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1
Maximano, Filipe Manuel Correia. "Armus : A novel link between Rac and Rab small GTPases." Thesis, Imperial College London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526397.
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Sadou, Amel. "Cross-talk between ral and rac pathways in the control of cell migration." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA11T010.
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Le mode de coordination parmi les différentes molécules qui régulent la migration reste très peu connu. Ce travail traite de deux voies de transduction régulant la migration: la voie Rac1/WRC (Wave Regulatory Complex) qui contrôle la formation du réseau d’actine au front des cellules migrantes, et la voie RalB/exocyst, dont les mécanismes moléculaires de son implication dans la motilité cellulaire étaient inconnus au début de cette thèse. Rac1 et RalB sont des petites protéines G des familles Rho et Ras, respectivement. Les complexes WRC et exocyst sont leurs effecteurs directs.Au cours de la recherche de connexions entre l’exocyst et des régulateurs de la migration, nous avons trouvé que deux sous-unités de l’exocyst, Exo70 et Sec6, interagissent directement in vitro avec Abi et Cyfip, respectivement, deux sous unités du WRC. De plus, nous avons trouvé que les sous-unités de l’exocyst peuvent interagir in vitro avec le WRC entier. Nous avons également montré que ces deux complexes s’associent in vivo. Sur le plan fonctionnel, l’exocyst est requis pour le positionnement du complexe WRC au front des cellules migrantes. D’autre part, nous avons également trouvé que deux autres sous- unités de l’exocyst Sec8 et Exo84, interagissent avec SH3BP1 (une RhoGAP) en double hybride et en co-immunoprécipitation. SH3BP1 se localise au front des cellules migrantes, et cette localisation dépend de l’exocyst. De façon intéressante, in vivo, la voie RalB/exocyst/SH3BP1 cible spécifiquement Rac1, et non Cdc42. Grâce à plusieurs approches, nous concluons que SH3BP1 est requis pour inactiver Rac1 au front. Dans notre modèle nous proposons que RalB/exocyst règulerait la migration cellulaire en véhiculant au front de migration deux éléments majeurs de la signalisation de Rac1 : son complexe effecteur WRC, qui stimule la nucléation de filaments d’actine et son régulateur négatif SH3BP1, une GAP qui promeut l’inactivation et le cycle GDP/GTP de Rac1. En conclusion, ce travail fournit de nouvelles connexions moléculaires et fonctionnelles entre l’exocytose polarisée et la dynamique de l’actine au cours de la motilité cellulaireVery little is known about the coordination and the integration among the different regulators of the motility process. This work deals with two migration-regulatory pathways: the Rac1/WRC (Wave Regulatory Complex) pathway that drives the formation of the actin polymerization network at the front of motile cells; and RalB/exocyst pathway for which the molecular mechanisms underlying its implication in cell motility were still largely unknown at the beginning of this thesis. Rac1 and RalB are small GTPases of the Rho and Ras family, respectively. WRC and exocyst complexes are their direct effectors.In searching for connections between the exocyst and migration regulators, we found that two subunits of the exocyst, Exo70 and Sec6, interact directly in vitro with two subunits of the WRC, Abi and Cyfip, respectively. Moreover, we found that exocyst subunits can interact in vitro with the whole fully-assembled WRC complex. We also showed that these two complexes associate in vivo. Functionally, the exocyst was required for WRC complex positioning at the front of migrating cells.On the other hand, we also found that two other subunits of the exocyst, Sec8 and Exo84, interact with SH3BP1 (a RhoGAP protein) by two-hybrid assay and by co-immunoprecipitation. SH3BP1 localizes at the leading edge and this localization is dependent on the exocyst. Interestingly, in vivo, the RalB/exocyst/SH3BP1 pathway specifically targets Rac1, and not Cdc42. By a combination of approaches we concluded that SH3BP1 is required to inactivate Rac1 at the front.In our model we propose that RalB/exocyst regulates cell migration by driving to the leading edge two key signaling elements of the Rac1 pathway: its effector WRC, that stimulates actin filament nucleation, and its negative regulator SH3BP1, a GAP promoting Rac1 inactivation and GDP/GTP cycling. In conclusion, this work provides novel molecular and functional links between polarized exocytosis and actin dynamics during cell motility
3
SADOU, AMEL. "CROSS-TALK BETWEEN RAL AND RAC PATHWAYS IN THE CONTROL OF CELL MIGRATION." Doctoral thesis, Università degli Studi di Milano, 2012. http://hdl.handle.net/2434/214614.
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SUMMARY (English)
Very little is known about the coordination and the integration among the different regulators of the motility process. This work deals with two migration-regulatory pathways: the Rac1/WRC (Wave Regulatory Complex) pathway that drives the formation of the actin polymerization network at the front of motile cells; and RalB/exocyst pathway for which the molecular mechanisms underlying its implication in cell motility were still largely unknown at the beginning of this thesis. Rac1 and RalB are small GTPases of the Rho and Ras family, respectively. WRC and exocyst complexes are their direct effectors.
In searching for connections between the exocyst and migration regulators, we found that two subunits of the exocyst, Exo70 and Sec6, interact directly in vitro with two subunits of the WRC, Abi and Cyfip, respectively. Moreover, we found that exocyst subunits can interact in vitro with the whole fully-assembled WRC complex. We also showed that these two complexes associate in vivo. Functionally, the exocyst was required for WRC complex positioning at the front of migrating cells.
On the other hand, we also found that two other subunits of the exocyst, Sec8 and Exo84, interact with SH3BP1 (a RhoGAP protein) by two-hybrid assay and by co-immunoprecipitation. SH3BP1 localizes at the leading edge and this localization is dependent on the exocyst. Interestingly, in vivo, the RalB/exocyst/SH3BP1 pathway specifically targets Rac1, and not Cdc42. By a combination of approaches we concluded that SH3BP1 is required to inactivate Rac1 at the front.
In our model we propose that RalB/exocyst regulates cell migration by driving to the leading edge two key signaling elements of the Rac1 pathway: its effector WRC, that stimulates actin filament nucleation, and its negative regulator SH3BP1, a GAP promoting Rac1 inactivation and GDP/GTP cycling. In conclusion, this work provides novel molecular and functional links between polarized exocytosis and actin dynamics during cell motility.
4
Di, Niro Gaetano. "Recycled aggregate concrete (RAC) for structural purposes." Thesis, University of Strathclyde, 1999. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=21124.
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The possibility of using demolished concrete waste as aggregate in fresh concrete in the production of prestressed concrete beams is checked in this research. As opposed to the use for road foundations or as fill-in material the use of the Recycled Aggregate (RA) for concrete structures requires more tests and processing of results. In fact to be able to use a material for construction it is essential to assess more than just its compressive strength. After the physical and chemical characteristics of the RA and the properties of both the wet and hardened Recycled Aggregate Concrete (RAC) have been determined, it is important to check if the mathematical models and numerical correlation normally used for design of ordinary concrete (such as mix-design procedure, design codes, non-linear analysis) are suitable for RAC. For this reason the main task of this investigations has been to ensure that RAC has satisfactory mechanical performance for structural use and later to guarantee a consistency of the results using methods checked for RAC. A mix-design procedure suitable for RAC to attain the desired workability and the target strength was the first step. Tests on durability of RA and RAC have been performed and the results reported. Finally three 15.0 metres span prestressd beams cast with different percentages of RA (one with 100% of RA, one with 100% of Natural Aggregate NA, and one with 50% of RA and 50% of NA) have been tested. The results show that it is practicable to make prestressed concrete elements using concrete made with Recycled Aggregate and that these elements can have satisfactory and predictable mechanical performance.
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Brentzel, Kelvin, Patrick Coronado, Barbie Brown, Parminder Ghuman, and Carol Harris. "A Regional Application Center (RAC) Ingest System." International Foundation for Telemetering, 1999. http://hdl.handle.net/10150/607319.
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International Telemetering Conference Proceedings / October 25-28, 1999 / Riviera Hotel and Convention Center, Las Vegas, NevadaOver the next ten years, NASA’s Earth Science Enterprise Program is scheduled to deploy a series of remote sensing satellites that require high-rate downlinks. As part of the program, a goal has been defined to provide the user community with a low-cost solution for receiving this Earth Science spaceborne remotely sensed data. This paper describes one approach, the High-Rate Ingest System (HRIS), which can serve as a gateway between the satellites and the information systems. HRIS is capable of ingesting a UQPSK downlink at rates up to 200Mbps in real-time and provide a level 0 data product with rapid turnaround. The commercial components of the HRIS include a high performance 3.1-meter antenna system, a DEC Alpha workstation, and a RAID storage system. Within the DEC Alpha workstation are advanced technology hardware and software components that will become available for commercialization. The paper describes the architecture and proposed application of the HRIS as a complete end-to-end ingest solution for regional sites. In addition, collaborative commercial efforts and technologies, along with Goddard’s technology prototyping efforts will also be presented as part of HRIS.
6
Fan, Wing-Tze. "Characterization of Ras-GRF2, a bifunctional guanine nucleotide exchange factor for the Ras and Rac GTPases." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ63720.pdf.
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Sadou, Amel. "Connexions entre les voies ral et rac dans le contrôle de la migration cellulaire." Phd thesis, Université Paris Sud - Paris XI, 2012. http://tel.archives-ouvertes.fr/tel-00701484.
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Le mode de coordination parmi les différentes molécules qui régulent la migration reste très peu connu. Ce travail traite de deux voies de transduction régulant la migration: la voie Rac1/WRC (Wave Regulatory Complex) qui contrôle la formation du réseau d'actine au front des cellules migrantes, et la voie RalB/exocyst, dont les mécanismes moléculaires de son implication dans la motilité cellulaire étaient inconnus au début de cette thèse. Rac1 et RalB sont des petites protéines G des familles Rho et Ras, respectivement. Les complexes WRC et exocyst sont leurs effecteurs directs.Au cours de la recherche de connexions entre l'exocyst et des régulateurs de la migration, nous avons trouvé que deux sous-unités de l'exocyst, Exo70 et Sec6, interagissent directement in vitro avec Abi et Cyfip, respectivement, deux sous unités du WRC. De plus, nous avons trouvé que les sous-unités de l'exocyst peuvent interagir in vitro avec le WRC entier. Nous avons également montré que ces deux complexes s'associent in vivo. Sur le plan fonctionnel, l'exocyst est requis pour le positionnement du complexe WRC au front des cellules migrantes. D'autre part, nous avons également trouvé que deux autres sous- unités de l'exocyst Sec8 et Exo84, interagissent avec SH3BP1 (une RhoGAP) en double hybride et en co-immunoprécipitation. SH3BP1 se localise au front des cellules migrantes, et cette localisation dépend de l'exocyst. De façon intéressante, in vivo, la voie RalB/exocyst/SH3BP1 cible spécifiquement Rac1, et non Cdc42. Grâce à plusieurs approches, nous concluons que SH3BP1 est requis pour inactiver Rac1 au front. Dans notre modèle nous proposons que RalB/exocyst règulerait la migration cellulaire en véhiculant au front de migration deux éléments majeurs de la signalisation de Rac1 : son complexe effecteur WRC, qui stimule la nucléation de filaments d'actine et son régulateur négatif SH3BP1, une GAP qui promeut l'inactivation et le cycle GDP/GTP de Rac1. En conclusion, ce travail fournit de nouvelles connexions moléculaires et fonctionnelles entre l'exocytose polarisée et la dynamique de l'actine au cours de la motilité cellulaire.
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Bishop, Anne Louise. "Functional analysis of the Rac binding protein POSH." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248466.
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Rooney, Claire. "A role for the Rac GEF, STEF, in cell migration, polarization and Ras-induced transformation." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492898.
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Tiam1 (for T-lymphoma invasion and metastasis-inducing protein) belongs to the Rho GEF family of proteins. In response to growth factors and cell-substrate interactions, Tiam1 selectively activates Rac. Using a two stage chemical carcinogenesis protocol (DMBA/TPA) it was previously shown that mice lacking Tiam1 are resistant to the development of Ras-induced skin tumours, suggestmg an important role for Tiam1/Rac signalling in tumourigenesis in vivo.
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Ni, Wenjun. "Involvement of Rac GTPase in p53-deficiency mediated lymphomagenesis." Cincinnati, Ohio : University of Cincinnati, 2006. http://rave.ohiolink.edu/etdc//view?acc_num=ucin1155831060.
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Xiao, Feipeng. "Development of fatigue predictive models of rubberized asphalt concrete (RAC) containing reclaimed asphalt pavement (RAP) mixtures." Connect to this title online, 2006. http://etd.lib.clemson.edu/documents/1171902609/.
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Francis, Richard Edward. "Functional and biochemical characterisation of a novel Rac binding protein." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429102.
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Tapon, Nicolas Alexandre Marie. "Identification of new targets for the Rho and Rac GTPases." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286591.
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Ng, Wai-Hung, and Tony Leung. "INVESTIGATION OF CHIRP INTERFERENCE ON M-FSK DEMODULATION USING RAC." International Foundation for Telemetering, 1990. http://hdl.handle.net/10150/613764.
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International Telemetering Conference Proceedings / October 29-November 02, 1990 / Riviera Hotel and Convention Center, Las Vegas, NevadaRecently, many satellite systems started to employ reflective-array compressor (RAC) to demodulate their M-FSK communication signals. Because the RAC’s time delay varies with the temperature, pilot-tones are usually introduced as the operational reference. In this paper, the basic chirp Fourier transform (CFT) is briefly reviewed. Then, investigation into possible pilot-tone interference caused by various chirp signals with RAC’s dispersive delay properties is presented and discussed.
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Ogg, Erinn-Lee. "The role of Tiam1/Rac signalling in the centriole cycle." Thesis, University of Manchester, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.684817.
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The mitotic spindle is a structure that facilitates the equal segregation of DNA into two daughter cells during mitosis. The centrosomes organise the mitotic spindle in to a bipolar conformation, and this arrangement is essential for maintaining faithful chromosome segregation. Deviations in centrosome number alter the structure of the spindle and this can promote multipolar cell divisions and large scale aneuploidy. Therefore centrosome number is tightly regulated in normal cells to prevent interference with bipolar spindle assembly and faithful chromosome segregation. Tumour cells often have supernumerary centrosomes. To prevent interference with bipolar spindle assembly extra centrosomes are clustered in to a bipolar spindle arrangement – preventing a multipolar cell division and intolerable levels of aneuploidy. However centrosome clustering can promote lagging chromosomes during anaphase, a major contributor to chromosomal instability. Chromosomal instability has been shown to enhance the malignant potential of tumour cells. Therefore it is important to understand the mechanisms involved in regulating centrosome number and how these become deregulated in cancer. Centrosome number is regulated by the centrioles, small barrel shaped organelles found within the core of the centrosome. We have identified Tiam1, a Rac specific guanine nucleotide exchange factor, as a novel regulator the centriole cycle. Tiam1 knockdown is sufficient to promote the assembly of multiple aberrant centriole structures in human tumour cell lines. These aberrant centriole structures behave like functional centrioles and correlate with an increase in lagging chromosomes at anaphase – suggesting these structures are capable of promoting chromosomal instability in human tumour cell lines. Moreover we have shown that Tiam1 regulates centriole number by preventing centriole re-duplication events and significantly this effect is independent of Rac activation. We have also identified MCM5 as a novel Tiam1 interactor. MCM5 has been identified in the literature as a regulator of centrosome re-duplication. Therefore we propose that Tiam1 and MCM5 co-operate to prevent centriole re-duplication in human tumour cell lines. These findings identify Tiam1 as a potential prognostic marker of centriole amplification and chromosomal instability in human tumours.
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Edme, Natacha. "Rôles des voies MAPK et Rac dans la transition épithélium-mésenchyme des cellules NBT-II activée par Ras." Paris 11, 2001. http://www.theses.fr/2001PA112298.
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La transition épithélium-mésenchyme (TEM) correspond à la perte du phénotype épithélial des cellules avec internalisation de leurs jonctions intercellulaires et à l'acquisition d'un phénotype fibroblastique avec acquisition de mobilité cellulaire. Le facteur de croissance épithélial (EGF) induit la TEM des cellules de carcinome vésical de rat NBT-II par une voie de signalisation dépendant des protooncogènes Ras et Src. Ras est une GTPase connue pour avoir plusieurs d'effecteurs, dont c-Raf qui active la voie MAPK, la PI3K, Ra1GDS, Rac. L'objectif de ce travail de thèse a été de déterminer quels sont les effecteurs de Ras activant la TEM. Par différentes approches, nous avons pu montrer que parmi tous les effecteurs de Ras, ce sont c-Raf et Rac qui jouent un rôle essentiel. En effet, l'inhibition de la voie qu'ils activent ou de leurs activités propres aboutit au blocage de la TEM induite par Ras ou par l'EGF. Bien que MEK1, un composant de la voie des MAPK et Rac1 pris isolément, ne soient pas suffisants pour induire la dispersion des cellules NBT-II, la coactivation de ces deux facteurs induit la TEM des cellules NBT-II. La migration des cellules induite par l'EGF ou Ras n'est pas inhibée par l'inhibiteur de la PI3K, ce qui indique que la PI3K ne participe pas à l'activation de la migration des cellules NBT-II. Afin de confirmer que Rac est le signal inducteur de la migration des cellules NBT-II, nous avons étudié les mécanismes d'activation de Rac dans les cellules NBT -II. L'EGF et la surexpression stable ou transitoire d'une forme active dominante de Ras induit l'activation de Rac. De plus, les mutants actifs de MEK1 et p110 n'activent pas Rac et l'inhibition de chacune de ces 2 voies ne bloque pas l'activité Rac induite par Ras ou l'EGF. D'une part, ces résultats suggèrent que l'activation de Rac par l'EGF et par Ras ne dépend pas des voies MAPK et PI3K et d'autre part, ils confirment que la voie PI3K ne participe pas à la migration cellulaire induite par RacCell dissociation and cell migration are two main components of epithelium- mesenchyme transitions (EMT). We have previously demonstrated that Ras is required in the accomplishment of both of these during the EGF-induced EMT of the NBT-II rat carcinoma cell line in vitro. In this study, we examined the downstream targets of Ras responsible for the dissociation and motility of NBT -II cells. Overexpression of activated forms of c-Raf and MEK1 (a component of the Mitogen Activated Protein Kinase pathway, MAPK), led to cell dissociation as inferred by the loss of desmosomes from the cell periphery. In contrast, active PI3K, Ra1A and Ra1B did not induce desmosome breakdown. The MEK1 inhibitor PD098059 inhibited EGF- and Ras-induced cell dispersion whereas the PI3K inhibitor LY294002 had no effect. Accordingly, among the partial loss of function mutants of Ras (RasV12) that distinguish between downstream targets of Ras, we found that the Raf-specific Ras mutants RasV12S35 and RasV12E38 induced cell dissociation. The PI3K- and Ra1GDS-activating Ras mutants had in contrast no effect on cell dispersion. However, MEK1 was unable to promote cell motility, whereas RasV12S35 and RasV12E38 induced cell migration, suggesting that another Ras effector was responsible for cell motility. We round that the small GTPase Rac is necessary for EGF-mediated cell dispersion since overexpression of a dominant-negative mutant of Rac1 (Rac1N17) inhibited EGF-induced NBT-Il cell migration. All stimuli that promoted cell migration also induced Rac activation. Finally, coexpression of active Rac1 and active MEK1 induced the motility of NBT-II cells suggesting that Ras mediates NBT-II cell scattering through the coordinate activation of Rac and Raf/MAPK pathways
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Smith, Harvey W. "Signalling from uPAR to the Activation of the Small GTPase Rac." Thesis, Institute of Cancer Research (University Of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499157.
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Ooi, Steen Kian Thye. "The role of RAC GTPases in B cell development and activation." Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406427.
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Shutes, Adam. "The small G-protein Rac nucleotide exchange and interactions with IQGAP." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272074.
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Nsaibia, Mohamed Jalloul. "Rôle d'autotaxine (ATX) dans le développement du rétrécissement aortique calcifié (RAC)." Doctoral thesis, Université Laval, 2018. http://hdl.handle.net/20.500.11794/31586.
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Le rétrécissement aortique calcifié (RAC), pathologie valvulaire la plus fréquente, est une maladie caractérisée par une minéralisation progressive de la valve. À l’heure actuelle, il n’existe aucun traitement médical efficace pouvant empêcher ou ralentir sa progression. Le remplacement valvulaire aortique (RVA) est le seul traitement disponible du RAC. Par conséquent, l'identification des principaux facteurs de risque ainsi que les processus moléculaires impliqués dans la pathogenèse du RAC représentent une nécessité primordiale pour développer des approches pharmacologiques. Le RAC est une maladie progressive caractérisée par une calcification ectopique des feuillets valvulaires. Pendant plusieurs années, elle était considérée comme une atteinte dégénérative liée au vieillissement. Néanmoins, de nombreuses études récentes ont révélé qu’il s’agit d’une maladie active. En effet, les premiers stades de cette maladie, nommée sclérose aortique, partagent plusieurs similitudes avec l’athérosclérose en termes de facteurs de risque associés. Il s’agit donc d’une pathologie complexe mettant en jeu plusieurs processus pathologiques, notamment la rétention des lipides et leur oxydation, l’inflammation chronique, le remodelage fibrotique et la calcification de la VA. À cet égard, l'identification des principaux facteurs de risque ainsi que les processus moléculaires par lesquelles les lipides favorisent la minéralisation de la valve aortique (VA) représentent une nécessité primordiale pour comprendre le mécanisme physiopathologique du RAC. Cela pourrait également aider à identifier de nouvelles cibles thérapeutiques et ouvre d’autres perspectives de recherche afin de développer de nouvelles thérapies médicales. Les objectifs généraux de mon projet de doctorat sont : (1) Étudier le rôle des lipides, en particulier l’axe lipoprotéine Lp (a)-autotaxine (ATX), dans la progression et le développement du RAC; (2) Élucider le mécanisme d’action par lequel l’acide lysophosphatidique (LPA), le produit final de l’enzyme ATX, favorise l’inflammation et la réponse ostéogénique des cellules interstitielles de la valve aortique (CIVs); (3) Déterminer le rôle de l’axe ATX-LPA dans un modèle murin du RAC.Calcific aortic valve disease (CAVD) is the most common valvular disease, which is characterized by a progressive mineralization of aortic valve. So far, there is no effective medical therapy able to stop or slow the natural course of this disease. Surgical aortic valve replacement is the only available treatments of severe symptomatic aortic stenosis. Therefore, identify the key factors as well as molecular processes involved in the pathogenesis of CAVD is crucial to develop efficient pharmaceutical approaches able to prevent or to slow the progression of aortic stenosis. CAVD is a progressive disease characterized by ectopic calcification of the aortic valve leaflets. It has long been considered as a degenerative process of the aortic valve linked to aging. However, a growing number of studies have revealed that this disease is an active process likely related to atherosclerosis. Therefore, CAVD seems to be a complex pathology involving several pathological processes, including lipid retention, oxidation, chronic inflammation, fibrotic remodeling and calcification. In this regard, assessment of the molecular process whereby lipids promote the mineralization of aortic valve is required to understand the pathophysiological mechanisms leading to CAVD. Furthermore, investigations are needed to identify therapeutic targets and to open novel therapeutic avenues for the treatment of CAVD. The general objectives of my PhD project are: (1) To determine the role of ATX in mediating lipid-induced mineralization of valve interstitial cells (VICs); (2) To understand the mechanisms and signaling pathways by which lysophosphatidic acid (LPA) promotes inflammation and the mineralization of the aortic valve; (3) To determine the role of ATX-LPA in a mouse model of CAVD.
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Baker, Martin James. "Rac activation and the different roles of Tiam1 and P-Rex1." Thesis, University of Cambridge, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709483.
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Edwards, David C. "LIM kinase : the connection between Rac/Cdc42 and the actin cytoskeleton /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1999. http://wwwlib.umi.com/cr/ucsd/fullcit?p9917949.
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Ferrari, Giovanna Maria. "The interaction of the α2 chimaerin SH2 domain with target proteins." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325678.
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Horst, Janina [Verfasser]. "Characterization of the ribosome-associated complex RAC from S. cerevisiae / Janina Horst." Konstanz : Bibliothek der Universität Konstanz, 2011. http://d-nb.info/1033059927/34.
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Bakewell, Clare Michelle. "Group 3 and Group 13 initiators for rac-lactide ring-opening polymerization." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/27290.
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This thesis describes the synthesis of a series of bis(quinolinolato)aluminium ethyl, (quinolinolato) gallium and (quinolinolato)zinc ethyl compounds which have been synthesised and fully characterised using spectroscopic techniques, elemental analyses and in some cases single crystal X-ray diffraction. The compounds are shown to be active initiators for the ring-opening polymerization of rac-lactide, with the activity being dependent on the metal, zinc > gallium > aluminium. All initiators show characteristics consistent with a controlled polymerization: predictable molecular weights and narrow polydispersities. The bis(quinolinolato)aluminium ethyl initiators all promote iso-selective ring-opening, with iso-selectivity values between 0.57 and 0.76. The degree of iso-selectivity is attributed to the steric hindrance imposed by the substituents on the ligands. The related gallium compounds show increased activity, whilst maintaining the good degree of stereocontrol. A series of yttrium phosphasalen compounds are also described and their activity for the ring-opening polymerization of rac-lactide is reported. The series of compounds vary at the diimine linker, the phenoxide substituents and at the alkoxide group. The compounds all show the rapid and controlled initiation of the ring-opening polymerization of lactide. The activity of the initiators was found to be dependent on the diimine linker: ethylene > cyclohexene > phenylene > propylene, and on the electron donating ability of the phenoxide substituent. All the initiators exerted a good degree of stereocontrol on the polymerization. Interestingly, the tacticity of the polymer was seen to switch from heterotactic polylactide (Ps 0.87) to isotactic polylactide (Pi 0.86), with the inclusion of an additional bonding nitrogen moiety in the diimine linker. The formation of isotactic polylactide using Group 3 initiators is extremely rare.
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Dubyk, Cara W. "The role of Rho and Rac GTPases in prostate cancer bone metastasis." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 96 p, 2009. http://proquest.umi.com/pqdweb?did=1889093521&sid=1&Fmt=2&clientId=8331&RQT=309&VName=PQD.
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Diekmann, Dagmar. "Structural and functional analysis of the small GTP-binding proteins rho and rac." Thesis, Institute of Cancer Research (University Of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283195.
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Asprodites, Nicole. "The Cloning and Characterization of Two ROP/RAC G-Proteins from Gossypium Hirsutum." ScholarWorks@UNO, 2005. http://scholarworks.uno.edu/td/233.
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Rop/Rac proteins are plant-specific monomeric guanosine triphosphate-binding proteins (G-proteins) with important functions in plant development. Until recently, only three cotton (Gossypium hirsutum) Rop/Rac G-protein genes were sequenced, representing subfamilies III and IV of the plant monomeric Gprotein family. In this project, members of subfamilies II and I were cloned, sequenced, and named GhRac2 and GhRac3, respectively. Using real-time reverse transcription PCR, expression of GhRac2 was highest during fiber elongation, decreasing significantly when cellulose biosynthesis began. Transcript abundance of GhRac3 doubled between fiber elongation and secondary wall synthesis, remaining constant until 20 days post-anthesis. Expression of GhRac2 and GhRac3 was compared between the unfertilized ovules of Gossypium hirsutum, Texas Marker 1 and two near-isogenic fiber-impaired mutants. Expression of GhRac2 and GhRac3 was significantly higher in wild type ovules than in Ligon lintless, a mutant impaired in fiber elongation, but was not different in Naked Seed, a mutant impaired in fiber initiation.
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Tsuji, Takahiro. "ROCK and mDia1 antagonize in Rho-dependent Rac activation in Swiss 3T3 fibroblasts." Kyoto University, 2003. http://hdl.handle.net/2433/148706.
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Doussau, Frédéric. "Roles de proteines g monomeriques rab3 et rac dans la liberation evoquee des neurotransmetteurs." Paris 6, 1999. http://www.theses.fr/1999PA066161.
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Mon travail de these porte sur les mecanismes moleculaires de la liberation vesiculaire des neurotransmetteurs. Pour cette etude, j'ai modifie la fonctionnalite de certaines proteines synaptiques (par des toxines et des proteines recombinantes mutees) et j'en ai determine electrophysiologiquement les consequences sur la transmission synaptique au niveau de synapses neuro-neuronales identifiees de l'aplysie (aplysia californica). J'ai d'abord analyse le mode d'action des neurotoxines clostridiales. Ces toxines sont des endopeptidases qui inactivent les snares, des proteines participant a l'exocytose des neurotransmetteurs. Puis j'ai etudie le role presynaptique de la proteine g monomerique rab3. En microinjectant dans le neurone presynaptique des proteines rab3 mutees et des neurotoxines clostridiales, j'ai montre que rab3-gtp est un regulateur negatif de la neuroexocytose qui interagit avec les snares. L'activite de rab3 depend aussi de l'etat du cytosquelette d'actine. J'ai egalement montre que, via ses effecteurs liant les ions ca 2 +, rab3 traduit un changement du calcium cytosolique en un changement de la quantite de neurotransmetteurs liberes. Plus particulierement rab3 participe a la facilitation synaptique a court terme. Enfin, j'ai montre que la proteine g monomerique rac (une gtpase de la famille rho), qui regule le cytosquelette d'actine, est presente sur la membrane des vesicules synaptiques et controle la liberation de neurotransmetteurs en agissant sur le recrutement des vesicules synaptiques sur leurs sites de fusion.
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Devlin, Renee. "Responsible Adult Culture (RAC) cognitive and behavioral changes at a community-based correctional facility /." Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1211297932.
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Hendesi, Honey. "CONNECTIVE TISSUE GROWTH FACTOR (CTGF/CCN2) REGULATES OSTEOBLAST CYTOSKELETAL REORGANIZATION AND MOTILITY AND ENHANCES DIFFERENTIATION VIA BINDING TO INTEGRIN RECEPTORS AND ACTIVATION OF DOWNSTREAM SIGNALINGS." Diss., Temple University Libraries, 2014. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/263674.
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Cell BiologyPh.D.
Connective Tissue Growth Factor (CTGF) is a matricellular protein that has been shown to mediate cell adhesion, and as a consequence, it regulates cell proliferation, migration, differentiation and gene transcription. Although previous in vivo and in vitro studies supported the anabolic role of CTGF in skeletogenesis, to date mechanisms of this effect remain unknown. So far, no specific receptor has been identified for CTGF, although previous studies have shown that integrins can serve as functional signaling receptors for CTGF. The CTGF-integrin interaction initiates intracellular signaling cascades that ultimately regulate cell cytoskeleton reorganization, gene transcription and cell function. To study the effect of CTGF on osteoblasts, we first conducted adhesion assays using the MC3T3-E1 osteoblastic cell line. We confirmed that osteoblasts adhere to rCTGF in a concentration-dependent manner and we showed this adhesion has characteristics of integrin mediated adhesions. Next, we used an array of blocking antibodies directed against the individual alpha and beta; integrin subunits that are known to be expressed in osteoblasts. Significant decreases in cell adhesion were observed upon treatment with anti-alpha-v or anti-beta1 blocking antibodies. Subsequent coimmunoprecipitation analyses demonstrated that CTGF interacts with alpha-v and beta1 integrins in osteoblasts. Furthermore, we showed that the specificity of this CTGF-integrin interaction occurs in the C-terminal domain (fourth module) of CTGF. The immunefluorescence staining of cells cultured on substrates of rCTGF, fibronectin (positive control) or BSA (negative control) demonstrated that osteoblast adhesion to rCTGF results in actin cytoskeleton reorganization, focal adhesion formation, enhanced cell spreading and Rac activation. These series of events are necessary for proper cell-matrix interaction and integrins' downstream signaling initiation. Next, through alkaline phosphatase (ALP) staining and activity assays, as well as Alizarin red staining, we demonstrated that osteoblast attachment to CTGF matrix enhances cell maturation, bone nodule formation and matrix mineralization. To investigate whether the effect of CTGF on osteoblast differentiation involves activation of specific signaling molecules, we performed Western blot and chromatin immunoprecipitation (ChIP) assays. Osteoblasts cultured on rCTGF expressed higher levels of both total and phosphorylated forms of focal adhesion kinase (FAK) and extracellular signal-regulated kinase (ERK) compared to the cells cultured on BSA. In addition, these osteoblasts showed an increase in runt-related transcription factor 2 (Runx2) binding to the osteocalcin gene promoter compared to the negative control. These experiments confirmed CTGF's effect on enhancing osteoblast differentiation through regulation of important signaling molecules. In another series of experiments, we used primary osteoblasts isolated from CTGF KO mice, their WT littermates, or WT cells infected to overexpress (OE) CTGF to study the effect of different levels of endogenous CTGF on osteoblast cytoskeleton reorganization and motility. Our assays showed enhanced cell adhesion, spreading and Rac expression in CTGF OE osteoblasts, while in CTGF KO osteoblasts, cell adhesion, spreading and Rac expression were significantly decreased. In contrast, CTGF OE osteoblasts that showed high adhesion and spreading, exhibited diminished cell motility and low levels of RhoA expression, while KO cells migrated quickly and expressed high levels of RhoA. Together, these experiments establish CTGF as an adhesion protein for osteoblasts; they demonstrate that the alpha-v beta1 integrin is a functional signaling receptor for CTGF; they confirm that osteoblast differentiation is enhanced when cultured on CTGF matrix through activation of regulatory signaling molecules; and finally, these experiments establish a role for CTGF in the regulation of small RhoGTPases expression, which in turn implies a significant role for CTGF in cell cytoskeleton reorganization and motility.
Temple University--Theses
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Yang, Qi. "A system biology approach to uncover the regulatory and effector hubs of Rac-family GTPases." Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=121446.
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Rho-family proteins are a major branch of the Ras superfamily of small GTPases. These proteins can be further subdivided into six subfamilies according to primary amino acid sequence identity, structural motifs and biological function: Rho, Cdc42, Rac, RhoBTB, RhoT and Rnd subfamily. Rho-family proteins are "molecular switches" and cycle between GDP-bound "inactive" state and GTP-bound "active" state by regulation of guanine nucleotide exchange factors (GEFs) and GTPases-activating proteins (GAPs). Rho GTPases have a large collection of effectors and are involved in numerous cellular and physiological processes, such as cytoskeletal reorganization, microtubule dynamics, cell polarity, gene expression and cell cycle progression. However, it is poorly understood how Rho GTPases select specific effectors for diverse physiologic functions. We hypothesize that the specificity of effector choice is dictated by the individual GEF or by scaffold proteins binding either the GEF or the Rho proteins. To test this hypothesis, I used a system biology approach which will determine the complete interactome of the Rac GTPases (Rac1, Rac2, Rac3, and RhoG) in their active and inactive conformation. Through this method, we tried to discover new Rac effectors, possible molecular scaffolds and the Rac:GEF and Rac:GAP specificity.Les protéines de la famille Rho forment une branche majeure de la superfamille des petites GTPases Ras. Ces protéines peuvent être subdivisées en six sous-familles selon leur identité de séquence d'acides aminés primaires, leur motifs structuraux et leur fonction biologique, soient les sous-familles: Rho, Cdc42, Rac, RhoBTB, RhoT et Rnd. Les petites GTPases agissent comme des "interrupteurs moléculaires" soit qu'elles vont osciller entre un état "inactif" (GTPase-GDP) et un état "actif" (GTPase-GTP), et ce cycle est régulé par des facteurs d'échange de nucléotides guanine (GEFs) et des protéines activatrices de GTPases (GAPs). Les GTPases Rho ont une multitude d'effecteurs et elles sont impliquées dans de nombreux processus cellulaires et physiologiques, tels que la réorganisation du cytosquelette, la dynamique des microtubules, la polarité cellulaire, l'expression génique et la progression du cycle cellulaire. Cependant, il est encore mal compris comment les GTPases Rho sélectionnent des effecteurs spécifiques pour les différentes fonctions physiologiques. Nous émettons l'hypothèse que le choix de l'effecteur est dictée par la GEF impliquée ou par une protéine d'échafaudage qui est soit liée à la GEF ou à la GTPase. Pour tester cette hypothèse, j'ai utilisé une approche de la biologie des systèmes qui déterminera l'interactome complet des GTPases Rac (Rac1, Rac2, RAC3 et RhoG) dans leur conformation active et inactive. Grâce à cette méthode, nous avons essayé de découvrir des nouveaux effecteurs de Rac, des protéines d'échafaudage, ainsi que des GEFs et des GAPs spécifiques pour Rac.
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MASSOL, PHILIPPE. "Role de l'actine dans la phagocytose : caracterisation de la fonction des proteines rac et cdc42." Aix-Marseille 2, 1999. http://www.theses.fr/1999AIX22035.
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La phagocytose est un processus qui consiste a ingerer des micro-organismes. La cellule qui phagocyte doit rearranger son cytosquelette d'actine pour permettre la formation d'un coupe phagocytaire, une structure contenant des microfilaments d'actine et qui va englober le micro-organisme afin de permettre son ingestion. Nous nous sommes interesses a la regulation du cytosquelette d'actine lors de la phagocytose faisant intervenir des recepteurs pour les portions constantes des immunoglobulines. Nous avons debute notre travail par l'etude des petites proteines g de la famille rho lors de la phagocytose. Ces proteines sont impliquees dans les rearrangements de l'actine suite a l'activation de cellules par des facteurs de croissance et nous avons demontre leur necessite durant les etapes tardives de la phagocytose par l'utilisation de diverses techniques de microscopie mais egalement en etudiant la dynamique de la phagocytose par videomicroscopie sur des cellules vivantes. Nous avons egalement montre que les tyrosine phosphatases jouent un role important durant la phagocytose. Enfin, nous avons mis au point un protocole de purification biochimique des coupes phagocytaires afin d'analyser leur composition.
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Robbe, Karine. "Le cycle d'activation de la protéine G Rac à la surface de la membrane lipidique." Paris 11, 2003. http://www.theses.fr/2003PA112292.
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Les protéines Rho comme toutes les petites protéines G lient les nucléotides à guanine, GDP ou GTP. La réaction d'activation des protéines Rho, qui correspond à l'échange d'un GDP par un GTP, est intrinsèquement très lente et nécessite la catalyse par des facteurs d'échange spécifiques, les protéines à tandem DH-PH. De plus, les protéines Rho sont ancrées à la membrane via groupement prényl mais sont en majorité solubilisées dans le cytosol par une protéine régulatrice appelée GDI possédant une poche hydrophobe où se loge le prényl. Nous avons étudié le mécanisme d'activation de Rac1, une protéine de la famille Rho, et le lien entre le cycle GDP/GTP et le cycle membrane/cytosol. Pour cela, nous avons reconstitué in vitro l'activation de Rac1 sur liposomes à partir du complexe Rac/GDI purifié. Nous avons montré que l'activation de Rac par le tandem DH-PH de la protéine Tiam1 nécessite la dissociation de Rac1 de GDI qui ne peut se faire qu'en présence de lipides anioniques. Par ailleurs, l'ancrage de Rac à la membrane favorisé la réaction d'activation suggérant un changement conformationnel du tandem DH-PH sur la membrane. La dissociation de GDI et l'ancrage de Rac-GDP à la membrane rend Rac également beaucoup plus sensible à la glucosylation par la toxine létale de Clostridium Sordelli. La présence de Phosphatidyl Sérine permet un recrutement membranaire du fragment catalytique de la toxine létale et augmente très fortement son activité de glucosylation sur Rac. Cela met en évidence dans la protéine bactérienne un domaine très spécifique pour la Phosphatidyl Sérine. L'ensemble de ces résultats souligne l'importance des interfaces protéines-membrane dans le cycle d'activation de la protéine RacAs all G proteins, Rho proteins bind guanine nucleotide, GDP or GTP. The activation reaction, which corresponds to the exchange of GDP by GTP, is intrinsically very slow and required catalysis by Rho specific exchange factors, containing a tandem of DH and PH domain. Moreover, Rho proteins are anchored at the lipidic membrane by a prenyl group, but are mostly soluble in the cytosol through the interaction of the prenyl with the hydrophobic pocket of a regulatory protein named GDI. We have studied the activation mechanism of Rac1, a Rho protein, and the link between the GDP/GTP cycle and the membrane/cytosol cycle. We have reconstituted Rac1 activation in vitro on liposomes using purified Rac/GDI complex. We showed that Rac activation by DH-PH tandem of Tiam1 required Rac dissociation from GDI, which can only occurs in the presence of anionic lipids. Moreover, the anchorage of Rac on the lipidic membrane facilitates the activation reaction suggesting a conformation change of the DH-PH tandem on the membrane surface. GDI dissociation and Rac-GDP membrane anchorage strongly facilitate the glucosylation of Rac by Clostridium Sordelli lethal toxin. The presence of Phosphatidyl Serine induces the recruitment lethal toxin to the membrane and strikingly enhances Rac glucosylation. A domain with a high specificity for Phosphatidyl Serine is present in this bacterial protein. Taken together, these results underline the importance of protein/lipid interactions in the Rac activation Cycle
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Fries, Sandra Jennifer [Verfasser]. "Structural and functional analysis of the RAC-Ssb system in Saccharomyces cerevisiae / Sandra Jennifer Fries." Konstanz : KOPS Universität Konstanz, 2019. http://d-nb.info/1238018025/34.
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Frasa, Marieke A. M. "Molecular mechanisms of disruption of E-cadherin adhesion induced by Arf6 and Rac small GTPases." Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/7618.
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Epithelial cells are characterised by a tight intercellular adhesion. Disassembly of E-cadherin-mediated cell-cell adhesion can induce a transition from a benign epithelial phenotype to an invasive mesenchymal phenotype. Therefore, understanding the underlying mechanisms leading to adherens junction disruption will provide insights into potential therapeutic agents to prevent tumour metastasis. The small GTPases Arf6 and Rac can each disassemble E-cadherin-based junctions, upon which epithelial cells scatter. Preliminary results in our lab showed that Rae requires PAK function during junction disassembly and that Arf6 disrupts keratinocyte junctions in a process dependent on Rac signalling. Crosstalk between Arf6 and Rac has been described previously, but.the exact molecular mechanisms involved during Arf6-induced junction disassembly are not known. A good candidate molecule to provide the link between Arf6 and Rac is GIT1. GIT1 interacts with active Arf6 by an Arf6GAP domain and induces Rac activation via binding to the RacGEF 0PIX. Rac regulates many cellular. processes in which no effector proteins have been yet identified, inclUding perturbation of cell-cell contacts. Using a keratinocyte eDNA library screen with active Rac as bait, a new Rac binding protein named Armus has been isolated previously. This protein is interesting as in addition to binding specifically to active Rac, it contains a TBC/RabGAP domain at its C-terminus, which is predicted to inactivate Rab small GTPases. Armus function is currently unknown. The aim of my PhD project was to test the involvement of GIT1, PAK and Armus in the disassembly of E-cadherin junctions induced by active Arf6 and Rac. I found that GIT1 and D-PIX might provide the link towards Rac signalling during Arf6induced junction disassembly. Furthermore, expression of the TBC/RabGAP domain of Armus can block Arf6-induced junction disruption by inactivating Rab7. In contrast, the Rac effector PAK1 does not playa role in Arf6-dependent junction disassembly. Moreover, I found that Armus and GIT1 are distributed on similar vesicular structures, suggesting that these proteins are spatially and functionally linked.
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Pinto, Ana Cristina Araujo. "Emprego de lagoas seriadas após reatores RAC-UASB para tratamento de águas residuárias de suinocultura." Universidade Federal de Minas Gerais, 2012. http://hdl.handle.net/1843/BUBD-92HEW4.
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This research presents the behavior of one facultative pond and three maturation ponds in series such as post-treatment effluent from a two stages anaerobic system, composed of an anaerobic baffled reactor (ABR) followed by an upflow anaerobic sludge blanket reactor (UASB), in full scale, treating swine effluent. The maturation ponds were worked in three different phases depending on the depth, being the first phase with 0.40 m, second with 0.60 m and third with 0.80 m. The parameters evaluated were: air temperature, pH; dissolved oxygen (DO); biochemical oxygen demand (BOD); chemical oxygen demand (COD); total solids (TS); total volatile solids (TVS); total suspended solids (TSS); volatile suspended solids (VSS); ammonia; total Kjeldahl nitrogen (NTK); nitrite (NO2); nitrate (NO3); phosphorus (Pt); coliforms; Escherichia coli and helminth eggs. At the end of the three phases the ponds, after dryingponds, the sludge was collected for analysis of the volume, weight, coliforms and viable helminth eggs. The global system showed efficiency of removal above of 98% and 96% for BOD and COD, respectively, given the standard of effluent discharge established by DN COPAM-CERH 01/2008, however the ammonia was very above the standard. The ponds were not efficient in the removal of nutrients and coliforms due to the low hydraulical detention time (HDT), however had produced effluent free of helminth eggs. The analysis of coliforms in t he ponds sludge attended reuses in agriculture, according to Resolution nº 375/06 of the CONAMA, for Escherichia coli, in ponds LF and LM3. The sludge showed high concentrations of viable helminth eggs not attend the standard of this Resolution.O trabalho apresenta o comportamento de uma lagoa facultativa e três de maturação em série, como pós-tratamento de efluente de um sistema anaeróbio em dois estágios, composto por um reator anaeróbio compartimentado (RAC) seguido de um reator anaeróbio de manta de lodo e fluxo ascendente (UASB), em escala real, tratando efluente de suinocultura. As lagoas de maturação foram trabalhadas em três fases diferentes em função da profundidade, sendo a primeira fase com 0,40 m, a segunda com 0,60 m e a terceira com 0,80 m. Os parâmetros avaliados foram: temperatura do ar; pH; oxigênio dissolvido (OD); demanda bioquímica de oxigênio (DBO); demanda química de oxigênio (DQO); sólidos totais (ST); sólidos totais voláteis (STV); sólidos suspensos totais (SST); sólidos suspensos voláteis (SSV); nitrogênio amoniacal (Nam.); nitrogênio total Kjeldahl (NTK); nitrito (NO2); nitrato (NO3); fósforo total (Pt); coliformes totais; Escherichia coli e ovos de helmintos. No final das três fases, após a secagem das lagoas, o lodo foi coletado para análise do volume, massa, coliformes e ovos viáveis dehelmintos. O sistema global apresentou eficiência de remoção acima de 98% e 96% para DBOt e DQOt, respectivamente, atendendo ao padrão de lançamento de efluentes estabelecido pela DN COPAM-CERH 01/2008, porém a amônia ficou muito acima do padrão. As lagoas nãoforam eficientes na remoção de nutrientes e coliformes devido ao baixo tempo de detenção hidráulica (TDH), porém produziram um efluente totalmente livre de ovos de helmintos. A análise de coliformes no lodo das lagoas atendeu ao padrão de reúso na agricultura, segundo a Resolução nº 375/06 do CONAMA, para Escherichia coli, nas lagoas LF e LM3. O lodo apresentou elevada concentração de ovos viáveis de helmintos não atendendo ao padrão desta Resolução.
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Gomez, John Clifford. "The role of CD18 and Rac₂ in regulating neutrophil production and release from the bone marrow." Cleveland, Ohio : Case Western Reserve University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1212179633.
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Warren-Paquin, Maude. "Regulation of synaptic plasticity at the Drosophila larval NMJ : the role of the small GTPase Rac." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112319.
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We are interested in understanding the molecular mechanisms that govern synaptic growth and plasticity. Recent evidence from several laboratories suggests that small GTPases play an important role in the promotion of neurite outgrowth; however, their role in the control of synaptic growth and functional plasticity is not well understood. The goal of this thesis is to investigate the role of small GTPases (including Rac, Rho and Cdc42) in the regulation of synaptic growth in vivo, using the Drosophila larval neuromuscular junction (NMJ) synapses as a model system. Our results show that presynaptic overexpression of Rac, but not of Rho or Cdc42, positively regulates both synaptic structure and function. Genetic loss of Rac leads to embryonic lethality, making it impossible to assess the full loss-of-function phenotype using conventional mutants. To circumvent this, we use the MARCM (Mosaic Analysis with a Repressible Cell Marker) technique to generate single motor neuron clones devoid of all genetic copies of Rac. Our data suggest that Rac activity is crucial for normal synaptic development. In support of this conclusion, we demonstrate that genetic removal of trio, a guanine nucleotide exchange factor (GEF) that is known to activate Rac, leads to a drastic reduction in the number of synaptic boutons. In addition, genetic removal of one copy of trio is sufficient to suppress the gain-of-function phenotype of Rac. Moreover, we demonstrate that partial removal of the fragile X mental retardation gene (dfmr1), a known suppressor of Rac, enhances the gain-of-function phenotype of Rac. Taken together, our findings support a model in which Rac signaling positively regulates synaptic growth and function at the Drosophila larval NMJ.
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Connolly, John Oliver. "The role of the small GTPase Rac in endothelial cell transformation by polyoma middle T antigen." Thesis, Queen's University Belfast, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266698.
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Bryan, Steven. "Rho/Rac GTP-binding proteins and their GTPase activating proteins in humans and in Dictyostelium discoideum." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266164.
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Yano, Tomoki. "Tara up-regulates E-cadherin transcription by binding to the Trio RhoGEF and inhibiting Rac signaling." Kyoto University, 2011. http://hdl.handle.net/2433/147340.
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Dalton, Lucy Ellen. "The in vivo role of RAC signalling in melanoma progression using zebrafish as a model organism." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509863.
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Pan, Dingxin. "P-Rex1 : regulation by Norbin and cooperation with Vav family Rac-GEFs in inflammatory neutrophil recruitment." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708001.
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Stephan, Ilona [Verfasser]. "Analyse der Aktivierung von Rac-GTPasen durch G-Protein-gekoppelte Rezeptoren in neutrophilen Granulozyten / Ilona Stephan." Ulm : Universität Ulm. Medizinische Fakultät, 2001. http://d-nb.info/1015269095/34.
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Lousa, Duarte António Domingues Louro de Matos. "Estudo do comportamento dinâmico de um reservatório hidropneumático." Master's thesis, Faculdade de Ciências e Tecnologia, 2011. http://hdl.handle.net/10362/6870.
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Dissertação para obtenção de Grau de Mestre em
Engenharia MecânicaO estudo dos fenómenos transitórios em condutas, baseado no método das características, assume grande relevância no projecto de instalações hidráulicas. A quantificação das pressões máximas e mínimas é de interesse fundamental para o dimensionamento da conduta e, para decidir sobre a necessidade de instalação de dispositivos de protecção. O presente trabalho tem como principal objectivo estudar o comportamento do reservatório hidropneumático. Desta forma, recorreu-se a simulações numéricas efectuadas com o programa AFT Impulse. As configurações geométricas das instalações simuladas foram criteriosamente escolhidas por forma a estudar separadamente: as sobrepressões, o efeito do volume do reservatório hidropneumático e da conduta e, finalmente, das perdas de carga. Neste estudo procedeu-se a uma análise em frequência da resposta do rac, utilizando técnicas de análise espectral. Os resultados obtidos permitiram concluir que instalações munidas de racs de pequenas dimensões registam pressões extremas superiores às medidas para uma mesma instalação sem sistema protector. O conjunto das simulações efectuadas permitiu concluir que o principal parâmetro a ter em conta na eficiência do rac é a relação entre o volume do reservatório e o da conduta a proteger. A comparação dos resultados numéricos com os obtidos por métodos clássicos (ábacos) permitiu concluir que muito embora permitam o dimensionamento dos racs não o fazem de forma optimizada. Acresce ainda que não podem ser aplicados em sistemas que apresentem alguma complexidade, como não linearidades ou geometrias complexas. Face aos actuais meios computacionais, os métodos numéricos baseados no método das características, permitem simular em tempo útil, muitas configurações para a instalação e desta forma optimizar o rac a instalar.
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Alexander, Lawrence. "Regulatory reform: A case study of the Regulatory Advisory Committee (RAC) and the Canadian Environmental Assessment Act." Thesis, University of Ottawa (Canada), 1996. http://hdl.handle.net/10393/10096.
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This paper examines a consensus-based approach to regulation making known as "regulation negotiation" or "regneg," and pursues the question, can regneg improve the performance of the federal regulatory process? Successfully implemented by the United States Environmental Protection Agency, regneg allows parties likely to be affected by a regulation to negotiate the substance of it. Although its use is rare in Canada, a similar process was used to help develop key regulations under the Canadian Environmental Assessment Act. The paper argues that the performance of any regulatory process can be measured by its ability to accommodate the views of a more diverse range of interests, improve the quality of regulations, and hold regulation makers to a higher standard of accountability. Based on the U.S. and Canadian experience, the paper suggests that in certain circumstances, and with some refinements, regneg is capable of improving the regulatory process in all of these areas.
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Nimitsiriwat, Nonsee. "Novel tin(II), zinc(II) and magnesium(II) initiators for the ring-opening polymerisation of rac-lactide." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424768.
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German, Ian. "Variation of ligand donor atoms in trivalent metal complexes and their impact on rac-Lactide polymerisation behaviour." Thesis, Imperial College London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.529360.
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