Dissertations / Theses on the topic 'Plasma membrane signaling'
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Alenkvist, Ida. "Epac2 signaling at the β-cell plasma membrane." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-284638.
Full textMahammad, Saleemulla. "Cholesterol in T cells homeostasis, plasma membrane organization and signaling /." Doctoral thesis, Stockholm : The Wenner-Gren Institute, Stockholm University, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-38357.
Full textAt the time of the doctoral defense, the following paper was unpublished and had a status as follows: Paper 2: Manuscript. Paper 3: In press.
Takahashi, Satoe. "Plasma Membrane Localization of Signaling Proteins in Yeast: a Dissertation." eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/364.
Full textMichael, James. "Regulation of Ras signaling and oncogenesis by plasma membrane microdomains." Diss., Temple University Libraries, 2016. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/377230.
Full textPh.D.
In this study, we assessed the contributions of plasma membrane (PM) microdomain targeting to the functions of H-Ras and R-Ras. These paralogues have identical effector-binding regions, but variant C-terminal targeting domains (tDs) which are responsible for lateral microdomain distribution: activated H-Ras targets to lipid ordered/disordered (Lo/Ld) domain borders, and R-Ras to Lo domains (rafts). We hypothesized that PM distribution regulates Ras effector interactions and downstream signaling. We used tD swap mutants, and assessed effects on signal transduction, cell proliferation, transformation, and tumorigenesis. R-Ras harboring the H-Ras tD (R-Ras-tH) interacted with Raf, and induced Raf and ERK phosphorylation similar to H-Ras. R-Ras-tH stimulated proliferation and transformation in vitro, and these effects were blocked by both MEK and PI3K inhibition. Conversely, the R-Ras tD suppressed H-Ras-mediated Raf activation and ERK phosphorylation, proliferation, and transformation. Thus, Ras access to Raf at the PM is sufficient for MAPK activation and is a principal component of Ras mitogenesis and transformation. Fusion of the R-Ras extended N-terminal domain to H-Ras had no effect on proliferation, but inhibited transformation and tumor progression, indicating that the R-Ras N-terminus also contributes negative regulation to these Ras functions. PI3K activation was tD-independent; however, H-Ras was a stronger activator of PI3K than R-Ras, with either tD. PI3K inhibition nearly ablated transformation by R-Ras-tH, H-Ras, and H-Ras-tR, whereas MEK inhibition had a modest effect on Ras-tH-driven transformation but no effect on H-Ras-tR transformation. R-Ras-tH supported tumor initiation, but not tumor progression. Whereas H-Ras-tR-induced transformation was reduced relative to H-Ras, tumor progression was robust and similar to H-Ras. H-Ras tumor growth was moderately suppressed by MEK inhibition, which had no effect on H-Ras-tR tumor growth. In contrast, PI3K inhibition markedly suppressed tumor growth by H-Ras and H-Ras-tR, indicating that sustained PI3K signaling is a critical pathway for H-Ras-driven tumor progression, independent of microdomains. In the second phase of the study, we investigated the combinatorial use of two drugs currently either in active use as anti-cancer agents (Rapamycin) or in clinical trials (OTX008), as a novel strategy to inhibit H-Ras-driven tumor progression. H-Ras anchored to the plasma membrane shuttles from the lipid ordered (Lo) domain to the lipid ordered/lipid disordered border upon activation, and retention of H-Ras at these sites requires Galectin-1 (Gal-1). We have previously found that genetically-mediated Lo sequestration of H-Ras inhibited MAPK signaling but not PI3K activation. Here we show that inhibition of Gal-1 with OTX008 sequestered H-Ras in the Lo domain, blocked H-Ras-mediated MAPK signaling, and attenuated H-Ras-driven tumor progression in mice. H-Ras-driven tumor growth was also attenuated by treatment with mTOR inhibitor Rapamycin, and this effect was further enhanced in tumors driven by Lo-sequestered H-Ras. These drugs also revealed bidirectional cross-talk in H-Ras pathways. Moreover, dual pathway inhibition with OTX008 and Rapamycin resulted in nearly complete ablation of H-Ras-driven tumor growth. These findings indicate that membrane microdomain sequestration of H-Ras with OTX008, coupled with mTOR inhibition, may support a novel therapeutic approach to treat H-Ras mutant cancers.
Temple University--Theses
Fröhlich, Florian. "Analysis of sphingolipid-signaling at the plasma membrane of Saccharomyces cerevisiae." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-120516.
Full textWang, Xing. "The locations and signaling of H-Ras on endosomes and plasma membrane." [Ames, Iowa : Iowa State University], 2008.
Find full textDinic, Jelena. "Plasma membrane order; the role of cholesterol and links to actin filaments." Doctoral thesis, Stockholms universitet, Wenner-Grens institut, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-62279.
Full textAt the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 2: Submitted. Paper 4: Manuscript.
Lam, Jonathan Lam. "Identification of mammalian cell signaling in response to plasma membrane perforation: Endocytosis of Listeria monocytogenes and The Repair Machinery." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1543497502225763.
Full textGouguet, Paul. "Deciphering the proteic partners of REMORIN, a membrane-raft phosphoprotein implicated in plant cell-to-cell communication." Thesis, Bordeaux, 2018. http://www.theses.fr/2018BORD0418.
Full textGroup 1 REMORINs are plant-specific proteins located at the plasma membrane. We have shown that StREM1.3 (REM) is a marker of lipid rafts, plasma membrane domains enriched in sterols and sphingolipids. In addition, REM is enriched in plasmodesmata channels (PD) which are anchored within the cell wall and enable intercellular communication between virtually all plant cells. We have demonstrated for the first time the physiological role of REM in plants, this protein is able to reduce the viral cell-to-cell movement of Potato Virus X (PVX) and other viruses. Moreover, the antiviral activity of REM is regulated by phosphorylation and leads to a modification of the pore size of PD via the accumulation of callose, a sugar polymer, around the neck regions of PD. In order to understand how REM is able to induce the accumulation of callose in these specific regions, a large set of proteins have been selected and the deciphering of their functions have been initiated in planta by transgenic approaches, in transient expression and on transgenic plants, which will be subjected to viral infections to study the spread of viruses. Protein interaction, biochemistry and imaging approaches were also used to study this question. This thesis aims at understanding the mechanisms of the REM interaction with its membrane partners during viral infection, focusing on the protein-protein interactions during the response to PVX. We will focus more particularly on PD proteins and membrane rafts that are most likely targeted during this interaction with viruses
LUNGHI, GIULIA. "GM1 OLIGOSACCHARIDE MODULATION OF CALCIUM SIGNALLING IN NEURONAL FUNCTIONS." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/792078.
Full textRusso, Hana. "Active Gasdermin D Forms Plasma Membrane Pores and Disrupts Intracellular Compartments to Execute Pyroptotic Death in Macrophages During Canonical Inflammasome Activation." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1499021688711516.
Full textLevchenko, Victor. "Studies of CA 2+ -signaling and CL-conductance changes in response to abscisic acid, voltage changes and cold, in the plasma membrane of guard cells." kostenfrei, 2009. http://nbn-resolving.de/urn/resolver.pl?urn=nbn:de:bvb:20-opus-45309.
Full textDI, BIASE ERIKA. "GM1 OLIGOSACCHARIDE ACCOUNTS FOR GM1 ROLE IN ENHANCING NEURONAL DEVELOPMENT ACTING ON TRKA-MAPK PATHWAY." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/692335.
Full textThe GM1 ganglioside is a mono-sialylated glycosphingolipid present in the outer layer of the cell plasma membrane and abundant in neurons. Numerous in vitro and in vivo studies highlight the role of GM1 not only as a structural component but also as a functional regulator. Indeed, GM1 enrichment in membrane microdomains promotes neuronal differentiation and protection, and the GM1 content is essential for neuronal survival and maintenance. Despite many lines of evidence on the GM1-mediated neuronotrophic effects, our knowledge on the underlying mechanism of action is scant. Recently, the oligosaccharide chain of GM1 (oligoGM1) has been identified as responsible for the neuritogenic properties of the GM1 ganglioside in neuroblastoma cells. The oligoGM1-mediated effects depend on its binding to the NGF specific receptor TrkA, thus resulting in the TrkA-MAPK pathway activation. In this context, my PhD work aimed to confirm the role of the oligoGM1, as the bioactive portion of the entire GM1 ganglioside, capable of enhancing the differentiation and maturation processes of mouse cerebellar granule neurons. First, we performed time course morphological analyses on mouse primary neurons plated in the presence or absence of exogenously administered gangliosides GM1 or GD1a (direct GM1 catabolic precursor). We found that both gangliosides increased neuron clustering and arborization, however only oligoGM1 and not oligoGD1a induced the same effects in prompting neuron migration. This result suggests the importance of the specific GM1 saccharide structure in mediating neuronotrophic effects. Then we characterized biochemically the oligoGM1-mediated effect in mouse primary neurons, and we observed a higher phosphorylation rate of FAK and Src proteins which are the intracellular key regulators of neuronal motility. Moreover, in the presence of oligoGM1 cerebellar granule neurons showed increased level of specific neuronal markers (e.g., β3-Tubulin, Tau, Neuroglycan C, Synapsin), suggesting an advanced stage of maturation compared to controls. In addition, we found that the oligoGM1 accelerates the expression of the typical ganglioside pattern of mature neurons which is characterized by high levels of complex gangliosides (i.e., GM1, GD1a, GD1b, and GT1b) and low level of the simplest one, the GM3 ganglioside. To study the mechanism of action of the oligoGM1, we used its tritium labeled derivative and we found that the oligoGM1 interacts with the cell surface without entering the cells. This finding suggests the presence of a biological target at the neuronal plasma membrane. Interestingly, we observed the TrkA-MAP kinase pathway activation as an early event underlying oligoGM1 effects in neurons. Our data reveal that the effects of GM1 ganglioside on neuronal differentiation and maturation are mediated by its oligosaccharide portion. Indeed, oligoGM1 interacts with the cell surface, thus triggering the activation of intracellular biochemical pathways that are responsible for neuronal migration, dendrites emission and axon growth. Overall, our results point out the importance of oligoGM1 as a new promising neurotrophic player.
Laurent, Nelson. "Caractérisation des mécanismes régulant les modifications de la structuration membranaire induites dans la signalisation des réponses de défense des plantes." Thesis, Bourgogne Franche-Comté, 2020. http://www.theses.fr/2020UBFCK026.
Full textSpatial distribution of pasma membranes (PM) components is tightly regulated to provide the cell an optimal physiological state. The level of order degree is a suitable parameter to study PM organization, reflecting the intensity of interactions taking place between PM components and so the level of their packing. During our work, we used the environment sensitive probe di-4-ANEPPDHQ to assess the level of order degree of tobacco BY-2 cells PM in different situations: during the time-course of cell regeneration and in the particular case of an elicitation by cryptogein.We measured that the level of order degree of PM is modulated during the slow process of cell regeneration. This regulation isn’t related to the cell wall neo-synthesis neither the cell morphology, but is correlated to the differentiation state. The mapping of the level of order degree along the PM perimeter of protoplasts and suspension cells revealed a global common organization with a mosaic like distribution of domains (288X288 nm) exhibiting high diversity of level of order degree. The two models differed by the organization of this mosaic, the cell PM exhibiting enrichment in highest ordered domains in a specific area between two adjacent cells. Then, we discus about a possible involvement of membrane trafficking in the regulation of the level of order degree allowing specific targeting of lipids/proteins, and subsequent cellular identity acquisition.A pharmacological approach allowed the identification of the reactive oxygen species involved in the PM reorganization observed at the surface of tobacco BY-2 cells in response to cryptogein. We report that H2O2 has similar effects on the PM level of order degree compared to cryptogein’s one, both acting doses dependently. Furthermore, a partial inhibition of the H2O2 accumulation occurring in response to cryptogein is linked to a partial inhibition in the increase of the level of order degree usually induced by cryptogein. Those results suggest that H2O2 could finely regulates The PM level of order degree during the response of tobacco cells to cryptogein. The potential mechanisms involved has been studied. Two current hypotheses were studied in parallel, and both were rejected. The first one involves a modification of PM composition by an arrival of ordered domain to the PM. In the second one, a de novo formation of PM component structure. So, we discuss about a new role for H2O2, which would act directly on the PM level of order degree
Salavessa, Laura. "Single-molecule analysis of IL-2 receptor reveals the importance of its clustering for endocytosis and signaling in lymphocytes Shigella promotes major alteration of gut epithelial physiology and tissue invasion by shutting off host intracellular transport Stoichiometry of receptors at the plasma membrane during their endocytosis using Total Internal Reflection Fluorescent (TIRF) microscopy live imaging and single molecule tracking." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL031.
Full textSignaling by the interleukin-2 receptor (IL-2R) is regulated by its clathrin-independent endocytosis (CIE) and subsequent degradation, while playing a critical role in immunity. Interestingly, CIE lacks a coat protein that drives pit formation, raising the question of how the CIE vesicle is initiated. Protein clustering generates forces that can induce membrane conformational changes. Notably, IL-2R has been shown to accumulate at the base of membrane protrusions, where receptors might cluster and thereby initiate the pit.To study the relevance of IL-2R clustering in its endocytosis, we generated a CRISPR-edited T cell line expressing GFP-IL-2Rᵧ and analyzed its stoichiometry at the plasma membrane, by TIRF microscopy coupled to a single-molecule endocytic tracking method. We identified distinct IL-2Rᵧ cluster populations. IL-2Rᵧ seems to reach the cell surface as a preassembled cluster to which further molecules are added, reaching an optimal cluster size that is key for its internalization. Binding of IL-2 promotes the formation of endocytic clusters and receptor uptake, highlighting the importance of clustering for CIE internalization.Moreover, we found that cholesterol depletion increases the proportion of large, non-endocytic clusters as well as IL-2R signaling. Disruption of the actin meshwork also promotes the formation of large clusters, yet it decreases IL-2R signaling. Thus, both factors regulate IL-2R endocytosis and signaling in a distinct manner. Our results provide new insights into the mechanisms regulating receptor signaling and CIE
Jeyaseelan, B. R. J. "PLASMA MEMBRANE SIALIDASE NEU3 SILENCING EFFECTS ON THE MOLECULAR PHENOTYPE OF MELANOMA CELLS." Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/480824.
Full textBernecic, Naomi Charlotte. "Identifying the regulatory mechanisms underlying cholesterol efflux from the sperm plasma membrane during capacitation." Thesis, The University of Sydney, 2019. http://hdl.handle.net/2123/20811.
Full textJames, Andrew. "Metabolic regulation of the plasma membrane calcium pump in pancreatic ductal adenocarcinoma." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/metabolic-regulation-of-the-plasma-membrane-calcium-pump-in-pancreatic-ductal-adenocarcinoma(0533b59c-e6ee-41fb-ad32-cb4784eadfa1).html.
Full textGreen, Toni. "Membrane Protein Complexes Involved in Thrombospondin-1 Regulation of Nitric Oxide Signaling." Diss., The University of Arizona, 2013. http://hdl.handle.net/10150/293333.
Full textMohamed, Tamer M. A. "Identification of the molecular mechanisms by which plasma membrane calcium ATPase isoforms 1 and 4 regulate cardiac signalling." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493674.
Full textBaggott, Rhiannon Rebecca. "Role of the plasma membrane calcium ATPase as a negative regulator of angiogenesis." Thesis, University of Wolverhampton, 2014. http://hdl.handle.net/2436/332139.
Full textFröhlich, Florian [Verfasser]. "Analysis of sphingolipid signaling at the plasma membrane of Saccharomyces cerevisiae / vorgelegt von Florian Fröhlich." 2010. http://d-nb.info/1007185333/34.
Full textHartung, Anke. "Localization of BMP receptors in distinct plasma membrane domains and its impact on BMP signaling." Doctoral thesis, 2006. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-18360.
Full textEndozytose von Wachstumsfaktor-Rezeptoren spielt eine entscheidende Rolle bei Aktivierung und Übertragung wie auch bei der Schwächung von Signalen. Störungen der Endozytose können schwere Krankheitsbilder hervorrufen, z.B. durch ihren Einfluss auf die Regulation der Rezeptormenge an der Zelloberfläche. BMPs sind Mitglieder der TGF-ß Superfamilie und sind involviert in die Regulation von Proliferation, Differenzierung, Chemotaxis und Apoptose. Zwei Arten von Transmembranproteinen, die Serin/Threonin-Kinase Aktivität besitzen, sind bedeutend für den BMP Signalweg – die BMP Rezeptoren BRI und BRII. Die Aktivierung von BRI und BRII erfolgt durch Ligandenbindung an präformierte Komplexe (PFCs) oder BMP2-induzierte Signalkomplexe (BISCs), die aus beiden Rezeptorarten bestehen. Wenn BMP2 an PFCs bindet, wird die Smad-Signalkaskade initiiert, wohingegen BISCs Smad-unabhängige Signale über p38 weiterleiten, was schließlich zur Produktion von alkalischer Phosphatase (ALP) führt. Das Feld der BMP Rezeptor Endozytose wurde noch nicht sehr ausführlich untersucht, genauso wenig wie die potentielle Rolle, die unterschiedliche Rezeptorlokalisierungen in verschiedenen Plasmamembran-Regionen bei der Initiierung der Signalwege, die durch PFCs bzw. BISCs aktiviert werden, spielen könnten. In der vorliegenden Arbeit wurden die Lokalisierung von BMP Rezeptoren in speziellen Membrandomänen sowie deren Einfluss auf die BMP Signalkaskade untersucht. Mittels Reinigung von Detergenz-resistenten Membranen (DRMs) aus Zelllysaten und anschließender Gradientenultrazentrifugation konnte gezeigt werden, dass BRI und BRII mit dem caveolären Markerprotein cav-1 kofraktionieren. Darüber hinaus interagieren beide Rezeptorarten mit cav-1 und kolokalisieren auch teilweise mit cav-1 an der Plasmamembran. Obwohl diese Ergebnisse auf ein eindeutiges Vorkommen der Rezeptoren in Caveolae schließen lassen, kofraktionieren sie auch mit DRMs in Zellen, die von Natur aus keine Caveolae ausbilden, woraus man eine zusätzliche nichtcaveoläre Raft-Lokalisierung schlussfolgern kann. Des Weiteren konnte BRII mittels Immun- Elektronenmikroskopie in „clathrin-coated pits“ (CCPs) lokalisiert werden. Im zweiten Teil der Arbeit wurde gezeigt, dass beide untersuchten Membranregionen die BMP Signalkaskade auf unterschiedliche Art und Weise beeinflussen. Es wurde bewiesen, dass Smad1/5 unabhängig von endozytotischen Vorgängen an der Plasmamembran phosphoryliert wird. Einerseits führte die Zerstörung von DRM-Regionen durch Cholesterindepletion zur spezifischen Inhibierung der BMP2-vermittelten ALP Produktion, ohne gleichzeitig die BMP Signalkaskade über Smads zu beeinflussen. Andererseits bewirkte eine spezifische Blockierung der Clathrin-vermittelten Endozytose eine Inhibition des BMP2-induzierten Smad-Signalwegs und auch der ALP Produktion, was auf ein Zusammenspiel von Smad-unabhängigen und Smad-abhängigen Signalwegen bei der ALP-Induzierung schließen lässt. Die Ergebnisse der vorliegenden Studie lassen die Schlussfolgerung zu, dass verschiedene endozytotische Wege und Membranregionen einen bedeutenden, regulatorischen Einfluss auf die BMP Signalkaskade ausüben. Weiterhin wurde festgestellt, dass die Membranlokalisierung von BMP Rezeptoren für das Einschlagen verschiedener Signalwege ausgehend von PFCs und BISCs verantwortlich ist
Hartung, Anke [Verfasser]. "Localization of BMP receptors in distinct plasma membrane domains and its impact on BMP signaling / vorgelegt von Anke Hartung." 2006. http://d-nb.info/980952336/34.
Full textBrejchová, Jana. "Úloha membránového cholesterolu v signalizaci delta-opioidního receptoru Korelace se strukturou plazmatické membrány." Doctoral thesis, 2014. http://www.nusl.cz/ntk/nusl-338451.
Full textLevchenko, Victor [Verfasser]. "Studies of Ca2+-signaling and Cl--conductance changes in response to abscisic acid, voltage changes and cold, in the plasma membrane of guard cells / vorgelegt von Victor Levchenko." 2009. http://d-nb.info/1000578437/34.
Full textMelcrová, Adéla. "Studium modelových membrán pokročilými fluorescenčními technikami a molekulárně dynamickými simulacemi." Doctoral thesis, 2019. http://www.nusl.cz/ntk/nusl-398649.
Full textOstašov, Pavel. "Vliv deplece cholesterolu na signální dráhu iniciovanou receptory spřaženými s G proteiny třídy Gq/G11." Doctoral thesis, 2011. http://www.nusl.cz/ntk/nusl-297733.
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