonstrated a much greater conservation of the CtrA binding motifs identified in S. meliloti. The CtrA binding motifs in S. meliloti identified by my analysis were not at all well conserved in C. crescentus, which was the most distantly related [alpha]-proteobacteria surveyed. These differences in cell cycle regulated transcription and the putative CtrA regulon between S. meliloti and C. crescentus thus appear to represent specific adaptations to the distinctive genome and unique intracellular symbiotic lifestyle of S. meliloti and illustrate the importance of S. meliloti as a model for cell cycle regulation in [alpha]-proteobacteria with similar intracellular lifestyles. The work presented in this thesis also describes the importance of CtrA regulation in S. meliloti during symbiosis with M. sativa. A crucial part of this symbiosis is a striking cellular differentiation (termed bacteroid differentiation), which includes changes in membrane permeability, cell elongation and branching, endoreduplication of the genome and loss of reproductive capacity and therefore a significant deviation from the free-living cell cycle program. Endoreduplication of the genome requires a decoupling of DNA replication and cell division, which could be achieved by down-regulation of the essential master cell cycle regulator CtrA. I tested the effects of CtrA depletion in S. meliloti and found that CtrA depletion induces a bacteroid-like state characterized by elongated and branched cells and highly elevated DNA content. I also show that S. meliloti CtrA has a comparable half-life to C. crescentus CtrA, but regulated proteolysis of CtrA may be different in the two species since we found CtrA proteolysis to be essential in S. meliloti. In addition, I demonstrate that the promoter and coding regions of C. crescentus ctrA cannot complement an S. meliloti ctrA chromosomal deletion during symbiosis even though they can do so in the free-living state. My attempts to identify the defects in the function C. cresentus ctrA promoter or coding region within M. sativa gave surprising results since S. melioti strains expressing C. crescentus CtrA from the S. meliloti ctrA promoter region and vice versa were able to establish an effective symbiosis with M. sativa. I discuss several possibilities to explain this apparent paradox, but further study is required to fully clarify this observation. Taken as a whole, my thesis work represents a significant advancement to the field of cell cycle research in S. meliloti and [alpha]-proteobacteria as a whole. The cell synchronization method I developed will greatly facilitate more comprehensive analysis of cell cycle regulation in S. meliloti. My microarray gene expression analysis provides a global view of cell cycle regulated transcription in S. meliloti, which can be used in more in-depth explorations of specific mechanisms of transcriptional regulation of cell cycle events in S. meliloti. Lastly, my study of CtrA function in S. meliloti establishes the importance of CtrA regulation during symbiosis with M. sativa.
by Nicole J. De Nisco.
Ph.D.