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Dissertations / Theses on the topic 'Cellular signals'

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Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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1

Manktelow, Emily Frances. "Structural studies of viral and cellular recoding signals." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611943.

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2

Papaioannou, Alexandra. "Fine-tuning UPR signals and subsequent cellular outputs." Thesis, Rennes 1, 2019. http://www.theses.fr/2019REN1B013.

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La présente thèse explore le monde de la biologie du stress du RE (réticulum endoplasmique). Une vue globale du RE et du stress du RE est d'abord fournie en commençant par les mécanismes de base impliqués pour aller vers de possibles applications cliniques. L'accent est ensuite mis sur le rôle crucial de l'UPR dans la cancérogénèse, qui est activée en réponse au stress du RE dans la micro-environnement de la tumeur. Après avoir passé en revue ces aspects, nous mettons en évidence des éléments manquants dans notre compréhension de la façon dont les signaux UPR sont affinés et conduisent soit à la restauration de l'homéostasie du RE et des cellules soit à la mort cellulaire. Parmi les branches de l'UPR, les signaux ATF6 et IRE1 deviennent notre sujet d'investigation en raison de leur convergence dans la régulation du facteur XBP1 favorisant la survie. D'une part, nous découvrons les mécanismes provenant du lumen du RE qui régulent l'activation de l'ATF6 en réponse au stress du RE et affectant la signalisation adaptative cellulaire de l'ATF6 en aval. D'autre part, nous observons l'existence d'un réseau autorégulateur de l'activité RNase de l’IRE1 consistant en un système tyrosine kinase-phosphatase ciblant la RtcB et impactant l'épissage de l'ARNm de XBP1. Ainsi, grâce à nos études, nous avons découvert un circuit de signalisation intégré capable d’ajuster avec précision les sorties cellulaires de l’activation conjointe ATF6 et IRE1 en réponse au stress du RE
The present thesis explores the world of ER (endoplasmic reticulum) stress biology. A global view of ER and ER stress is first provided with a transition from the basic mechanisms involved to possible clinical applications. The focus is then placed to the crucial role of the UPR in carcinogenesis that is activated in response to ER stress in the micro-environment of the tumor. After reviewing these aspects, we point to missing parts in our comprehension of how UPR signals are fine-tuned and lead to either restoration of ER and cell homeostasis or cell death. Among the UPR branches, ATF6 and IRE1 signaling become our focus of investigation because of their convergence in the regulation of the pro-survival factor XBP1s. On the one hand, we unravel mechanisms originating from the ER lumen that regulate the ATF6 activation in response to ER stress and affect its downstream cell adaptive signaling. On the other hand, we witness the existence of an auto-regulatory network of IRE1 RNase activity consisted of a tyrosine kinase-phosphatase system that targets RtcB and impacts on XBP1 mRNA splicing. Hence, through our studies we uncover an integrated signaling circuit that can fine-tune the cellular outputs of the joint ATF6 and IRE1 activation in response to ER stress
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3

Thomson, Ty M., and Drew Endy. "Rapid Characterization of Cellular Pathways Using Time-Varying Signals." International Conference on Systems Biology, 2005. http://hdl.handle.net/1721.1/29803.

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The use of traditional tools for the discovery and characterization of biological systems has resulted in a wealth of biological knowledge. Unfortunately, only a small portion of the biological world is well-understood to date, and the study of the rest remains a daunting task. This work involves using time-varying stimuli in order to more rapidly interrogate and characterize signaling pathways. The time-dependent stimulation of a signaling pathway can be used in conjunction with a model of the pathway to efficiently evaluate and test hypotheses. We are developing this technology using the yeast pheromone signal transduction pathway as a model system. The time-varying stimuli will be applied to the yeast cells via a novel microfluidic device, and the pathway output will be measured via various fluorescent reporters. The output of the pathway can then be compared to the output from a computational model of the pathway in order to test hypotheses and constrain our knowledge of the pathway. Initial work shows that a computational model can be used to identify stimuli time-courses that increase the parameter sensitivity, meaning that corresponding experiments could potentially be much more informative.
Poster presented at the 2005 ICSB meeting, held at Harvard Medical School in Boston, MA.
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4

Madhavan, Shashi D. "Biomechanical signals mediate cellular mechano-transduction and gene regulation." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1195234773.

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5

Brandman, Onn. "Feedback loops shape cellular signals in space and time /." May be available electronically:, 2008. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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6

Osuna, José A. "The recognition of acoustical alarm signals with cellular neural networks /." [S.l.] : [s.n.], 1995. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=11058.

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7

Wong, Stephanie A. "Physical and Molecular Pathways Involved in Cellular Sensing of Mechanical Signals." Research Showcase @ CMU, 2016. http://repository.cmu.edu/dissertations/878.

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Mechanical properties of the extracellular environment provide important cues that regulate cell behavior. Particularly, the cellular response to substrate rigidity has become an important parameter to consider in disease treatment as well as tissue engineering. The goal of this thesis is to understand how adherent cells sense and respond to external rigidity cues. It has been challenging to study the mechanism that drives the preferential migration of cells towards stiffer substrates at a rigidity border due to difficulties in capturing cells as they transiently encounter a rigidity interface. Using a model system developed for testing cellular responses at a simulated rigidity border, I find that NIH 3T3 cells preferentially localize to the rigid portion of the model system. Cells use filopodia extensions to probe substrate rigidity in front of the leading edge and use substrate strain to determine whether the filopodia protrusions retract or expand to occupy the area. Myosin II mediated contractility is necessary to generate forces for both probing the substrate and retraction in response to substrate strain. Focal adhesion kinase null (FAK -/-) cells, known to be defective in durotaxis, are able to readily cross the rigidity border, while reexpression of focal adhesion kinase (FAK) rescues rigidity sensing. The model experimental system allows efficient analyses of conditions affecting rigidity sensing of cells. The results suggest that enhanced Rho activity, likely through Rho downstream effector mDia1, may underlie many rigidity sensing defects including those caused by FAK deficiency and microtubule disassembly. Additionally, I show that probing mechanisms at the front of a cell are used not only for probing rigidity but for sensing the state of migration. Design of a new checkerboard micropattern with alternating adhesive and non-adhesive areas revealed that the appearance of new traction forces and focal adhesions at the leading edge promotes the downregulation of pre-existing traction forces and focal adhesions that lag behind. These results suggest that in migrating cells continuous protrusion and mechanical probing directly in front of existing adhesions modulates traction force build up and serves as a key mechanism for regulating mechanical output in response to physical cues.
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8

Lau, See-yan. "A study of intracellular signals of K-opioids in non-neuronal cells /." Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19667139.

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9

Park, Edward S. "Microfluidic chamber arrays for testing cellular responses to soluble-matrix and gradient signals." Diss., Georgia Institute of Technology, 2011. http://hdl.handle.net/1853/39471.

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This work develops microfluidic technologies to advance the state-of-the-art in living cell-based assays. Current cell-based assay platforms are limited in their capabilities, particularly with respect to spatial and temporal control of external signaling factors, sample usage, and throughput. The emergence of highly quantitative, data-driven systems approaches to studying biology have added further challenges to develop assay technologies with greater throughput, content, and physiological relevance. The primary objectives of this research are to (i) develop a method to reliably fabricate 3-D flow networks and (ii) apply 3-D flow networks to the development and testing of microfluidic chamber arrays to query cellular response to soluble-matrix signal combinations and gradient signaling fields. An equally important objective is for the chamber arrays to be scaled efficiently for higher-throughput applications, which is another reason for 3-D flow networks. Two prototype chamber arrays are designed, modeled, fabricated, and characterized. Furthermore, tests are performed wherein cells are introduced into the chambers and microenvironments are presented to elicit complex responses. Specifically, soluble-matrix signaling combinations and soluble signal gradients are presented. The study of complex biological processes necessitates improved assay techniques to control the microenvironment and increase throughput. Quantitative morphological, migrational, and fluorescence readouts, along with qualitative observations, suggest that the chamber arrays elicit responses; however further experiments are required to confirm specific phenotypes. The experiments provide initial proof-of-concept that the developed arrays can one day serve as effective and versatile screening platforms. Understanding the integration of extracellular signals on complex cellular behaviors has significance in the study of embryonic development, tissue repair and regeneration, and pathological conditions such as cancer. The microfluidic chamber arrays developed in this work could form the basis for enhanced assay platforms to perform massively parallel interrogation of complex signaling events upon living cells. This could lead to the rapid identification of synergistic and antagonistic signaling mechanisms that regulate complex behaviors. In addition, the same technology could be used to rapidly screen potential therapeutic compounds and identify suitable candidates to regulate pathological processes, such as cancer and fibrosis.
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10

Heessen, Stijn. "Regulation of the ubiquitin-proteasome system : characterization of viral and cellular stabilization signals /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-600-6/.

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11

Fong, Lai-ping Iris, and 方麗萍. "Modulation of dendritic cell differentiation, maturation by exogenous and endogenous "danger" signals." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31971015.

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12

劉思恩 and See-yan Lau. "A study of intracellular signals of K-opioids in non-neuronal cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31214290.

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13

BOAVENTURA, ALBERTO MAGNO SILVEIRA. "EVALUATION OF ESTIMATION METHODS OF DIRECTION OF ARRIVAL OF SIGNALS IN CELLULAR COMMUNICATIONS SYSTEMS." PONTIFÍCIA UNIVERSIDADE CATÓLICA DO RIO DE JANEIRO, 1998. http://www.maxwell.vrac.puc-rio.br/Busca_etds.php?strSecao=resultado&nrSeq=7529@1.

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EMPRESA BRASILEIRA DE TELECOMUNICAÇÕES
Este estudo tem por objetivo contribuir para emprego de antenas adaptativas em sistemas de comunicação sem fio. É feita uma revisão dos métodos de estimação de ângulo de chegada e de sua utilização na formação de feixe. O desempenho de alguns métodos baseados em subspace fitting é comparado através de simulação considerando quatro cenários. O primeiro supões apenas a presença de ruído. Os demais consideram os modelos típicos de espalhamento local, ou seja, espalhamento aleatório dos ângulos de chegada.
This work intends to contribute for the employment of the Adaptive Antennas in Wireless Communications. In this way, a review of methods for direction of arrival estimation and beamforming is presented. The performance of some subspace fitting direction of arrival estimation methods is evaluated by simulation considering four propagation scenarios: The first assumes only additive white Gaussian noise; The three others consider typical models for local scattering, which means a random angular spread of angle of arrival.
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14

Ma, Leung Hang. "Characterization of calcium signals during the blastula period of zebrafish (danio rerio) embryogenesis /." View abstract or full-text, 2007. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202007%20MA.

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15

Fong, Lai-ping Iris. "Modulation of dendritic cell differentiation, maturation by exogenous and endogenous "danger" signals." Click to view the E-thesis via HKUTO, 2003. http://sunzi.lib.hku.hk/hkuto/record/B31971015.

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16

Leitao, Beatriz Belchior. "The role of the SUMO pathway in the cellular responses to oxidative stress signals in human endometrium." Thesis, Imperial College London, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544293.

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17

Dumond, Mathilde. "From cellular variability to shape reproducibility : mechanics and morphogenesis of Arabidopsis thaliana sepal." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSEN047/document.

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Les organismes produisent des organes de formes similaires, malgré une forte variabilité intrinsèque. La régulation de la forme des organes a été largement étudiée, cependant la robustesse des formes est encore mal comprise. Une plante telle qu’Arabidopsis possède de nombreux sépales, notre système modèle car il est possible d’étudier leur variabilité. Comme les cellules végétales contrôlent leur croissance à travers les propriétés mécaniques de leur paroi, ma thèse vise à étudier le lien entre mécanique cellulaire et robustesse des formes.J’ai d’abord cherché à comprendre si la forme des organes est influencée par la réaction cellulaire aux contraintes mécaniques induites par la croissance. J’ai validé cette hypothèse grâce un modèle mécanique, et fait des prédictions de la forme des sépales qui ont été confirmées expérimentalement par un collaborateur.D’autre part, j’ai mesuré les propriétés mécaniques de la paroi qui se révèlent spatialement hétérogènes. L’ajout de cette hétérogénéité dans le modèle conduit à des organes de forme variable. J’ai obtenu des formes robustes en ajoutant de la variabilité temporelle, et j’ai montré que, contre-intuitivement, le niveau de variabilité spatiale est anti-corrélé avec la robustesse des formes.Ces prédictions ont été testés en étudiant un mutant présentant des formes de sépales variables. J’ai en particulier montré que les propriétés mécaniques de ce mutant étaient moins variables spatialement que le sauvage. Ainsi, ma thèse a permis de mieux comprendre la régulation de la robustesse de forme des organes, en particulier en montrant que la variabilité des propriétés mécaniques peut conduire à une robustesse des formes
Developmental robustness is the ability to produce similar phenotypes despite intrinsic variability.Regulation of organ shape has been widely studied, but regulation of organ shape reproducibility is yet to be elucidated.A. thaliana sepals, flower external organs, can be used to study such robustness : each plant produces more than 60 flowers, allowing variability measurement.Plant cells modulate their surrounding cell wall stiffness and anisotropy to control growth, thus my PhD aims at elucidating the role of cell wall mechanics on organ shape robustness.Cells sense their physical environment and accordingly adjust their cell wall mechanics: we studied whether the strength of this feedback influenced organ shapes. Using a model, I showed that a strong feedback lead to the formation of a pointy sepal tip; this prediction was experimentally validated by a PhD student of the team.Measurements of the cell wall mechanical properties using atomic force microscopy (AFM) showed that they were highly spatially variable. When this variability was added in the model, the organ shapes were variable. To get reproducible shapes, I increased the temporal variability of the mechanics: it smoothed the spatial variability over time. Likewise, decreasing spatial variability reduced organ shape robustness. These theoretical results suggest that spatial and temporal variability influence shape robustness.To experimentally test these results, our collaborators identified a mutant displaying less robust sepal shapes. Using AFM, I showed that the spatial variability was reduced in the mutant, confirming that mechanical spatial variability influenced shape robustness
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18

Bhrigu, Gargi. "Sorting Signals, Domain Conformation and Interdomain Interactions in CFTR Misprocessing and Rescue." University of Toledo Health Science Campus / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=mco1268659408.

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19

Lira, Junior Mario de Andrade. "Environmental factors and plant-to-bacteria signals effects on nodulation and nodule development of pea." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=38075.

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With the projected increase in global population, unprecedented increases in crop production will be needed and legume crops are one of the primary means of achieving these increases. The legume-Rhizobium symbiosis is the single most important source of biologically fixed nitrogen in agricultural systems but, as a biological system it is complex, and very sensitive to environmental effects, such as available soil nitrogen, soil pH (both high and low), soil salinity and extremes of soil temperature. Each of these may affect the delicate signal exchange process that occurs during symbiosis establishment. To better understand the effect of environmental factors on signal exchange and nodulation, we conducted four experiments, under controlled-environment conditions, with pea (Pisum sativum) as the model legume. The first experiment studied the effects of available nitrogen, the second the effects of low soil pH, the third the effect of soil salinity and the fourth the effects of low soil temperature. In all experiments the plants were inoculated with Rhizobium leguminosarum bv. viceae cells previously treated with 10 x 10-3 M of hesperitin or naringenin, or not treated (control). In all experiments plants were destructively sampled at 10, 20, 30 and 40 days after inoculation (in two experiments samplings were also conducted at 15 DAI), and data on plant and nodule variables were collected. To allow for a better understanding of the effects of flavonoids on nodule development an image analysis technique was developed that permitted us to measure every individual nodule at each sampling. This provided a more precise picture of nodule development over time than would have been possible with previous methods. Our results indicated that addition of flavonoids had positive effects on nodulation, both in number and size of nodules produced, and that the positive effects were greatest at the most inhibitory levels of the environmental factors tested, and at earlier sampling
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20

Mouradi, Rand. "Wireless Signals and Male Fertility." Cleveland State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=csu1318571631.

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21

Huang, Yun. "Integration of Extracellular and Intracellular Calcium Signals: Roles of Calcium-Sensing Receptor (CASR), Calmodulin and Stromal Interaction Molecule 1 (STIM1)." Atlanta, Ga. : Georgia State University, 2008. http://digitalarchive.gsu.edu/chemistry_diss/28/.

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Thesis (Ph. D.)--Georgia State University, 2008.
Title from title page (Digital Archive@GSU, viewed July 1, 2010) Jenny J. Yang, committee chair; Edward Brown, Giovanni Gadda, Zhi-ren Liu, committee members. Includes bibliographical references (p. 230-258).
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22

Coronato, Nicola [Verfasser], Paul Gottlob [Akademischer Betreuer] Layer, and Bodo [Akademischer Betreuer] Laube. "Identification of cellular and molecular signals involved in neural retina specification in the developing chick embryo / Nicola Coronato ; Paul Gottlob Layer, Bodo Laube." Darmstadt : Universitäts- und Landesbibliothek Darmstadt, 2017. http://d-nb.info/1137624752/34.

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23

Khattar, Mithun. "Modulation of TCR Signals Reprograms Immune Tolerance in Transplantation and Type-1 Diabetes." University of Toledo Health Science Campus / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=mco1329231545.

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24

Moskalenko, Bogdan, and Богдан Дмитрович Москаленко. "Temperatures influence of nanocircuits." Thesis, National Aviation University, 2021. https://er.nau.edu.ua/handle/NAU/50365.

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Tougav P. D. Logic Devices Implementated using Quantum Cellular Automata. // Journal Applied Physics. 1994, #3, p.p. 49-53. 2. Melnik O. S. Myshynsky A. V. Cipher Nanodevices. // Proc. of the XV Int. Conf. "Electronics and Applied Physics." T. Shevchenko National University of Kyiv. 22-26.10.2019, p.p. 41-43.
The purpose of this article was to prove that the main element (ME) together with the inverter, ie the universal ME, is a functionally complete element base of one-electron nanochemistry. During the simulations of the element operation, it was proved that the temperature directly affects the operation of logic nanoschemas on cellular machines that use most elements. Therefore, research and modeling of their effectiveness is an urgent task.
Метою даної статті було довести, що основний елемент (МЕ) разом з інвертором, тобто універсальний МЕ, є функціонально повною елементною базою одноелектронної нанохімії. Під час симуляцій роботи елементу було доведено що температура безпосередньо впливає на роботу логічних наносхем на квантових автоматах, що використовують більшість елементів. Тому дослідження та моделювання їх ефективності - актуальне завдання.
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25

Ruppert, Shannon Moore. "Signals Delivered By Interleukin-7 Regulate The Activities Of Bim And JunD In T Lymphocytes." Doctoral diss., University of Central Florida, 2012. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/5475.

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Interleukin-7 (IL-7) is an essential cytokine for lymphocyte growth that has the potential for promoting proliferation and survival. While the survival and proliferative functions of IL-7 are well established, the identities of IL-7 signaling components in pathways other than JAK/STAT, that accomplish these tasks remain poorly defined. To this end, we used IL-7 dependent T-cells to examine those components necessary for cell growth and survival. Our studies revealed two novel signal transducers of the IL-7 growth signal: BimL and JunD. IL-7 promoted the activity of JNK (Jun N-terminal Kinase), and that JNK, in turn, drove the expression of JunD, a component of the Activating Protein 1 (AP-1) transcription factors. Inhibition of JNK/JunD blocked glucose uptake and HXKII gene expression, indicating that this pathway was responsible for promoting HXKII expression. After a bioinformatics survey to reveal possible JunD-regulated genes activated early in the IL-7 signaling cascade, our search revealed that JunD could control the expression of proteins involved in signal transduction, cell survival and metabolism, including Pim-1. Pim-1, an IL-7 induced protein, was inhibited upon JNK or JunD inhibition. Our hypothesis that JunD positively regulated proliferation was confirmed when the proliferation of primary CD8+ T-cells cultured with IL-7 was impaired upon treatment with JunD siRNA. These results show that the IL-7 signal is more complex than the JAK/STAT pathway, activating JNK and JunD to induce rapid growth through the expression of metabolic factors like HXKII and Pim-1. When metabolic activities are inhibited, cells undergo autophagy, or cell scavenging, to provide essential nutrients. Pro-apoptotic Bim was evaluated for its involvement in autophagy. Bim is a BH3-only member of the Bcl-2 family that contributes to T-cell death. Partial rescue of T-cells occurs when Bim and the interleukin-7 receptor are deleted, implicating Bim in IL-7-deprived T-cell apoptosis. Alternative splicing results in three different isoforms: BimEL, BimL, and BimS. To study the effect of Bim deficiency and define the function of the major isoforms, Bim-containing and Bim-deficient T-cells, dependent on IL-7 for growth, were used. Loss of Bim in IL-7-deprived T-cells delayed apoptosis, but blocked the degradative phase of autophagy. The conversion of LC3-I to LC3-II was observed in Bim-deficient T-cells, but p62, which is degraded in autolysosomes, accumulated. To explain this, BimL, was found to support acidification of lysosomes associated with autophagic vesicles. Key findings showed that inhibition of lysosomal acidification accelerated death upon IL-7 withdrawal only in Bim-containing T-cells, indicating that in these cells autophagy was protective. IL-7 dependent T-cells lacking Bim were insensitive to inhibition of autophagy or lysosomal acidification. BimL co-immunoprecipitated with dynein and Lamp1-containing vesicles, indicating BimL could be an adaptor for dynein to facilitate loading of lysosomes. In Bim deficient T-cells, lysosome-tracking probes revealed vesicles of less acidic pH. Over-expression of BimL restored acidic vesicles in Bim deficient T-cells, while other isoforms, BimEL and BimS, associated with intrinsic cell death. These results reveal a novel role for BimL in lysosomal positioning that may be required for the formation of functional autolysosomes during autophagy.
ID: 031001292; System requirements: World Wide Web browser and PDF reader.; Mode of access: World Wide Web.; Error in paging: p. v followed by 1 unnumbered page and then followed by p. ii-vii.; Adviser: Annette R. Khaled.; Title from PDF title page (viewed March 1, 2013).; Thesis (Ph.D.)--University of Central Florida, 2012.; Includes bibliographical references (p. 99-121).
Ph.D.
Doctorate
Molecular Biology and Microbiology
Medicine
Biomedical Sciences
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26

Song, Hao. "Hematopoietic cell lineage switching mediated by zebrafish STAT1B." Thesis, University of Oregon, 2010. http://hdl.handle.net/1794/10913.

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xi, 38 p. : ill. (some col.) A print copy of this thesis is available through the UO Libraries. Search the library catalog for the location and call number.
A critical question for developmental biology is the mechanism by which cells make fate decisions. In the hematopoietic system, stem cells differentiate into several different cell types, but the mechanisms that affect this process are incompletely known. Understanding these mechanisms is important because abnormal regulation of hematopoiesis can result in disease. STAT1 protein plays crucial roles in mediating innate immunity by transducing interferon signals, but recent results have also related STAT1 to hematopoietic cell differentiation. Here we cloned a previously uncharacterized zebrafish co-ortholog of the human STAT1 gene we call stat1b and investigated the functions of two zebrafish Stat1 proteins in hematopoiesis. The advantage of the zebrafish model is that, due to a whole genome duplication (WGD), some human genes have two co-orthologs in zebrafish. During evolution, co-orthologs have retained or acquired similar, complimentary, or new functions. Both stat1a and stat1b encode all four characteristic domains of the human STAT1 protein. Phylogenetic and conserved synteny analyses showed that stat1b and stat1a arose as duplicates in the teleost genome duplication event, and these analyses clarified the historical origin of the entire vertebrate STAT gene family. RT-PCR demonstrated maternal expression of both stat1a and stat1b . Expression of stat1b, but not stat1a, was detected in hematopoietic domains of embryos by in situ hybridization. Morpholino knockdown of stat1b , but not stat1a, mRNA expression resulted in a decrease in expression of the myeloid cell marker genes spi and mpx and an increase in expression of the hematopoietic progenitor marker gene scl and the erythrocyte marker gene gatal. These results show that in zebrafish, Stat1b protein functions in the commitment of hematopoietic cells to a myeloid cell fate.
Committee in charge: William Cresko, Chairperson, Biology; John Postlethwait, Advisor, Biology; Judith Eisen, Member, Biology; Jan Spitsbergen, Member, Not from U of O; J. Andrew Berglund, Outside Member, Chemistry
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27

Ogese, Monday. "Definition of antigenic determinants in drug hypersensitive patients : an integrated clinical, chemical and cellular approach to quantify and characterize the drug signals presented to T-Lymphocytes." Thesis, University of Liverpool, 2014. http://livrepository.liverpool.ac.uk/18733/.

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Idiosyncratic drug hypersensitivity remains a major challenge as it causes high morbidity and mortality. This is complicated by the multiple risk factors implicated and the inability to predict these reactions during the early stages of drug development. Thus, this study attempted to delineate the molecular pathomechanism(s) involved in sulfamethoxazole (SMX) hypersensitivity. The reactive metabolite, nitroso-SMX (SMX.NO) generated through the hepatic bioactivation of SMX has long been hypothesised as a major trigger of these reactions. SMX hypersensitivity has been used as a paradigm to study the role of drug metabolism in the activation of T-cells as the synthetic nitroso metabolite is available for functional studies. Metabolism of SMX in hepatic tissue has been extensively studied. CYP2C9 and Myeloperoxidase (MPO) are implicated in the formation of SMX.NO. However, it is unclear whether the SMX.NO generated in the liver migrates to the skin; the primary target in SMX hypersensitivity. It is possible that localised SMX metabolism by immune cells resident in the skin are implicated in the observed reactions. ELISA data revealed SMX metabolism in EBV-transformed B-cells used as antigen presenting cells (APCs). SMX-metabolism was significantly inhibited by methimazole. Furthermore, Western blotting and RT-PCR analyses suggested the presence of low concentrations of MPO in EBV-transformed B-cells. Interestingly, RT-PCR revealed mRNA expression of flavine containing monooxygenases (FMO1-5), TPO and LPO but the protein levels of these enzymes were not detected in immune cells. Subsequent experiments involved the generation and LC-MS/MS characterization of SMX.NO-modified MPO adducts. Although SMX.NO formed both the sulphinamide and N-hydroxysulfinamide adducts, drug specific T-cell clones failed to proliferate in response to drug-modified peptides. Since SMX.NO binds to multiple cellular proteins, it is assumed that peptides derived from the modified protein interact with a number of diverse HLA molecules to activate T-cells. However, the HLA molecules that interact with SMX.NO-modified peptides have not been defined. This study therefore examined the HLA molecules that present SMX.NO (derived peptides) to T-cells. T-cell clones (TCCs) were generated from 5 hypersensitive patients with cystic fibrosis. Fast growing TCCs from 2 SMX hypersensitive patients were used for HLA restriction studies. Drug-specific proliferative response, cytokine secretion and cytolytic markers were measured using [3H]-thymidine incorporation and ELIspot assays. Anti-human class I and class II (DR, DP, and DQ) antibodies were used to determine HLA restriction of drug-specific T-cell activation. APCs expressing similar or different HLAs were used to define the alleles involved in the presentation of SMX.NO-derived antigens to T-cells. A total of 1578 clones were tested for SMX.NO reactivity. Seventy-seven CD4+ clones were activated to proliferate and secrete IFN-ϒ, IL-5, IL-13 and granzyme-B by SMX.NO. Only one TCC was CD8+No cross reactivity with SMX was observed. The SMX.NO-specific response of clones was blocked with antibodies against MHC class II and HLA-DQ. Clones from 2 patients (Patient 1: HLA-DQB1*05:01:01G/ DQB1*06:03:01G; Patient 2: HLA-DQB1*02:01:01G/DQB1*02:01:01G) were used to define the DQ alleles involved in the presentation of SMX.NO derived antigens. SMX.NO-specific responses were detected with heterologous APCs expressing HLA-DQB1*05:01 (patient 1) and HLA-DQB1*02:01 (patient 2), but not other HLA-DQB1 alleles. Activation of PD-1 on T-cells is thought to inhibit antigen-specific T-cell priming and regulate T-cell differentiation. Thus, this study sought to measure the drug-specific activation of naïve T-cells after perturbation of PD-L1/PD-1 binding and investigate whether PD-1 signalling influences the differentiation of T-cells. Naive T-cells were co-cultured with monocyte-derived dendritic cells in the presence of SMX.NO for a period of 8 days (±PD-1/2 block) and T-cell priming investigated using readouts for proliferation and cytokine secretion. Priming of naïve T-cells against SMX.NO was found to be more effective when PD-L1 signalling was blocked. Drug-specific TCCs generated through priming and from hypersensitive patients were found to secrete IFN-γ, IL-5 and IL-13. More detailed analysis revealed two different cytokine signatures. Clones secreted either FasL/IL-22 or granzyme B. The FasL/IL22 secreting clones expressed the skin homing receptors CCR4, CCR10 and CLA and migrated in response to CCL17/CCL27. PD-1 was stably expressed at different levels on clones; however, PD-1 expression did not correlate with the strength of the antigen-specific proliferative response or the secretion of cytokines/cytolytic molecules. In conclusion, this study used a variety of in vitro assays to investigate the multiple factors involved in the pathomechanism of SMX hypersensitivity. A clear understanding of mechanisms of drug hypersensitivity will provide insights that aid drug design and reduce the frequency of such reactions.
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Hempel, Felix [Verfasser], and Markus [Akademischer Betreuer] Hoth. "Organic electrochemical transistors based on PEDOT : PSS for the sensing of cellular signals from confluent cell layers down to single cells / Felix Wolfgang Hempel ; Betreuer: Markus Hoth." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2020. http://d-nb.info/1212433653/34.

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29

Hempel, Felix Wolfgang [Verfasser], and Markus [Akademischer Betreuer] Hoth. "Organic electrochemical transistors based on PEDOT : PSS for the sensing of cellular signals from confluent cell layers down to single cells / Felix Wolfgang Hempel ; Betreuer: Markus Hoth." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2020. http://d-nb.info/1212433653/34.

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30

Lavik, Andrew R. "The Role of Inositol 1,4,5-Trisphosphate Receptor-Interacting Proteins in Regulating Inositol 1,4,5-Trisphosphate Receptor-Dependent Calcium Signals and Cell Survival." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1448532307.

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31

Rong, Yiping. "Bcl-2 Regulates Proapoptotic Calcium Signals by Interacting with the Inositol 1, 4, 5-Trisphosphate Receptor." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1228322705.

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32

Biver, Galadrielle. "Identification and characterization of the control of murine MSC differentiation by the ADP receptors P2Y12 and P2Y13." Doctoral thesis, Universite Libre de Bruxelles, 2014. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209334.

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Extracellular nucleotides act as local intercellular messengers. In response to various stimuli, nucleotides can be released from the cytosol of damaged cells, exocytosis vesicles and efflux through membrane channel. In the extracellular fluids, nucleotides are rapidely degraded by ecto-nucleotidases, such as CD39,CD39L1 and CD73. Extracellular nucleotides activate the P2 receptor family .This family of receptors can be divided into 2 groups: P2X1-7R ( ionotropic receptors) and P2YR ( G protein-coupled receptors). Nowadays, there are eight accepted human P2Y receptors: P2Y1,2,4,6,11,12,13,14.

To determine the physiological roles of P2Y receptor family, our laboratory generated different strains of P2Y knockout mice (P2Y4 ,6 and 13). In collaboration with A. Gartland ,I. And Arnett TR Orriss ( Sheffield and London University) ,it has been observed that the P2Y13R-/- mice exhibit an impaired bone tissue metabolism that leads to a reduction in the volume of the femoral trabecular bone and the number of trabeculae. This phenotype is correlated with the decrease in the number of osteoblasts at the endo-cortical bone surface .

We therefore examined whether P2Y13 R activation was involved in the osteogenic differentiation of mesenchymal stem cells (MSCs). In the first part of our work we have shown that :

Induction of the MSCs differentiation is associated with the release of ATP and its conversion to ADP (agonist of the P2Y13R). ATP release probably involves the pannexine1 while the conversion of ATP into ADP is probably due to the activity of the ecto-nucleotidase CD39L1.

ADP stimulation of P2Y13 R+/+ (but not P2Y13 R-/-) adherent bone marrow stromal cells (BMSC) increased significantly the formation of alkaline phosphatase-colony forming units (CFU-ALP), as well as the expression of osteoblastic genes such as Osterix involved in the maturation of pre-osteoblasts into osteoblasts. The number of CFU-ALP obtained from P2Y13 R-/- BMSC and the level of osteoblastic gene expression after osteogenic stimulation were also strongly reduced compared to those obtained in wild-type cell cultures. In contrast, when P2Y13 R-/- BMSCs were incubated in an adipogenic medium, the number of adipocytes generated and the level of adipogenic gene expression (PPARγ2 and Adipsin) were higher than those obtained in P2Y13 R+/+ MSC. We also observed a significant increase of the number of bone marrow adipocytes in tibia of P2Y13 R-/- mice.

The P2ry12 gene deletion (also activated by ADP) also affects the ability of BMSCs to differentiate into osteoblasts but stimulates adipogenic differentiation.

In a second part of our work ,we have shown that the pro- osteogenic action of P2Y13R is indirect. Indeed ,this receptor is not expressed by MSCs but by adherent myeloid cells present in the bone marrow cell cultures (characterized by the expression of CD11b and CD45 markers) .In addition, we observed that following receptor activation by ADP ,these myeloid cells produce BMP2 factor.

We therefor propose that the stimulation of MSCs differentiation induces CD45- adherent cells to release ATP that is converted into ADP, most probably by the up-regulated CD39L1 ectonucleotidase. This ADP stimulates P2Y12R and P2Y13R expressed by CD45+/CD11b+ myeloid cells leading to the release of the osteogenic factor BMP2. This cytokine favours the maturation of pre-osteoblasts into osteoblasts and concomitantly inhibits the maturation of pre-adipocytes.


Doctorat en Sciences
info:eu-repo/semantics/nonPublished

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33

Hennig, Katharina. "Dynamique des forces motiles et brisure de symétrie chez la cellule migrante." Thesis, Université Grenoble Alpes (ComUE), 2018. http://www.theses.fr/2018GREAY040/document.

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La motilité cellulaire directionnelle au cours du développement de l'organisme et des tissus, l'homéostasie et la maladie nécessite une rupture de symétrie. Ce processus repose sur la capacité des cellules individuelles à établir une polarité avant-arrière, et peut se produire en l'absence de signaux externes. L'initiation de la migration a été attribuée à la polarisation spontanée des composants du cytosquelette, tandis que l'évolution spatio-temporelle des forces du cytosquelette résultant de l'interaction mécanique cellule-substrat continue n'a pas encore été résolue. Ici, nous établissons un test de migration microfabriqué unidimensionnel qui imite un environnement fibrillaire complexe in vivo tout en étant compatible avec les mesures de force à haute résolution, la microscopie quantitative et l'optogénétique. La quantification des paramètres morphométriques et mécaniques révèle un comportement de stick-slip générique initié par un détachement stochastique des contacts adhésifs d'un côté de la cellule dépendant de la contractilité, qui est suffisant pour conduire la motilité cellulaire directionnelle en absence de polarité du cytosquelette préétablie ou de gradients morphogènes. Un modèle théorique valide le rôle crucial de la dynamique d'adhésion au cours de la rupture de symétrie spontanée, en proposant que le phénomène examiné puisse émerger indépendamment d'un système auto-polarisant complexe
Directional cell motility during organism and tissue development, homeostasis and disease requires symmetry breaking. This process relies on the ability of single cells to establish a front-rear polarity, and can occur in absence of external cues. The initiation of migration has been attributed to the spontaneous polarization of cytoskeleton components, while the spatio- temporal evolution of cytoskeletal forces arising from continuous mechanical cell-substrate interaction has yet to be resolved. Here, we establish a one- dimensional microfabricated migration assay that mimics complex in vivo fibrillar environment while being compatible with high-resolution force measurements, quantitative microscopy, and optogenetics. Quantification of morphometric and mechanical parameters reveals a generic stick-slip behavior initiated by contractility-dependent stochastic detachment of adhesive contacts at one side of the cell, which is sufficient to drive directional cell motility in absence of pre-established cytoskeleton polarity or morphogen gradients. A theoretical model validates the crucial role of adhesion dynamics during spontaneous symmetry breaking, proposing that the examined phenomenon can emerge independently of a complex self-polarizing system
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34

Pinidiyaarachchi, Amalka. "Digital Image Analysis of Cells : Applications in 2D, 3D and Time." Doctoral thesis, Uppsala universitet, Centrum för bildanalys, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9541.

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Light microscopes are essential research tools in biology and medicine. Cell and tissue staining methods have improved immensely over the years and microscopes are now equipped with digital image acquisition capabilities. The image data produced require development of specialized analysis methods. This thesis presents digital image analysis methods for cell image data in 2D, 3D and time sequences. Stem cells have the capability to differentiate into specific cell types. The mechanism behind differentiation can be studied by tracking cells over time. This thesis presents a combined segmentation and tracking algorithm for time sequence images of neural stem cells.The method handles splitting and merging of cells and the results are similar to those achieved by manual tracking. Methods for detecting and localizing signals from fluorescence stained biomolecules are essential when studying how they function and interact. A study of Smad proteins, that serve as transcription factors by forming complexes and enter the cell nucleus, is included in the thesis. Confocal microscopy images of cell nuclei are delineated using gradient information, and Smad complexes are localized using a novel method for 3D signal detection. Thus, the localization of Smad complexes in relation to the nuclear membrane can be analyzed. A detailed comparison between the proposed and previous methods for detection of point-source signals is presented, showing that the proposed method has better resolving power and is more robust to noise. In this thesis, it is also shown how cell confluence can be measured by classification of wavelet based texture features. Monitoring cell confluence is valuable for optimization of cell culture parameters and cell harvest. The results obtained agree with visual observations and provide an efficient approach to monitor cell confluence and detect necrosis. Quantitative measurements on cells are important in both cytology and histology. The color provided by Pap (Papanicolaou) staining increases the available image information. The thesis explores different color spaces of Pap smear images from thyroid nodules, with the aim of finding the representation that maximizes detection of malignancies using color information in addition to quantitative morphological parameters. The presented methods provide useful tools for cell image analysis, but they can of course also be used for other image analysis applications.
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35

Masri, Bernard. "Fonction endothéliale du récepteur de l'apeline : étude de la cascade de transduction et implications physiologiques." Toulouse 3, 2004. http://www.theses.fr/2004TOU30181.

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Notre équipe a caractérisé un nouveau récepteur, msr/apj, qui est exprimé par les cellules endothéliales durant la formation des vaisseaux et du cœur. En 1998, le ligand endogène (baptisé apeline) du récepteur a été isolé par une équipe japonaise. Dans le but de comprendre la fonction endothéliale de cette nouvelle voie de signalisation, nous avons analysé les différentes cascades de transduction activées par l'apeline dans des CHO exprimant de manière stable msr/apj. Dans ces cellules, l'apeline engendre une inhibition de l'adénylylcyclase, et induit une activation des ERKs et de la p70S6 kinase. Grâce à l'expression stable de sous-unités a de protéines G insensibles à la toxine pertussique, nous avons montré que la stimulation des ERK est dépendante de ai2 et indépendante de Ras. La stimulation de la p70S6 kinase implique préférentiellement ai1, une PI3 Kinase, Akt, et mTOR. De manière intéressante, nous avons observé que les HUVEC (Human Umbilical Vein Endothelial Cells) expriment naturellement le récepteur de l'apeline. L'apeline engendre aussi une activation de la p70S6K dans ces cellules et induit leur prolifération. Cependant, ces cellules expriment naturellement l'apeline qui peut engendrer une désensibilisation autocrine. Cette désensibilisation peut être obtenue en aigu après un prétraitement des CHO par l'apeline ou en chronique avec des CHO coexprimant le récepteur et l'apeline. La délétion du domaine C-terminal du récepteur bloque la désensibilisation associée au couplage avec la sous-unité ai2 et l'activation des ERK. Ce récepteur représente donc une nouvelle cible pharmacologique pour les pathologies associées à une néovascularisation telles que le développement des tumeurs solides et les rétinopathies ischémiques
Our team have characterized a new receptor, msr/apj, which is expressed in the endothelium of newly forming heart and blood vessels. In 1998, the endogenous ligand (named apeline) of this receptor was isolated by a Japanese laboratory. In order to understand the endothelial function of this new signaling pathway, we analyzed the various signal transduction pathways activated by apelin in CHO cells which stably express msr/apj. In these cells, apelin induces inhibition of adenylylcyclase, and activation of ERKs and p70S6 kinase. The stable expression of pertussis toxin insensitive a subunits of G proteins led us to demonstrate that ERK stimulation is ai2 dependent and Ras independent. The p70S6 kinase stimulation preferentially involves ai1, a PI3 Kinase, Akt, and mTOR. Interestingly, we observed that HUVEC (Human Umbilical Vein Endothelial Cells) endogenously express the apelin receptor. In these cells, apelin induces the activation of p70S6K and leads to their proliferation. However, these cells also express apelin which can induce an autocrine desensitization of the receptor. This desensitization can be obtained after acute pretreatment of the CHO by apelin or observed with CHO cells co-expressing the receptor and apelin. The deletion of the receptor C-terminal domain abolishes the desensitization associated with the coupling with the ai2 subunit and the ERK activation. Thus, this receptor represents a new pharmacological target for pathologies associated with a neovascularization such as the solid tumors development and ischemic retinopathy
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36

L'Allemain, Gilles. "Mécanisme d'action des facteurs de croissance : étude des évènements précoces dans la transmission du signal mitogénique." Nice, 1986. http://www.theses.fr/1986NICE4047.

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37

Haugh, Jason Michael 1972. "Cellular compartmentation effects in receptor-mediated signal transduction." Thesis, Massachusetts Institute of Technology, 1999. http://hdl.handle.net/1721.1/85364.

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38

Leahy, Rachel A. "Signal Transduction and Cellular Differentiation in Airway Epithelium." Kent State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=kent1352673026.

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39

Jouaville, Laurence Sophie. "Modulation mitochondriale des signaux calciques intracellulaires." Bordeaux 2, 1996. http://www.theses.fr/1996BOR28441.

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40

Gammon, Benjamin Matthew. "Signal transduction in the cellular slime mould Dictyostelium discoideum." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279872.

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41

Najari, Moghadam Nima. "On Multiantenna Cellular Communications: From Theory to Practice." Doctoral thesis, KTH, Teknisk informationsvetenskap, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-207623.

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Today, wireless communications are an essential part of our everyday life. Both the number of users and their demands for wireless data have increasedtremendously during the last decade. Multiantenna communicationsis a promising solution to meet this ever-growing traffic demands. However, impairments that exist in most practical communication networks may substantially limit the performance of a multiantenna system. The characterizationof such a performance loss and how to minimize that are still largelyopen problems. The present thesis addresses this important research gap. Inparticular, we focus on three major impairments of a multiantenna cellularnetwork: impairment in the channel state information (CSI), interference andimpairment in the transceiver hardware components.To fully realize the benefits of multiantenna communications, the users need to acquire a certain level of information about their propagation environment; that is, their corresponding CSI. In practice, the CSI is not known bythe users and should be acquired by allocating part of the network resourcesfor pilot transmission. This problem is mainly important in the systems with a large number of antennas, as in general the required network resources for CSI acquisition scales with the number of transmitting antennas. Theproblem of CSI acquisition in a single-cell multiuser multiple-input multipleoutput(MIMO) system is addressed in this thesis. A linear spatial precodingand combining scheme for pilot transmission is proposed. This scheme requiresless number of network resources for channel estimation compared tothe conventional schemes. The gains of the proposed scheme are characterized by finding an upper-bound and a lower-bound on the channel estimation error.Moreover, as an ultimate performance metric, an achievable sum-rate ofthe network is formulated and analyzed numerically.Due to the broadcast nature of the wireless channels, the performanceof the users in a network is intertwined; the desired signal of one user mayinterfere other users. Hence, the interference is another major impairment inwireless communication systems. In this thesis, the practical challenges of aninterference management technique, namely MIMO interference alignment isinvestigated by implementation on a multiuser MIMO testbed. Then, in thecontext of interference alignment, the problem of optimal power allocation forpilot and data transmission is studied and verified by the measurements.The impairment in the hardware components of the transceivers, that is, any deviation of the components from their ideal behavior, degrades the performance of a communication system. In particular, the impact of nonlineartransmitter power amplifiers (PA)s is investigated in this thesis. First, consideringa memoryless third-order polynomial model for the PAs, a model forthe transmitted nonlinear distortion signal from a multiantenna transmitter isproposed and validated by measurements. This model implies that the spatialdirection of the transmitted distortion is dependent on the spatial directionof the desired signal. Then, this model is extended for a general arbitrary order polynomial model. Exploiting the developed distortion model, the energyefficiency of a multiantenna system operating at millimeter wave frequenciesis studied.

QC 20170523

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42

Radnosrati, Kamiar. "On Timing-Based Localization in Cellular Radio Networks." Licentiate thesis, Linköpings universitet, Reglerteknik, 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-148074.

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The possibilities for positioning in cellular networks has increased over time, pushed by increased needs for location based products and services for a variety of purposes. It all started with rough position estimates based on timing measurements and sector information available in the global system for mobile communication (gsm), and today there is an increased standardization effort to provide more position relevant measurements in cellular communication systems to improve on localization accuracy and availability. A first purpose of this thesis is to survey recent efforts in the area and their potential for localization. The rest of the thesis then investigates three particular aspects, where the focus is on timing measurements. How can these be combined in the best way in long term evolution (lte), what is the potential for the new narrow-band communication links for localization, and can the timing measurement error be more accurately modeled? The first contribution concerns a narrow-band standard in lte intended for internet of things (iot) devices. This lte standard includes a special position reference signal sent synchronized by all base stations (bs) to all iot devices. Each device can then compute several pair-wise time differences that corresponds to hyperbolic functions. Using multilateration methods the intersection of a set of such hyperbolas can be computed. An extensive performance study using a professional simulation environment with realistic user models is presented, indicating that a decent position accuracy can be achieved despite the narrow bandwidth of the channel. The second contribution is a study of how downlink measurements in lte can be combined. Time of flight (tof) to the serving bs and time difference of arrival (tdoa) to the neighboring bs are used as measurements. From a geometrical perspective, the position estimation problem involves computing the intersection of a circle and hyperbolas, all with uncertain radii. We propose a fusion framework for both snapshot estimation and filtering, and evaluate with both simulated and experimental field test data. The results indicate that the position accuracy is better than 40 meters 95% of the time. A third study in the thesis analyzes the statistical distribution of timing measurement errors in lte systems. Three different machine learning methods are applied to the experimental data to fit Gaussian mixture distributions to the observed measurement errors. Since current positioning algorithms are mostly based on Gaussian distribution models, knowledge of a good model for the measurement errors can be used to improve the accuracy and robustness of the algorithms. The obtained results indicate that a single Gaussian distribution is not adequate to model the real toa measurement errors. One possible future study is to further develop standard algorithms with these models.
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43

Pat, Betty Kila. "Signal transduction pathways in renal fibrosis /." St. Lucia, Qld, 2003. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17739.pdf.

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44

Chang, Wen-Tsan. "Molecular studies of signal transduction and development." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360212.

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45

Moulager, Mickael. "Intégration séquentielle des signaux métaboliques et circadiens dans le contrôle de la division cellulaire d'Ostreococcus tauri." Perpignan, 2008. http://www.theses.fr/2008PERP0874.

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L’horloge circadienne et l’état métabolique sont deux paramètres cellulaires contrôlant de nombreux processus. Mieux connaître les voies d’entrée de ces deux paramètres dans le contrôle de la division cellulaire est essentiel. Chez le picoeucaryote Ostreococcus tauri, ces contrôles se produisent de manière séquentielle au cours de la phase G1. La dissection moléculaire du contrôle métabolique a été réalisée
Circadian clock and metabolic status are two cellular parameters controlling a lot of processes. Better understand input pathways of these two parameters are critical for knowledge of cell division regulation. In the picoeucaryote Ostreococcus tauri, these controls occur in a sequential way along G1. Molecular dissection of the metabolic control was performed
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46

Chasseriau, Jacques. "Coopération entre Bcr-Abl et p95vav pour l'induction de la mobilité cellulaire médiée par les GTPases de la famille Rho." Poitiers, 2006. http://www.theses.fr/2006POIT2302.

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La protéine chimère Bcr-Abl résulte de la translocation chromosomique réciproque t(9 ;22). Cette protéine existe sous deux formes principales : p190bcr-abl, responsable de la Leucémie Aiguë Lymphoblastique, et p210bcr-abl, responsable de la Leucémie Myéloïde Chronique. La seule différence structurale entre ces deux formes est la présence chez p210bcr-abl du domaine DH (Dbl Homology) de Bcr, porteur d'une activité d'échange pour les petites protéines G de la famille Rho. De plus, la protéine p95vav, présentant également un domaine DH, est complexée sous forme activée aux deux formes de Bcr-Abl. Bcr-Abl intervient dans de nombreuses voies de signalisation comme l'inhibition de l'apoptose, la prolifération ou la réorganisation du cytosquelette d'actine. Le travail présenté dans ce mémoire a permis de démontrer que dans l'activation des GTPases de la famille Rho induite par Bcr-Abl, Vav est responsable de l'activation de Rac1 et Bcr-Abl de RhoA. L'activation de Cdc42, induite en partie par Vav, passe certainement par une autre protéine à activité facteur d'échange qui reste à identifier. De plus, nos résultats suggèrent l'existence d'une synergie entre les domaines DH des protéines GEF, facilitant l'activation des GTPases. Enfin, nous avons pu démontrer que l'activité facteur d'échange de Vav n'est pas indispensable au pouvoir transformant de Bcr-Abl et qu'un autre domaine de Vav y participe. Au niveau de la mobilité cellulaire induite par Bcr-Abl, nous avons montré que les mouvements amoeboïdes sont liés à l'activation de RhoA, ce qui contredit certaines données de la littérature. Enfin, nous avons mis en évidence une nouvelle voie d'activation de Rac1 impliquant la protéine Vav2 et la GTPase RhoG. Ces éléments nous ont permis de faire évoluer le modèle d'activation différentielle des petites protéines G de la famille Rho dans le cadre des leucémies et nous avons proposé ce modèle, centré sur l'activation différentielle de RhoA, pour le suivi moléculaire des patients
The chimerical oncogene BCR-ABL is known to induce autonomous motility of leukemic cells. We previously showed that p210bcr-abl responsible for chronic myelogenous leukaemia activates RhoA and Rac1, while p190bcr-abl, associated with acute lymphoid leukaemia, although devoid of a DH domain activates Rac1, but not RhoA. Moreover p95vav is present in an activated state in complex with Bcr-Abl. Here, we investigated the regulation of GEF activities in the BCR-ABL complex. For that purpose, different GEF activity mutants of Vav and of BCR-ABL were constructed and stably transfected in Ba/F3 cells. We demonstrated that RhoA is exclusively activated by the DH domain of p210bcr-abl, while Rac1 activation was only due to Vav. We show that p210bcr-abl induces a specific amoeboid mobility which is due to RhoA activity, while p190bcr-abl induces a rolling type mobility associated with Rac1 activity. Finally, our results reveal a synergistic mechanism between BCR-ABL and Vav GEFs. Moreover, we demonstrated the presence of Vav2 and GTPase RhoG in the complex with Bcr-Abl. This new signaling pathway cooperates with Vav to activate Rac1 and probably Cdc42. Recently, using blood patient samples, we proved that our model of differential activation of Rho GTPases in leukemia disease is valid. We proposed a molecular study to follow up the leukemia diseases of patients
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Rogers, Laura Ann. "Membranes as a hub for cellular signaling /." Access full-text from WCMC, 2007. http://proquest.umi.com/pqdweb?did=1481668281&sid=2&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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48

Kim, Hyun Ji. "Development and signal transduction in Dictyostelium." Thesis, University of Oxford, 1999. http://ora.ox.ac.uk/objects/uuid:4ed80c6e-adc8-46d6-aeaf-c853cef7af77.

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Dictyostelium, is a simple eukaryote that multiplies as separate amoebae. However when nutrients are no longer available it embarks on a developmental programme in which the amoebae collect together by chemotaxis and the resulting aggregates eventually transform into fruiting bodies consisting of a cluster of spores held up on a cellular stalk. The entire process of development normally takes about 24 hours. However there are mutants, termed rapidly developing mutants (rde) which complete development in about two-thirds of this time. RdeA null mutants have been reported to have elevated levels of cyclic AMP that may lead to increased activity of the enzyme, cAMP dependent protein kinase (PKA). I started my work by measuring total cAMP levels in an rdeA mutant along with an aca-/rdeA- double mutant that is expected to have very low level of cAMP due to the absence of the adenylyl cyclase, AC A. Two Dictyostelium adenylyl cyclases were known at the beginning of my work; one is AC A the aggregative enzyme, and the other ACG, expressed only during spore germination. Contrary to expectation, I detected cAMP in aca-/rdeA cells. This raised the question of which enzyme was responsible for producing this cAMP. In collaboration with Dr.Pauline Schaap, I discovered a novel adenylyl cyclase that I initially detected in rdeA and regA mutants but not in wild-type cells. The product of the rdeA gene, RDEA was thought to be an H2-module histidine phosphotrasferase of the kind acting in multi-step phosphorelays. Similarly REGA was believed to be a response regulator associated with a cAMP-phosphodiesterase. It had been proposed that RDEA phosphorylates REGA in a multi-step phosphorelay and it had been shown that it is the phosphorylated form of REGA that is active as a cAMP-PDE. I therefore thought that cAMP produced by the novel AC could be protected in rdeA mutants by the absence of the REGA cAMP-PDE activity and this idea was supported by my finding that the enzyme activity could also be detected in wild-type (aca-) cells when REGA-PDE was inhibited by IBMX. In order to investigate further the proposed phosphorelay model, I tested for possible interaction between RDEA and REGA using the yeast two-hybrid system and also measured intracellular cAMP-phosphodiesterase activity in rdeA and regA mutants. I found that the interaction between RDEA and REGA appeared to be too transient to be detected in the two-hybrid system. In addition rdeA and regA mutants seemed to have levels of intracellular cAMP-phosphodiesterase activity similar to wild type. However REGA-PDE activity measured specifically by immuno-precipitation was completely absent in the regA mutant. It therefore appeared that there is another intracellular cAMP-phosphodiesterase, in addition to the REGA PDE, in Dictyostelium and that the latter cannot be easily detected in total cell lysates. One possible explanation is that the novel adenylyl cyclase exists together with REGA in a complex (that may also include PKA) and that REGA PDE preferentially destroys the cAMP made by the novel adenylyl cyclase. I conclude that rdeA and regA mutants may develop rapidly due to high PKA activity induced by the accumulation of cAMP made by the novel AC when the REGA cAMP-PDE activity is absent.
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49

Harding, Angus Silas. "A biochemical analysis of the MAP kinase pathway in mammalian cells /." A biochemical analysis of the MAP kinase pathway in mammalian cellsRead the abstract of the thesis, 2003. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17885.pdf.

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50

Grandbarbe, Luc. "Rôle de la voie de signalisation Notch dans la différenciation des cellules souches neurales." Université Louis Pasteur (Strasbourg) (1971-2008), 2002. http://www.theses.fr/2002STR13050.

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Le système nerveux central est constitué de 3 types cellulaires majeurs : neurones, oligodendrocytes et astrocytes. Ces cellules dérivent toutes d'un précurseur commun capable d'auto-renouvellement, de prolifération quasi infinie in vitro et multipotentiel : la cellule souche neurale. Dans ce mémoire, nous avons étudié le rôle de la voie de signalisation Notch dans le déterminisme neurones versus cellules gliales, au cours du processus développemental qui conduit de la cellule souche neurale aux neurones, aux oligodendrocytes et aux astrocytes. Pour cela, nous avons utilisé le système in vitro des neurosphères, qui représente la descendance clonale des cellules souches neurales. La première partie de notre travail a consisté de mettre au point les cultures de neurosphères et à montrer que les neurosphères produisaient neurones, oligodendrocytes et astrocytes dans des proportions reproductibles. L'obtention de neurosphères à partir d'embryons Dll1LacZ, mutants pour le gène Delta like 1 (Dll1) a montré que Dll1 n'était pas nécessaire à la production et au maintien des cellules souches neurales. Les neurosphères mutantes Dll1Lac présentent une augmentation du nombre de neurones par rapport aux neurosphères de type sauvage. Cette augmentation a lieu aux dépens des cellules gliales, oligodendrocytes et astrocytes. Le phénotype des neurosphères mutantes peut être sauvé quand les neurosphères Dll1LacZ sont incubées en présence de milieu conditionné par des neurosphères sauvages pendant la phase de prolifération et/ou la phase de différenciation. Les expériences d'activation transitoire de la voie Notch par addition d'une forme soluble de ligand ont montré que la fonction Notch intervenait à deux stades de la neurogenèse : Dans une première étape, la voie Notch empêche les précurseurs de s'engager dans la voie de développement neuronal et les oriente irréversiblement vers la voie gliale. Dans une seconde étape, la voie Notch inhibe la différenciation neuronale et oligodendrocytaire, tandis qu'elle active la différenciation des astrocytes
The central nervous system comprises three major cell types: neurons, oligodendrocytes and astrocytes. All these cell-types derive from a common multipotential precursor cell, capable of self-renewing, and which is referred to as a neural stem cell. To elucidate the role of Notch signaling on the generation of neurons and glia, we made use of the in vitro neurosphère system which is clonally derived from neural stem cells through the selective action of EGF. Neurospheres prepared from Dll1lacZ mutant embryos display an increase of neurons at the expense of both oligodendrocytes and astrocytes. This mutant phenotype could be rescued when Dll1lacZ spheres were grown and/or differentiated in the presence of WT neurospheres conditioned medium. Time-dependant activation of Notch by soluble forms of ligands indicates that Notch acts in two steps. Initially, it acts on the cell fate choice by negatively regulating the neuronal fate and promoting the glial cell fate. In a second step, Notch promotes differentiation of astrocytes and inhibits differentiation of both neurons and oligodendrocytes
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