Dissertationen zum Thema „Signalling“
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Schelfaut, Roselien. „Integrin Signalling“. Thesis, Uppsala University, Department of Medical Biochemistry and Microbiology, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6265.
Integrins are receptors presented on most cells. By binding ligand they can generate signalling pathways inside the cell. Those pathways are a linkage to proteins in the cytosol. It is known that tumor cells can survive and proliferate in the absence of a solid support while normal cells need to be bound to ligand. To understand why tumour cells act that way, we first have to know how ligand-binding to integrins affect the cell. This research field includes studies on activation of proteins by integrins and the following protein-protein interactions.
The part of the research that I did, focused on the activation of PI3K by integrins and the question whether Ras is included in that pathway. I also studied the conformation changes of the integrins and tried to identify factors which regulate these changes.
Known is that Ras can activate PI3K. But we wanted to know if this is a step in the activation of PI3K by integrins. So if this would be a fact then Ras must be activated by integrins.
To see if integrins could activate Ras I did a pull down assay. GTP loaded Ras was isolated through its affinity for Raf. Only when Ras is in its activated state then it is GTP loaded, otherwise it is GDP loaded. In the experiment we also compared the β1A and the β1B splice variants. As result we could see that both splice variants probably can activate Ras. By blotting with anti-PI3K antibody we looked if PI3K had bound to Ras but no clear result could be obtained.
Integrins presented on blood cells are mostly in the inactive state while adherent cells have integrins which are mostly in the active state. PI3K has been shown, for blood cells, to be involved in the conformation regulation of integrins. Possibly, there is a positive circle that for blood cells just has to be switched on. It could be that the integrins in adherent cells are active because the cells are adhesive. By being adhesive, PI3K is activated. PI3K may then activate the integrins, through which the integrins stay in the active state. This circle could be broken at two points: we could inhibit PI3K or we could make the cells un-adhesive. I analysed this in cell attachment assay and by binding of conformation-specific integrin antibodies in FACScan. From the results we could not find any evidence that the whole idea around the positive circle is correct. Surprisingly we saw that the integrin value at the surface decrease if you add PI3K inhibitor. This could be due to distribute recirculation of integrins from the cytoplasm to the cell surface.
β1- and β3-integrins are both widely spread, but no functional difference could be shown already. Previous results suggest that there is a difference between migrations of those two types. To ensure this suggestion I did a wound assay. Hereby I compared the migration of different cell types, with different integrins on their surface and on different ligands.
Demuth, Dirk Geoffrey. „Cannabinoid signalling“. Thesis, University of Hertfordshire, 2004. http://hdl.handle.net/2299/14229.
Potter, Timothy James. „Transmembrane signalling“. Thesis, University of Sheffield, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275041.
O'Byrne, Declan. „CD28 and associated signalling elements of T lymphocyte signalling“. Thesis, University of Bath, 1998. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266468.
Shivdasani, Anish Anil. „Hedgehog signalling, TGF-β signalling and spermatogenesis in Drosophila melanogaster“. Thesis, University of Sheffield, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408836.
Jordan, Lindsay. „Signalling Towards IRES“. Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/19946.
Anderson, Ian Paul. „Met receptor signalling“. Thesis, University of Liverpool, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526784.
Clynes, David Alexander. „Signalling to chromatin“. Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496840.
Samuels, Michael L. „Yeast stress signalling“. Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368116.
Is'Harc, Hayaatun. „JAK/STAT signalling“. Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272414.
Stephens, Sebastien. „Novel Osteoclast Signalling“. Thesis, Griffith University, 2010. http://hdl.handle.net/10072/365823.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
Full Text
Halilagic, Aida. „Retinoid signalling in forebrain development and COUP-TF and retinoid signalling“. Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399574.
Altosaar, Katrin. „Dimer-dependent allosteric modulation within GPCR signalling complexes can influence signalling diversity“. Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114353.
Les récepteurs couplés aux protéines G (RCPG) constituent le plus grand groupe de récepteurs de la surface cellulaire, qui traduisent les signaux environnementaux en réponses cellulaires via leurs protéines G associées. Contrairement à notre compréhension initiale, la majorité des RCPG ne fonctionnent pas en tant que monomères, mais possiblement en tant que dimères ou même oligomères. Les approches actuelles de conception de médicament estiment que lors de la liaison d'un médicament aux deux récepteurs d'un dimère quelconque, ces derniers fonctionnent potentiellement indépendamment l'un de l'autre. Cependant, cette notion a été reconsidérée par une étude récente montrant que la liaison d'un ligand aux deux récepteurs peut les altérer par voie de communication allostérique. Alors qu'un premier récepteur peut être requis pour initialiser la signalisation, un second peut contrôler ou modifier ces signaux, n'ayant pas nécessairement une signalisation directe comme résultante. Dans l'étude suivante, basée sur la notion de modulation allostérique au sein d'homodimère et d'hétérodimère, les changements de signalisation en aval ainsi qu'au niveau du complexe récepteur/protéine G/effecteur (RGE) ont été étudiés et comparés en réponse à différentes combinaisons de ligands pour chaque protomère. En utilisant une combinaison d'essais de signalisation de calcium, d'adénosine monophosphate cyclique (cAMP) et de protéine kinase activée par des agents mitogènes (MAPK), une interaction fonctionnelle entre le récepteur dopaminergique D2 et le récepteur de l'ocytocine (D2R/OTR) a été démontrée dans les cellules HEK 293. Des expériences d'immunoprécipitation, de transfert d'énergie de résonance par bioluminescence (BRET) et de microscopie confocale ont révélé la présence d'hétérodimère entre le D2R et l'OTR in vitro, ce qui pourrait expliquer la nature des interactions fonctionnelles allostériques. En utilisant la technique de BRET, la dynamique fonctionnelle du complexe RGE dans les cellules HEK 293 a été examinée chez deux autres hétérodimères, soit celui composé du récepteur adrénergique β2 et du récepteur cannabinoïde CB1 (β2AR/CB1R) et l'hétérodimère β2AR/OTR, afin de déterminer comment ils traduisent les évènements de signalisation. Ces études démontrent donc qu'une interaction fonctionnelle peut survenir sur le plan de la conformation du complexe de signalisation. Par conséquent, la signalisation d'un RCPG peut être modulée par son récepteur partenaire au niveau des effecteurs ou au niveau du complexe de signalisation lui-même. Pour cette raison, il serait impératif de réanalyser in vivo les propriétés allostériques d'hétérodimères putatifs, ce qui pourrait expliquer certains effets secondaires d'une multitude de médicaments et ce qui pourrait impliquer des changements majeurs dans la façon de concevoir de nouveaux médicaments.
Bryon, K. H. R. „Multiple dopamine signalling pathways antagonize RHO-1 signalling in the nervous system“. Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1419852/.
Li, Xiaolei. „Quadgate forward-signalling pipelines“. Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.442597.
Melford, Steven K. „Calcium signalling in megakaryocytes“. Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364104.
Rebocho, Ana Paula da Mota Torres. „Cellular signalling by Araf“. Thesis, University of London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531334.
McVeigh, P. „Neuropeptide signalling in nematodes“. Thesis, Queen's University Belfast, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411747.
Lindqvist, Susanne. „Colonic crypt calcium signalling“. Thesis, University of East Anglia, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327537.
Sun, Yan. „Cannabinoids and PPARa signalling“. Thesis, University of Nottingham, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431260.
Greig, Aina Vibeke Hiller. „Purinergic signalling in skin“. Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407987.
Brickell, Laura. „Wound signalling Arabidopsis thaliana“. Thesis, University of York, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286054.
Jai-Yoon, Sul. „Calcium signalling in astrocytes“. Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391921.
Sarafimidis, Ioannis. „Polyketide signalling in Dictyostelium“. Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615971.
Lau, C. I. „Hedgehog signalling in haematopoiesis“. Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1428443/.
Benford, Heather Elizabeth. „Signalling in hypothalamic tanycytes“. Thesis, University of Warwick, 2014. http://wrap.warwick.ac.uk/62112/.
Gagliardi, M. „Endocytosis and wingless signalling“. Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1353109/.
Bond, Alistair. „Purinergic signalling in osteoblasts“. Thesis, University of Liverpool, 2012. http://livrepository.liverpool.ac.uk/11293/.
Káradóttir, Raghildur Póra. „Neurotransmitter signalling to oligodendrocytes“. Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1446463/.
Hiskens, Richard Andrew. „The interaction of activator of G protein signalling 1 (AGS1) with signalling components“. Thesis, University of Warwick, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422078.
Brodin, Greger. „Smad7 in TGF-β Signalling“. Doctoral thesis, Uppsala University, Ludwig Institute for Cancer Research, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1949.
Members of the transforming growth factor-β (TGF-β) superfamily of growth and differentiation factors regulate a vast array of biological functions in the adult, and are of great importance in governing cell fate determination and patterning in the developing embryo. The TGF-β signal is propagated intracellularly by Smad proteins resulting in transcriptional responses. Smad6 and Smad7 are inhibitory Smads known to downregulate the TGF-β signal and thereby possibly modulating the biological response. This thesis describes a functional analysis of the inhibitory Smad7 from an in vitro and in vivo perspective.
The prostate gland is dependent on androgens for its growth and differentiation. Androgen withdrawal can cause regression and apoptosis in normal and malignant prostate. Previous studies suggest a role for TGF-β in the apoptotic mechanism. We investigated the expression levels of Smad proteins in the rat ventral prostate as well as in an androgen sensitive prostate tumor model (Dunning R3327 PAP) by immunohistochemistry. We observed an increased immunoreactivity for Smad3, Smad4 and phosphorylated Smad2 in the rat ventral prostate epithelial cells after castration, as well as in the prostate tumor cells. Expression of inhibitory Smad6 and Smad7 were also increased in both normal and malignant prostate in response to castration.
Several studies have shown that Smad7 is upregulated in response to TGF-β stimuli, suggesting a role in a negative feedback loop attenuating the TGF-β response. We investigated the molecular mechanism behind that response by studying the transcriptional regulation of the Smad7 gene. We identified a palindromic Smad binding element (SBE) in the promoter. Point mutations introduced into the SBE abolished transcriptional activation via TGF-β. We also observed that mutating or deleting binding motifs for Sp1 and AP-1, led to an attenuation of the TGF-β mediated transcriptional induction as well as the basal promoter activity.
Gene ablation of Smad proteins has revealed specific physiological and developmental roles. We analysed mice targeted on the Smad7 locus. The mice appeared viable and fertile with a slight reduction in litter size, suggesting a perinatal loss. Biochemical analysis of mouse embryonic fibroblasts (MEFs) showed no major difference between wild type and mutant MEFs.
Cargill, James. „Multitone signalling on telephone lines“. Thesis, University of Ottawa (Canada), 1988. http://hdl.handle.net/10393/5543.
Law, Robert. „PDE3A signalling in blood platelets“. Thesis, University of Hull, 2016. http://hydra.hull.ac.uk/resources/hull:13761.
Tadros, Amir. „Novel pathways in microvascular signalling“. Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/29504.
Kaplan, Andrew Daniel. „Purinoceptor signalling in skeletal cells“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq28500.pdf.
Day, Jonathan Robert Stewart. „Therapeutic inhibition of thrombin signalling“. Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434321.
Haines, Nicola. „Mutational analysis of hedgehog signalling“. Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365823.
Saltmarsh, Esther Joy. „Calcium signalling in neutrophil behaviour“. Thesis, Cardiff University, 2008. http://orca.cf.ac.uk/55796/.
Ludlow, Melanie Joanna. „Purinergic signalling in dictyostelium discoideum“. Thesis, University of Leicester, 2009. http://hdl.handle.net/2381/7450.
Allen, John Cronin. „Neutrophil signalling via Fcγ receptors“. Thesis, University of Liverpool, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.494099.
Brennan, Damian Frederick. „Structural studies of MAPK signalling“. Thesis, Institute of Cancer Research (University Of London), 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511162.
Lee, Sue Chin. „Spatial signalling of phosphatidic acid“. Thesis, University of Strathclyde, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510804.
Dawson, M. A. F. „JAK-STAT signalling at chromatin“. Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598423.
McGouran, Joanna. „Probing sugar-plant-soil signalling“. Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526091.
Moon, Alice E. „Immune signalling in insect cells“. Thesis, Kingston University, 2009. http://eprints.kingston.ac.uk/20407/.
Zhou, Zhigang. „TNF signalling in endothelial cells“. Thesis, University of East Anglia, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.435077.
Iessi, Elisabetta. „TRAIL signalling regulation by ezrin“. Phd thesis, Université de Bourgogne, 2011. http://tel.archives-ouvertes.fr/tel-00695336.
Chen, Daliang. „Cell signalling in Paracoccidioides brasiliensis“. Thesis, Durham University, 2006. http://etheses.dur.ac.uk/2655/.
Schweinzer, Paul Gernot. „Three essays on signalling games“. Thesis, Birkbeck (University of London), 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.442064.
Woodroffe, P. J. „Mathematical modelling of cell signalling“. Thesis, University of Nottingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416886.