Tesis sobre el tema "GTPase"
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Normandin, Caroline. "Identification et caractérisation de GTPases Activating Proteins spécifiques à la petite GTPase RAB21". Mémoire, Université de Sherbrooke, 2017. http://hdl.handle.net/11143/11544.
Texto completoAbstract : Autophagy is defined as the lysosomal degradation and recycling of cellular constituents. At basal levels, autophagy eliminates protein aggregates or damaged organelles. In condition of stress, such as in condition of nutritional deficiency, hypoxia or cancer treatments, autophagy allow cells to adapt and survive. Therefore, autophagy is an essential system required for survival and maintenance of cellular homeostasis. It is thus essential to identify the cellular entities and mechanisms regulating this process. RAB GTPases were identified as master regulators of autophagy. These particular proteins act as molecular switches for the rapid execution of cellular responses. RABs are activated by Guanine Nucleotide Exchange Factors (GEF) whereas GTPase Activating Proteins (GAP) accelerates RAB deactivation. RAB21 is essential in the late stages of autophagy. Indeed, RAB21 is activated by nutritional deficiency, via its GEF MTMTR13, to allow trafficking of a SNARE required for autophagic flux. During starvation, RAB21 is deactivated which suggest that a GAP could negatively regulate RAB21 activity. However, to date no GAP for RAB21 has been identified. An eye modifier genetic screen in Drosophila was performed to identify potential RAB21 GAPs and some candidates were identified. As a result of this screen, the GAP TBC1D25 was identified as interacting with RAB21. Moreover, this interaction was increased by starvation. Proximity ligation assays revealed that the RAB21-TBC1D25 interaction partially localized at early endosomes. Moreover, prolonged activation of RAB5, located at early endosomes, inhibited RAB21-TBC1D25 interaction. Further experiments will be carried out to explain these results. With respect to the roles of autophagy in cancer, RAB21 was shown to be overexpressed in cells with high autophagic flux as well as in some colon cancer tumors. Importantly, the expression of Tbc1d25 in these same tumors does not appear to be increased, indicating that TBC1D25 could be an autophagic inhibitor specific to cells with a high autophagic flow. My work suggests that TBC1D25 could function as a GAP to negatively regulate RAB21 activity in condition of prolonged starvation.
Visvikis, Orane. "GTPase Rac1 et ubiquitination". Paris 5, 2007. http://www.theses.fr/2007PA05P622.
Texto completoThis thesis has been dedicated to the study of the regulation by ubiquitination of a signaling protein, the Rac1 GTPase. I have shown that the degradative ubiquitination of Rac1 affects poorly its splice variant Rac1b, and requires JNK activity, which is stimulated by Rac1 but not by Rac1b. In addition, I have described a non-degradative ubiquitination of Rac1, which could participate in pathogen endocytosis during bacterial infection. Searching for the enzyme responsible for specific Rac1 ubiquitination, I have identified a RING finger protein, Unkempt, as a new effector of Rac1. I have shown that this potential ubiquitin ligase, which is activated by Rac1, could be involved in the ubiquitination of BAF60b, a component of the chromatin remodeling complex SWI/SNF. Moreover, I have observed that Rac1 stimulates histone H2A mono-ubiquitination. Thus, Rac1 GTPase could be involved in novel pathways by controlling chromatin remodeling
Peurois, François. "Activation des petites GTPases à la périphérie des membranes". Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLN037.
Texto completoSmall GTPases are major regulators of many cellular processes. Nucleotide exchange factors (GEF) activate small GTPases. Deregulation of the activation of small GTPases is at the origin of several diseases, such as certain diabetes and cancers. GTPases and GEFs interact together at the periphery of cell membranes. Beyond a simple place of co-localization, biological membranes have physicochemical properties directly impacting the activation of small GTPases by GEFs. This thesis project is based on three axes, 1) to propose an experimental strategy to quantitatively measure the effects of membranes in this activation 2) to establish a model of the activation at the periphery of membranes of the GEF EPAC1, a therapeutic target in heart diseases, 3) to characterize known ArfGEF inhibitory small molecules in a membrane context. The results showed that membranes modified GEF catalytic efficiency, and questioned their specificity towards small GTPases. The membranes also appear as partners for the activation of EPAC1 in cooperation with cAMP. These effects could be explained by a co-localization between GEF and GTPases on the membranes surfaces, a conformational rearrangement of the GEF induced by membranes, a modification of lateral diffusion of the GEF, or a catalytically advantageous geometry of the GEF-GTPase-membrane complex. Finally, understanding the involvement of membranes in this activation leads us to imagine new therapeutic inhibition strategies
Chan, King-chung Fred y 陳敬忠. "Functional characterization of StAR-related lipid transfer domain containing 13 (DLC 2) RhoGAP in the nervous system". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43278449.
Texto completoChan, King-chung Fred. "Functional characterization of StAR-related lipid transfer domain containing 13 (DLC 2) RhoGAP in the nervous system". Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43278449.
Texto completoKeller, Laura. "Conception de nano-anticorps conformationnels comme nouveaux outils d'étude de l'activité des GTPases de la sous-famille RHOA". Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30005/document.
Texto completoRHOA small GTPase belongs to a subfamily acting as a molecular switch activating major signaling pathways that regulate cytoskeletal dynamics and a variety of cellular responses such as cell cycle progression, cytokinesis, migration and polarity. RHOA activity resides in a few percent of GTP loaded protein, which is finely tuned by a crosstalk between regulators of the GTPase cycle. Manipulating a single RHO at the expression level often induces imbalance in the activity of other RHO GTPases, suggesting that more specific tools targeting these active pools are needed to decipher RHOA functions in time and space. We decided to use single domain antibodies, also known as VHH or nanobodies, as a new tool for studying RHOA activation. We produced and screened a novel fully synthetic phage display library of humanized nanobodies (NaLi-H1) to develop conformational sensors of the GTP loaded active conformation of RHO subfamily. We obtained several high affinity nanobodies against RHOA's active form which we characterized as RHO active antibodies in vitro and RHO signaling blocking intrabodies in cellulo. These new tools will facilitate and improve our current knowledge of this peculiar protein subfamily and will be a paradigm for the study of other RHO related small GTPases
Tillement, Vanessa. "Régulation de la GTPase RHOB par phosphorylation". Toulouse 3, 2005. http://www.theses.fr/2005TOU30175.
Texto completoRhoB belongs to the Rho family (RhoA, RhoB and RhoC) of the low molecular weight GTPases, regulated by cycling between GDP and GTP bound state. We have shown that RhoB is also regulated by phosphorylation. On contrast to RhoA, which is phosphorylated by PKA, RhoB is specifically phosphorylated by Casein kinase 1 (CK1) and Calmodulin kinase II in vitro and in vivo. Mass spectrometry analysis has shown that CK1 phosphorylates RhoB on its C-terminal sequence on serine 185. With CK1 inhibitors we have shown that CK1-mediated phosphorylation of RhoB inhibits its binding to one of its effector, thus inhibiting its activity. Finally, preliminary results strongly suggest that RhoB phosphorylation by CK1 is implicated in the regulation of the intracellular trafficking of internalized EGF receptor
Paul, Florian [Verfasser]. "Developing quantitative GTPase affinity purification (qGAP) to identify interaction partners of Rho GTPases / Florian Paul". Berlin : Freie Universität Berlin, 2015. http://d-nb.info/1069532711/34.
Texto completoPaul, Florian Ernst Rudolf Benjamin [Verfasser]. "Developing quantitative GTPase affinity purification (qGAP) to identify interaction partners of Rho GTPases / Florian Paul". Berlin : Freie Universität Berlin, 2015. http://d-nb.info/1069532711/34.
Texto completoKoraïchi, Faten. "Etude de l'activation de la GTPase RhoB par complémentation split-GFP tripartite". Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30081.
Texto completoRhoB is a small GTPase that is rapidly activated in response to growth factors and cellular stress. It regulates fundamental biological processes such as cell migration, angiogenesis, DNA repair, apoptosis and response to anticancer therapies. Small GTPases activity is tightly regulated by their subcellular localization. However, RhoB activation had never been investigated in living cells. In this work, we have adapted and validated an innovative method of protein-protein interactions analysis using tripartite split-GFP complementation, for the sensitive and specific detection of small GTPases activation in living cells. Then, we developed an optimized cellular model by combining the tripartite split-GFP technology with an anti-GFP intrabody fluorescence-enhancer to detect the regulation of RhoB activation with high spatial resolution. This biosensor highlighted the translocation of active RhoB from endosomes to accumulate at the plasma membrane upon serum stimulation, revealing a novel membrane signaling platform of RhoB. Future studies based on this biosensor will enable the analysis of RhoB activation profile and other small GTPases upon various stimuli or in different cellular contexts, as well as the identification of the GTPases partners and activation modulators
Belbachir, Nadjet. "Mécanismes physiopathologies du syndrome de Brugada : caractérisation d'un nouveau gène morbide Rad GTPase". Thesis, Nantes, 2017. http://www.theses.fr/2017NANT1015/document.
Texto completoBrugada syndrome (BrS) is a rare inherited cardiac disorder linked to high risk of ventricular arrhythmias and sudden death. In the present day, only 30% of BrS cases have known genetic causes. Most of these mutations have been identified in the SCN5A gene that encodes the cardiac voltage-gated sodium channel NaV1.5. We identified a rare variant in the RRAD gene encoding for the small G protein Rad GTPase, in a familial case of BrS. The aim of this work was to elucidate the mechanisms by which the RRAD p.R211H variant could lead to BrS. First, an overexpressing model was developed using neonatal mouse cardiomyocytes to define the involvement of Rad in the electrical function of cardiomyocytes. Then, cardiac cells were derived from human induced pluripotent stem cells reprogrammed from the carriers of the Rad mutation in order to investigate the phenotype induced at the cellular level. Furthermore, a knock in mouse has been generated to study the impact of this same mutation on the organ level. The three models summarized in a complementary way the phenotype caused by the Rad mutation on the electrical activity at the cellular and the organ levels. The mutation seem to trigger structural defects in the cardiomyocytes that can be involved in the electrical defects related to the disease. The present study is the first report of the potential link between Rad GTPase and BrS. The phenotype reported recapitulates the classical electrophysiological signature of the disease but also associates cytoskeleton disturbances
Seviour, Elena Genevieve. "Regulation of the small GTPASE ARF6". Thesis, University of Bristol, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492445.
Texto completoAtkinson, Gemma C. "Evolution of the translational GTPase superfamily". Thesis, University of York, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.479486.
Texto completoDavidson, Anthony Christopher. "Salmonella manipulation of Arf GTPase networks". Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708908.
Texto completoWu, Guang. "ROP GTPASE signaling in tip growth /". The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486546889380932.
Texto completoFoucher, Anne-Emmanuelle. "Caractérisation biochimique de YphC, une protéine de Bacillus subtilis à deux domaines GTPases impliquée dans la biogenèse du ribosome". Grenoble, 2010. http://www.theses.fr/2010GRENV040.
Texto completoGenome sequencing programs have revealed many genes of unknown function. The systematic disruption of these genes revealed the essentiality for some of them. Studying orphan proteins became of first importance as they are ideal targets for new antibacterial compounds. YphC is a GTPase from Bacillus subtilis that meets these criteria. It is well conserved throughout bacterial kingdom but is not found in eukaryota or archeas, strengthening the choice of this protein as a future target for antibacterial drugs. YphC has the particularity to possess two GTPase domains in tandem. As a unique protein, we decided to study YphC from a biochemical point of view to better understand its catalytic mechanism. We overexpressed and purified the protein, either wild type or mutants. We measured its enzymatic constants and characterize potassium activation effect on its hydrolytic activity. We showed that YphC displays a high GTPase activity and that GD1 bears the majority of this activity. GD2 would thus have a regulatory role in the protein. We also studied the role of YphC in vitro. We showed that the protein was able to interact with ribosome from Bacillus subtilis in a nucleotide dependant manner, suggesting that YphC plays a role in ribosome biogenesis
Mitteau, Romain. "Régulation par la phosphorylation d’un module Rho GTPase dans la levure Saccharomyces cerevisiae". Thesis, Bordeaux 2, 2013. http://www.theses.fr/2013BOR22084/document.
Texto completoThe eukaryotic cell cycle is characterized by abrupt and dynamic changes in cellular polarity as chromosomes are duplicated and segregated. Those dramatic cellular events require coordination between the cell cycle machinery and polarity regulators. The mechanisms underlying this coordination are not well understood. In the yeast S. cerevisiae, as in other eukaryotes, the GTPase Cdc42 plays an important role in the regulation of cell polarity. Cdc42 regulators constitute a GTPase module that undergoes dynamic phosphorylation during the cell cycle by conserved kinases including Cyclin-Dependent Kinase 1 (Cdk1) and p21-activated kinase (PAK). These kinases and substrates may link cell polarity to the cell cycle progression. Using in vitro approaches, we have reconstituted the phospho-regulation of the Cdc42 Guanine Nucleotide Exchange Factor (GEF), Cdc24. We have identified a possible mechanism of Cdc24 regulation involving a scaffold-dependent increase in Cdc24 phosphorylation by Pak and Cdk1. This phosphorylation moderately increases the affinity of Cdc24 for another GTPase module component, the scaffold Bem1. Moreover, by testing the effect of other GTPase module components on the phosphorylation of Cdc24, and thus on its interaction with the scaffold, we identified an antagonistic function for the GTPase Activating Protein (GAP) Rga2. Our in vivo data of rga2 mutants suggest that Rga2 phosphorylation by Cdk1 inhibits its GAP activity. We propose a tentative model to explain the inhibition of Cla4 by Rga2 and its presence in a complex containing Cdc24 and Bem1. The presence of the GAP protein in the complex may be a mechanism that reduces Cdc24 phosphorylation in case of a mistargetting of the complex in order to downregulate the GEF/Scaffold dimer. Since the PAK component of the GTPase module is itself activated by Cdc42 activity, our results are consistent with a model in which inputs from the cell cycle lead to auto-amplification of the Cdc42 GTPase module. In S. pombe, polarised growth requires a gradient of activation of Cdc42 due to GEF and GAP segregation. Here we show that all Cdc42 GAPs localise to the polarised site during the cell cycle. Those localisations are consistent with a requirement of Cdc42 cycling to maintain a polarity cap. Our results may suggest that Cdc42 GAPs localisations in S. cerevisiae are different from current knowledge in S. pombe
Slaymi, Chaker. "Rôle de la GTPase atypique RhoU dans l'homéostasie intestinale". Thesis, Montpellier 2, 2014. http://www.theses.fr/2014MON20127.
Texto completoIn Mammals, the intestinal epithelium is renewed every 4-6 days through the stem cells located at the bottom of crypts. The renewal depends on signals from the micro-environment and requires a proliferation phase of stem cells, then a differentiation and apoptosis/desquamation phases of epithelial cells. Wnt signaling plays a major role in intestinal homeostasis by the action of two reversed gradients along the axis crypt/ lumen: canonical Wnt signaling, active in the bottom of crypts, control proliferation while non canonical signaling, active in the top of the crypts control cell differentiation. It was shown that these two pathways are regulator of the atypical GTPase RhoU/Wrch1. The RhoU protein activates spontaneously, its activity is directly proportional to its expression level in the cell and is expressed as in gastric and colorectal tumors. In view of these informations, our objectives were therefore to characterizethe morphological changes induced by conditional invalidation of RhoU in the intestinal epithelium of mice and to determine the mechanisms of action. Our results show that RhoU depletion is not lethal. However, it induces an increase of cell density (+20%) and a disruption of the epithelium structure in the top of the colonic crypts. This increase affects both absorptive and secretory lineages. However, the absence of RhoU induced over-representation of secretory lineage. In colorectal tumor cell line DLD-1, we have shown that the absence of RhoU mimics the phenotype of cell density increase observed in mice. RhoU invalidationdid not change the distribution of cell cycle phases and mitosis, however, it reduces the number of apoptotic cells in the colon of mice and in the DLD-1 cells. RhoU invalidation reduced Hippo signaling and altered cell contractility via the increase of the protein MLC2 phosphorylation. Recent work has shown that the reduction of MLC2-P level is necessary for the caspase protein activation by an apoptotic stimulus. Suggesting that the perturbation of contractility may be the cause of this apoptosis decrease which is the main cause responsible of this phenotype. Finally, RhoU is a regulator of the intestinal homeostasis in micevia its moderating role of cell death
Bery, Nicolas. "Nouvelle stratégie de ciblage de la GTPase RhoB : développement d'intracorps conformationnels sélectifs et leur fonctionnalisation en tant qu'inhibiteurs intracellulaires de l'activité de RhoB". Toulouse 3, 2014. http://thesesups.ups-tlse.fr/2734/.
Texto completoRhoB GTPase shares more than 85% of homology with RhoA and RhoC. These proteins switch between an active conformation bound to GTP and an inactive one bound to GDP. Deregulations of their expression and/or their activity are often found in many cancers. To date, no selective inhibitor of these GTPases has been developed in order to block selectively Rho's activity. This project showed an original approach targeting RhoB's activity. After a new single domain antibody library characterization, its validation using the phage display technology against various antigens gave many highly functional antibodies in many applications. Set up of a new direct screening strategy of intracellular antibody (intrabody) raised against RhoB allowed us to identify several conformational intrabodies of RhoB active form, one of them discriminating RhoB from its homologs RhoA and RhoC. Intrabody functionalization with an Fbox domain driving target to degradation led to the identification of the first efficient selective RhoB activity inhibitory strategy. These work demonstrated that RhoB activity knockdown with functionalized intrabodies increased migration and invasion of pulmonary cells. In conclusion this tool will allow to determine if RhoB activity could be a new therapeutic target and open new perspectives to study GTPases activity
Kawano, Yoji, Takeshi Yoshimura y Kozo Kaibuchi. "Smooth muscle contraction by small GTPase Rho". Nagoya University School of Medicine, 2002. http://hdl.handle.net/2237/5374.
Texto completoNozawa, Atsuko. "Rab35 GTPase recruits NPD52 to autophagy targets". Kyoto University, 2018. http://hdl.handle.net/2433/230994.
Texto completoYarwood, Sam. "Calcium signalling and the small GTPase Ras". Thesis, University of Bristol, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492619.
Texto completoKirsten, Marie Lis. "Biophysical studies of Rab GTPase membrane binding". Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/6964.
Texto completoVignal, Emmanuel. "Polymérisation de l'actine GTPases de la famille Rho : caractérisation et étude d'un effecteur de la Petite GTPase RhoG". Montpellier 2, 2001. http://www.theses.fr/2001MON20042.
Texto completoGhiaur, Gabriel. "The role of Rho GTPases in hematopoietic stem cell biology RhoA GTPase regulates adult HSC engraftment and Rac1 GTPases is important for embryonic HSC /". Cincinnati, Ohio : University of Cincinnati, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1204374567.
Texto completoAresta, Sandra. "Etude de la protéine Gem, un membre de la superfamille Ras". Paris 11, 2001. http://www.theses.fr/2001PA112281.
Texto completoGem is a recently identified protein belonging to the branch RGK of the Ras superfamily of GTPases. Gem is induced in several cell types upon mitogen stimulation, and it presents N- and C-terminal extensions of unknown function when compared to Ras as well as several amino acid substitutions in key positions for GTP binding and hydrolysis. With the aim of identifying Gem partners, and in particular those interacting with its N-terminal extension, we have developed a new vector for two-hybrid studies where the bait is fused through its C-terminus with the N-terminus of the DNA-binding domain (DBD) of LexA, therefore, possessing an inverted polarity as compared with a classical two-hybrid vector. We have validated this system by showing that it allows the same specific interactions between Ras and Ra1 GTPases with their effectors and regulators as a classical two-hybrid vector, and that it even shows an increased sensibility. We have built a two-hybrid cDNA library from Jurkat cells that we have screened for Gem partners with two different baits: (i) the first 82 amino acids of Gem fused to the N-terminus of LexA DBD; (ii) full-length Gem fused to the C-terminus of GAL4 DBD. Amongst the 20 different clones obtained, two have been studied further. Their cDNAs coded for an isoform of the 4. 1N protein, and for a novel protein containing a RhoGAP domain. We have shown that the new RhoGAP protein is capable of increasing the intrinsic GTPase activity of GTPases belonging to the Rho/Rac/Cdc42 branch, in vitro as well as in vivo, and we have demonstrated by co-immunoprecipitation that Gem is able to interact with this protein in eukaryotic cells. These results suggest that Gem could be implicated in the regulation of Rho GTPases function
Gloor, Yvonne. "The Arf GTPase exchange factor Sec7p interaction network:". Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-ds-1202827858817-78960.
Texto completoJilkina, Olga. "The function of Ral GTPase in human platelets". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ41614.pdf.
Texto completoSaunders, Amy Elizabeth. "GIMAP1 : a small GTPase involved in lymphocyte survival". Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612535.
Texto completoErasmus, Jennifer Carr. "Small Pho GTPase Signalling Downstream of E-cadherin". Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.503823.
Texto completoGraham, Deborah Louise. "The catalytic mechanism of Rho-GTPase-activating protein". Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322212.
Texto completoLumb, Jennifer. "Exploration of Rab GTPase function in Trypanosoma brucei". Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608669.
Texto completoKwiatkowska, Aneta, Sebastien Didier, Shannon Fortin, Yayu Chuang, Timothy White, Michael Berens, Elisabeth Rushing et al. "The small GTPase RhoG mediates glioblastoma cell invasion". BioMed Central, 2012. http://hdl.handle.net/10150/610207.
Texto completoBousquet, Emilie. "Rôle de la GTPase RhoB dans l'oncogenèse pulmonaire". Toulouse 3, 2010. http://thesesups.ups-tlse.fr/1007/.
Texto completoLung cancer is the leading cause of cancer-related death worldwide and this is largely due to late diagnosis and a high metastatic potential. This highlights the need for a better understanding of the molecular mechanisms involved in lung cancer initiation and progression. It has previously been shown in the laboratory that overexpression of RhoB GTPase inhibits cell transformation in cells expressing Ras and an inverse correlation between RhoB expression and lung cancer progression, this loss of expression occurs between carcinoma in situ and invasive carcinoma. To define more precisely the role of RhoB in different stages of lung oncogenesis, we have analysed the effect of its inhibition on the phenotype of lung cells to mimic the loss of RhoB. This work showed that inhibition of RhoB does not induce transformation of bronchial cells but increases migratory and invasive capabilities of bronchial cells and the migratory phenotype. Moreover, this work has helped to show that RhoB regulates the migratory and invasive phenotype via the regulation of Akt1 and Rac1 GTPase. The RhoB inhibition in bronchial cells, induced by the Ras oncogene, frequently mutated in Iung cancer, critical for stimulation of their migratory and invasive properties through the regulation of the kinase Akt1. All these data suggest that RhoB is involved in tumor progression, notably the acquisition of migratory and invasive properties, rather than in the initiation of pulmonary carcinogenesis and that RhoB has a critical role in the metastasis of lung cancer
Hu, Shuang. "Rho GTPase Signaling Modulates Neurotransmission in Caenorhabditis elegans". University of Toledo / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1365182177.
Texto completoLi, Hai. "ROP GTPASE signaling in cell development of Arabidopsis /". The Ohio State University, 2000. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488191667181129.
Texto completoPatwardhan, Anand. "Role of the small GTPase RAB6 in pigmentation". Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB090.
Texto completoMercey, Olivier. "Interactions des microARN de la famille miR-34/449 avec les voies de signalisation intracellulaire : rôle dans la différenciation des cellules multiciliées chez les vertébrés". Thesis, Université Côte d'Azur (ComUE), 2016. http://www.theses.fr/2016AZUR4119/document.
Texto completoVertebrate multiciliated cells (MCC) project hundreds of motile cilia at their apical surface which coordinately beat to generate a directional fluid flow necessary for many biological functions including airway cleansing. Biogenesis of multiple cilia (multiciliogenesis) follows different key cellular steps corresponding to a cell cycle arrest, a massive multiplication of centrioles which then migrate to the apical surface to form basal bodies, from which cilia elongate. In 2011, my host laboratory evidenced that the miR-34/449 family of microRNAs control vertebrate multiciliogenesis by inducing the cell cycle arrest and by repressing the Notch pathway. My thesis work has revealed a new role of miR-34/449 by demonstrating that they modulate expression and activity of small GTPases to drive the apical reorganization of the actin network, a prerequisite for basal body anchoring. Besides, I have identified and characterized variant sequences of canonical miR-34/449 family, named isomiRs. Whereas these isomiRs share common biological functions with canonical miR-34/449 miRNAs, they may also contribute to a complementary effect by targeting specific transcripts. Finally, the last part of my work has contributed to the identification of the conserved role of the BMP pathway in the control of multiciliogenesis. I have evidenced some molecular mechanisms by which the BMP signal controls this phenomenon. Importantly, I demonstrated that BMP inhibition promotes regeneration of tracheal MCC in vivo in an asthmatic mouse model. Overall, our findings offer an unprecedented opportunity to develop novel therapeutic strategies to treat diseases associated with ciliary disorders
Wakade, Rohan Sanjay. "Rôle de GTPase de type Rab, Ypt6, chez le pathogène fongique opportuniste de l’homme, Candida albicans". Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2017. http://www.theses.fr/2017AZUR4064.
Texto completoCandida albicans is a harmless constituent of the human microbiota that causes superficial infections as well as life threatening infections in immune compromised individuals. The transition from a budding form to the highly polarized hyphal form is associated with virulence and requires cytoskeleton reorganization and sustained membrane trafficking. In a range of eukaryotes, Ras related protein in the brain (Rab) G proteins and their regulators have been shown to play a central role in membrane traffic. The objective of this work is to understand the role of Rab proteins, in particular Ypt6, the homolog of Human Rab6, in the morphological transition and virulence of C. albicans. To this aim, I generated loss of function mutants and found that YPT6 is not essential for viability, yet was critical for cell wall integrity and invasive hyphal growth, with ypt6 hyphal filaments shorter compared to that of the wild type (WT). Furthermore, YPT6 was important for virulence in two murine candidiasis models. I determined that Ypt6 was localized at the late Golgi compartment during hyphal growth, where it co-localized with Arl1, a small GTPase of the Arf (ADP Ribosylation Factor) family, also required for hyphal growth and virulence. Interestingly, overexpression of YPT6 specifically rescued the hyphal growth defect of the arl1 mutant, but not the converse. Further characterization of the ypt6 deletion mutant showed that the number of Golgi cisternae is increased in this mutant compared to that of WT strain, suggesting an alteration of Golgi integrity. In addition, using live cell imaging I showed that the distribution of Actin binding protein 1 (Abp1), which is a reporter for actin patches, was altered in the ypt6 mutant, in that it was no longer restricted to the tip of the filament, as is observed in WT cells. These data suggest that the defect in hyphal growth maintenance of the ypt6 deletion mutant is at least partly associated with an alteration of the distribution of endocytic sites. Thus, I identified a critical role of Ypt6 during invasive hyphal growth and virulence in the human fungal opportunistic pathogen C. albicans and revealed an interaction between Ypt6 and Arl1 in the hyphal growth process
Verma, Sunil Kumar. "Studies on the signalling of the small GTPase Rap1". Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491743.
Texto completoCordeiro, Joao. "Modulation of Rho GTPase signalling during vaccinia virus infection". Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/17273/.
Texto completoLourie, Josephine Anna. "Regulation of the small GTPase ras1p in Schizosaccharomyces pombe". Thesis, Institute of Cancer Research (University Of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312913.
Texto completoWhite, Angeline. "The role of the BipA GTPase in Salmonella enteritidis". Thesis, University of Southampton, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370065.
Texto completoZhao, Wenye. "Rab27a : ligand and interactome discovery for a secretory GTPase". Thesis, Imperial College London, 2017. http://hdl.handle.net/10044/1/57954.
Texto completoWallace, S. "Analysis of Rho GTPase signalling pathways regulating epithelial morphogenesis". Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19565/.
Texto completoWinsor, James. "Energetics of Lipid Bilayer Fusion by the GTPase Atlastin". Research Showcase @ CMU, 2018. http://repository.cmu.edu/dissertations/1204.
Texto completoNi, 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.
Texto completoSmith, Gregory R. "Identification and characterization of GTPase activating proteins for CDC42 /". view abstract or download file of text, 2001. http://wwwlib.umi.com/cr/uoregon/fullcit?p3024536.
Texto completoTypescript. Includes vita and abstract. Includes bibliographical references (leaves 90-98). Also available for download via the World Wide Web; free to University of Oregon users.
Kamkar, Fatemeh. "Pftaire1 (Cyclin Dependent Kinase14): Role and Function in Axonal Outgrowth During the development of the CNS". Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32860.
Texto completoSingh, Komudi. "Oxidant-Induced Cell Death Mediated By A Rho Gtpase In Saccharomyces cerevisiae". Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view.cgi?acc%5Fnum=osu1227716169.
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