Tesis sobre el tema "RhoA"
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Chinestra, Patrick. "Conception de biosenseurs des protéines RhoA, RhoB, RhoC". Toulouse 3, 2012. http://thesesups.ups-tlse.fr/1715/.
Texto completoOur team is interested in understanding the mechanisms of deregulation of cell signaling pathways in the development and maintenance of tumor processes and their consequences in response to anti-tumor therapies. We focuse on Rho proteins as well as on their regulators. They are involved in signaling pathways of cell receptors leading to changes in adhesion, proliferation, motility and balance survival / cellular death. RhoA, RhoB and RhoC are small GTPases switching from an active state (GTP-bound) to an inactive state (GDP-bound) and the homology of which is close to 85%. Overexpression of RhoA and RhoC protein has been described in many tumors; in contrast, there was a decreased expression of RhoB in melanoma and lung cancer. Engineering antibody fragment specific of Rho active conformations, namely biosensors, would allow in situ assessment of these proteins activation in healthy or tumour samples. These tools could be further developed towards diagnosis or prognosis usage, or could even define novel therapeutics markers and be used to answer more fundamental question as their cellular localization, their role in cell migration, or their spatio-temporal activation. Starting from the scFvC1 previously isolated in the group and which is selective for RhoA, RhoB and RhoC active conformations, we have created by random mutagenesis a second library and performed a phage display selection with two aims: 1°) increase the C1 scFv affinity to enhance its interaction potential with active native Rho proteins in order to improve its performance in immuno-histology or to use it as an intracellular antibody. 2°) select variants with a selectivity towards strictly only one of the three Rho excluding the others despite their strong homology. We show that our strategy allowed an affinity increase of scFv and also a selectivity modulation as one variant preferentially binds RhoA and C. Moreover, in contrast to scFvC1 these scFvs immuno-precipitate active endogenous Rho Proteins in eukaryotic cells. In parallel, we have established a method allowing the labelling of an anti-RhoB scFv from the lab, by fusing it to an intein that induce covalent binding of a biotin fluorescent analogue. This approach will improve immuno-histological techniques using fluorescent biosensors
Huppertz, Tilman [Verfasser]. "Charakterisierung der Rekrutierungsdomäne der kleinen Rho-GTPasen RhoA und RhoC / Tilman Huppertz". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2009. http://d-nb.info/1023697491/34.
Texto completoZandvakili, Inuk. "RhoA as a Potential Target in Lung Cancer". University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1445342196.
Texto completoWill, Laura Christine [Verfasser]. "Charakterisierung der Interaktion von p120ctn mit den Rho-GTPasen RhoA und RhoC / Laura Christine Will". Gießen : Universitätsbibliothek, 2019. http://d-nb.info/1178320073/34.
Texto completoWill, Laura [Verfasser]. "Charakterisierung der Interaktion von p120ctn mit den Rho-GTPasen RhoA und RhoC / Laura Christine Will". Gießen : Universitätsbibliothek, 2019. http://d-nb.info/1178320073/34.
Texto completoSoliman, Hesham. "The RhoA/Rho kinase pathway in diabetic cardiomyopathy". Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/43439.
Texto completoSrivastava, Kirtiman. "Pathophysiological role of RhoA/Rho-kinase under oxygen-glucose deprivation/reperfusion and hyperglycaemia". Thesis, University of Nottingham, 2013. http://eprints.nottingham.ac.uk/13533/.
Texto completoArd, Ryan. "Regulation of RhoA Activation and Actin Reorganization by Diacylglycerol Kinase". Thesis, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/22669.
Texto completoBendris, Nawal. "Nouvelles fonctions de la Cycline A2 : régulation de l’invasion cellulaire et de la transition épithéliomésenchymateuse". Thesis, Montpellier 2, 2011. http://www.theses.fr/2011MON20079.
Texto completoCancer aggressiveness is often associated with metastases occurrence and their dissemination can arise following an epithelial to mesenchymal transition (EMT). Cyclin A2 expression is lower in metastases relative to primary colon adenocarcinoma of matched human tumors. This manuscript describes new links between Cyclin A2 and Actin cytoskeleton remodeling in fibroblasts. This regulation requires a cytoplasmic localization of the protein and its N-terminal domain, which is unable to bind CDKs. This new Cyclin A2 activity appears to be mediated by its binding to RhoA. Accordingly, the activity of its GEF is potentiated when Cyclin A2 is present, in vitro. Furthermore, we used a normal mammary epithelial cell line and identified another Cyclin A2 partner, RhoC. Cyclin A2 depletion in this context leads to a reciprocal RhoGTPase activation where RhoA activation is impaired and that of RhoC is increased. Moreover, cell invasiveness is increased in a collagen matrix following Cyclin A2 knockdown in these cells. In addition, the epithelial cells acquire mesenchymal properties, which are exarcerbated by the expression of RasV12 and are characteristic of an EMT. Our work completes the network involving cell cycle proteins in motility. These novel functions of Cyclin A2 will hopefully help to understand the impact of its deregulation in cancer
Keller, 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
Böhringer, Christian. "The role of RhoA in corticogenesis". Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-148975.
Texto completoAgard, Christian. "Nouvelles approches pharmacologiques expérimentales ciblant la voie RhoA/Rho kinase dans l'hypertension artérielle pulmonaire". Nantes, 2009. http://www.theses.fr/2009NANT2091.
Texto completoBei, Yihua. "Implications de la voie RhoA/Rho-kinases dans la physiopathologie des atteintes vasculaires et interstitielles pulmonaires des maladies respiratoires chroniques : études humaines et expérimentales chez la souris". Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05T011/document.
Texto completoThe RhoA/Rho-kinases (ROCK) pathway plays a pivotal role in the pathophysiology of pulmonary hypertension (PH) as its abnormal activation leads to endothelial dysfunction, sustained vasoconstriction and pulmonary vascular remodeling. According to the international classification of PH, chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD) represent two main causes of PH associated with chronic respiratory diseases. These two causes have in common major pathophysiological mechanisms such as endothelial dysfunction, vascular remodeling and interstitial fibrosis. The aims of the present study were to investigate the role of the RhoA/ROCK pathway in the pathophysiology of lung vascular and interstitial injuries in COPD and ILD with or without development of PH, and to study the molecular mechanisms associated with regulation of the RhoA/ROCK pathway in each of these situations.The pulmonary endothelial dysfunction is an essential event in the initiation and progression of COPD. Although the role of the RhoA/Rho-kinase pathway in pulmonary endothelial dysfunction has been demonstrated in smokers with normal lung function, little is known about its role in patients with COPD. The results of our first study demonstrated an increase in RhoA and ROCK activity in pulmonary arteries of patients with COPD, simultaneously with an altered pulmonary endothelial-dependent vasodilation. The increased RhoA activity in patients with COPD was correlated with an impairment of the gene expression and activity of endothelial NO synthase (eNOS).PH associated with pulmonary fibrosis (PF) considerably worsens prognosis of ILD. The results of our second study showed an activation of the RhoA/ROCK pathway in lung tissues of mice intoxicated by intratracheal instillation of bleomycin (BLM). BLM induced severe PF and PH in mice, associated with an increased RhoA and ROCK activity in the lung. We further demonstrated that long-term treatment with fasudil, a selective ROCK inhibitor, reduced BLM-induced lung inflammation, lung fibrosis and PH in mice, at least in part, via inhibition of Smad2/3 phosphorylation in TGF-β1 signaling.PF and PH represent two leading causes of death in patients with systemic sclerosis (SSc). In our third study, we investigated the role of the RhoA/ROCK pathway in the pathophysiology of skin fibrosis and lung injuries in a murine model of SSc induced by intradermal injection of hypochlorous acid (HOCl). We demonstrated that HOCl-induced skin fibrosis was associated with an activation of the RhoA/ROCK pathway in the fibrotic skin, and that long-term treatment with fasudil reduced both skin and lung fibrosis through inhibition of the phosphorylation of Smad2/3 and ERK1/2 in the fibrotic skin.These results suggest the implications of the RhoA/ROCK pathway in the pathophysiology of lung vascular and interstitial injuries in COPD and ILD with and without development of PH. The RhoA/ROCK pathway might be a promising therapeutic target for patients with COPD or ILD with and without PH
Gluth, Markus. "Untersuchungen zum Einfluss von RhoA und der RhoA Effektorkinase PKN auf die TNF-induzierte Barrieredysfunktion in humanen intestinalen Epithelzellen". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2012. http://dx.doi.org/10.18452/16529.
Texto completoInflammatory bowel diseases are relapsing systemic inflammatory diseases of the gastrointestinal tract associated with high morbidity and costs. A plethora of studies demonstrated that impaired intestinal barrier function is a key step in the pathogenesis of inflammatory bowel diseases and that the cytokine tumor necrosis factor alphpa (TNF) is of pivotal importance for this effect. Although the small GTPase RhoA has been implicated in the control of tight junction function, its role in TNF induced barrier dysfunction is not entirely understood due to the complexity of its downstream signaling pathways. Therefore, the contribution of RhoA and its effector kinase PKN on TNF induced barrier dysfunction was investigated in vitro. An inducible expression system that allowed the doxycyline controlled expression of a constitutively active (CA) RhoA and PKN mutant as well as a dominant negative (DN) PKN mutant was generated. Induction of CA RhoA expression led to an impaired epithelial barrier. Simultaneous Interferon-gamma and TNF treatment also resulted in barrier perturbation, but this defect was attenuated when CA RhoA was expressed. As treatment with TNF resulted in activation of the RhoA effector kinase PKN, this protein constitutes a candidate molecule for the mediation of these effects. Inhibition of PKN by inhibitory compounds as well as expression of a dominant negative PKN mutant aggravated TNF-induced barrier dysfunction, characterized by a decline in transepithelial electrical resistance and increased ion permeability. These alterations were accompanied by an increase in myosin light-chain and NF-kappaB p65 subunit phosphorylation level as well as morphological changes of the tight junctions. Conversely, expression of a CA PKN mutant attenuated or prevented these changes. These results provide support for a potential role of the RhoA effector kinase PKN in modulating the barrier disrupting effects of TNF in the intestinal epithelium.
Stirling, Lee. "Dual Roles for Rhoa/Rho-Kinase in the Regulated Trafficking of a Voltage-Sensitive Potassium Channel". ScholarWorks @ UVM, 2009. http://scholarworks.uvm.edu/graddis/223.
Texto completoKaarbo, Mari y n/a. "The Role of RhoA in Early Heart Development". Griffith University. School of Biomolecular and Biomedical Science, 2005. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20060105.091005.
Texto completoSahai, Erik Anand. "Functional analysis of RhoA and its effector molecules". Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300839.
Texto completoKaarbo, Mari. "The Role of RhoA in Early Heart Development". Thesis, Griffith University, 2005. http://hdl.handle.net/10072/366791.
Texto completoThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
Full Text
Krause, Sven Matthias. "Small Rho-GTPase function in myelinating cells of the vertebrate peripheral nervous system with focus on RhoA /". Zürich : ETH, 2008. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=17732.
Texto completoTurner, Stephanie J. "RhoA, B, and C in cancer study of statin-induced changes in Rho signaling, and identification of isoform-specific Rho effectors /". Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p3359512.
Texto completoTitle from first page of PDF file (viewed July 7, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 77-106).
Silva, Gisele Espinha Teixeira da. "Sinalização da GTPase RhoA nas respostas celulares após estresse genotóxico promovido por radiação ultravioleta". Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/87/87131/tde-19102016-165552/.
Texto completoThe RhoA GTPase signaling pathway acts on many cellular processes. To evaluate this possible RhoA function after stress caused by ultraviolet radiation, mutant clones expressing RhoA in its constitutively active or dominant negative forms were generated. After exposure of the cells to ultraviolet radiation, cell lines showed a higher sensitivity and a delayed recovery capacity when the RhoA activity is reduced. The impaired repair reduced the cells proliferation and survival under RhoA deficiency. In cell lines deficient in NER pathway, we notice that these cell lines, have a further reduced ability to repair damaged DNA under RhoA inhibition.
Yusuf, Muhammad Zuhair. "cAMP signaling reverses platelet spreading via inhibition of RhoA". Thesis, University of Hull, 2016. http://hydra.hull.ac.uk/resources/hull:14381.
Texto completoLawder, John J. "The Role of RhoA in GPR116 Mediated Alveolar Homeostasis". University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1563526829841322.
Texto completoDel, Re Dominic Pasquale. "RhoA as a mediator of cardiomyocyte survival and apoptosis". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3316411.
Texto completoTitle from first page of PDF file (viewed Sept. 9, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 121-141).
Jatho, Aline. "The role of the monomeric GTPase RhoA in cardiac fibroblasts". Doctoral thesis, Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2014. http://hdl.handle.net/11858/00-1735-0000-0023-98EA-5.
Texto completoLima, Victor Vitorino. "Papel da O-glicosilação com N-acetil-glucosamina (O-GlcNAc) nas alterações vasculares associadas a altos níveis de endotelina-1". Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/17/17133/tde-15082013-114532/.
Texto completoLIMA, V.V. O-GlcNAcylation contributes to the vascular effects of ET-1 via activation of RhoA/Rho-kinase pathway. 2012. 106 f. Ph.D. Thesis - Faculdade de Medicina de Ribeirão Preto Universidade de São Paulo, Ribeirão Preto, 2012. Glycosylation with O-linked -N-acetylglucosamine (O-GlcNAc) is a highly dynamic post-translational modification that plays a key role in signal transduction pathways. The cycling of O-GlcNAc is controlled by two enzymes: UDP-NAc transferase (OGT) and O-GlcNAcase (OGA). Whereas OGT catalyses the addition of O-GlcNAc to the hydroxyl group of serine and threonine residues of a target protein, OGA catalyses the hydrolytic cleavage of O-GlcNAc from post-translationally-modified target. Proteins with an important role in vascular function are targets for O-GlcNAcylation and we have recently shown that the vascular content of O-GlcNAc-proteins is augmented in arteries from DOCA-salt rats. Since endothelin-1 (ET-1) production is increased in the vasculature of salt-sensitive forms of hypertension, we tested the hypothesis that O-GlcNAc contributes to the vascular effects of ET-1, via activation of the RhoA/Rho-kinase pathway. Incubation of rat aortas or vascular smooth muscle cells (VSMCs) with ET-1 (0,1 mol/L) produced a time-dependent increase in O-GlcNAc levels, decreased expression of O-GlcNAc transferase (OGT) and -N-acetylglucosaminidase (OGA), key enzymes in the O-GlcNAcylation process. Overnight treatment of aortas with ET-1 increased phenylephrine (PE) vasoconstriction. ET-1 effects were not observed when vessels were previously instilled with anti-OGT antibody or after incubation with an OGT inhibitor (ST045849, 100 mol/L). Aortas from DOCA-salt rats, which exhibit increased pre-pro-ET-1 expression, displayed increased contractions to PE and augmented levels of O-GlcNAc proteins. Treatment of DOCA-salt rats with atrasentan (ETA antagonist) abrogated augmented vascular levels of O-GlcNAc and prevented increased PE vasoconstriction. Aortas from rats chronically infused with low rate of ET-1 (2 pmol/Kg/min, 14days) exhibited increased O-GlcNAc-proteins and enhanced PE responses. These changes are similar to those induced by PUGNAc (OGA inhibitor which increases O-GlcNAc levels). ET-1 as well as PUGNAc augmented contractions to PE in endothelium-denuded rat aortas, an effect that was abolished by the Rho kinase inhibitor Y-27632 (1 mol/L). Incubation of VSMCs with ET-1 did not change expression of ROCK-, ROCK-, CPI-17, MYPT-1 or MLC, but increased phosphorylation levels of MYPT-1 (Thr853), CPI-17 (Thr38) and MLC (Thr18/Ser19). The effects of ET-1 on MYPT-1, CPI-17 and MLC phosphorylation were prevented by the OGT inhibitor and OGT siRNA transfection, as well as by atrasentan. ET-1 increased RhoA expression and activity in VSMCs, and this effect was abolished by OGT siRNA transfection and OGT inhibition. ET-1 also augmented expression of PDZ-Rho GEF and p115-Rho GEF in VSMCs and this was prevented by OGT siRNA, OGT inhibition (ST045849) and ETA receptor blockade (atrasentan, 1 mol/L). In conclusion, our data strongly suggest that ET-1 augments O-GlcNAc levels and this modification contributes to increase vascular contractile responses, via activation of the RhoA/Rho-kinase pathway. We speculate that the modulatory effect of ET-1 on O-GlcNAcylation may represent a novel mechanism underlying the vascular effects of the peptide.
Assis, Welton Ferreira de [UNESP]. "Efeitos da manutenção em ambiente enriquecido em aspectos cognitivos e nas proteínas AKT, RhoA e RhoE musculares de ratos diabéticos". Universidade Estadual Paulista (UNESP), 2016. http://hdl.handle.net/11449/150223.
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O diabetes mellitus é um quadro patológico que traz diversas complicações como prejuízos metabólicos, endócrinos, cognitivos, sarcopenia, emagrecimento, hiperfagia e polidispia. Estudos prévios têm demonstrado que a manutenção de animais em ambiente enriquecido traz um conjunto de benefícios através dos estímulos que oferece, sendo a atividade física um desses estímulos. Apesar disso, poucos estudos investigaram os efeitos da manutenção de animais diabéticos em ambiente enriquecido. Desta forma, a presente dissertação teve por objetivos investigar os efeitos do diabetes na atividade física realizada no ambiente enriquecido e investigar os efeitos do ambiente enriquecido em parâmetros bioquímicos, morfométricos, cognitivos e nas proteínas AKT, RhoA e RhoE musculares. Para isso, na primeira etapa do desenho experimental, ratos wistar foram distribuídos em dois grupos: controle e diabetes. O diabetes foi induzido por estreptozotocina via intraperitonial (50 mg/kg) e os animais foram inseridos em gaiolas amplas contendo objetos coloridos e rodas de atividade com contador de giros. O rastreamento foi realizado pelo sistema para análises cinemáticas, Digital Video For Biomechanics - Windows 32 bits (DVIDEOW® ) e software Matlab® . Na segunda etapa do desenho experimental, os animais foram distribuídos nos seguintes grupos: controle, diabetes e diabetes gaiola enriquecida. O diabetes foi induzido por estreptozotocina via intraperitonial (50 mg/kg) e os animais foram mantidos em gaiolas padrão ou ambiente enriquecido. A massa corporal, ingestão hídrica e alimentar foram coletadas duas vezes por semana e a glicemia no início e final do experimento. Ao final do período experimental foi registrado o comprimento corporal e coletadas amostras do músculo gastrocnêmio para as análises da fosforilação da AKT e expressão de RhoA e RhoE. Para estas análises, foram utlizados o teste t ou Mann-Whitney para as análises entre dois grupos e análise de variância (ANOVA) two way, com posthoc de Bonferroni (significância de 5%) para as demais análises. O software SPSS® foi utilizado para as análises. O diabetes reduziu o acúmulo de atividade física no ambiente enriquecido. A manutenção no ambiente enriquecido amenizou o aumento da hiperglicemia e melhorou, parcialmente, o desempenho no labirinto aquático de Morris dos animais diabéticos. A redução na massa corporal, índice de Lee e o aumento na ingestão hídrica e alimentar nesses animais diabéticos não foram influenciados pelo ambiente enriquecido. Ainda, neste período de 6 semanas, não houve efeitos do diabetes ou do ambiente enriquecido na fosforilação da AKT e expressão das proteínas RhoA e RhoE. Pode ser concluído que a manutenção no ambiente enriquecido traz benefícios aos animais diabéticos, apesar deste realizar menos atividade física que animais controles.
Diabetes mellitus is a pathological condition that brings several complications such as metabolic, endocrine, cognitive loss, sarcopenia, weight loss, hyperphagia and polydipsia. Previous studies have shown that keeping animals in enriched environment brings a set of benefits through the stimuli it provides, and the physical activity is one of these stimuli. Despite this, few studies have investigated the effects of the maintenance of animals in diabetic enriched environment. The present dissertation aimed to investigate the effects of diabetes on physical activity performed in the enriched environment and to investigate the effects of enriched environment on biochemical parameters, morphometric, cognitive, and AKT, RhoA and RhoE proteins in the muscle. For this, in the first step of the experimental design, wistar rats were distributed into two groups: control and diabetes. Diabetes was induced streptozotocin via intraperitoneal (50 mg/kg) and the animals were placed in large cages, containing colored objects and the wheels of activity and a counter of revolutions. The tracking was carried out by the system for analysis, kinematics, Digital Video For Biomechanics - 32-bit Windows (DVIDEOW®) and Matlab® software. In the second step of the experimental design, the animals were distributed into the following groups: control, diabetic and diabetic - enriched cage. Diabetes was induced streptozotocin via intraperitoneal (50 mg/kg) and the animals were kept in cages of standard or enriched environment. The body mass, the intake of water and food were collected twice per week and the blood glucose at the beginning and end of the experiment. At the end of the experimental period was recorded and the length of the body and collected samples of the gastrocnemius muscle for the analysis of the phosphorylation of AKT and expression of RhoA and RhoE. For these analyses, were used the t test or the Mann-Whitney test for analyses between two groups and analysis of variance (ANOVA) two way, with posthoc Bonferroni (significance of 5%) for all other analyses. The software SPSS® was used for the analyses. Diabetes reduced the accumulation of physical activity in the enriched environment. The maintenance in the enriched environment slowdown the increase of hyperglycemia and improved, in part, the performance of the diabetic animals in the water maze of Morris. The reduction in the body mass, index of Lee and the increase in the intake of water and food of these diabetic animals were not influenced by the enriched environment. Still, in this period of 6 weeks, there were no effects of the diabetes or from the enriched environment in the phosphorylation of AKT and expression of the RhoA and RhoE proteins. It can be concluded that maintenance in enriched environment brings benefits to the animals and diabetic patients, although this perform less physical activity than control animals.
Assis, Welton Ferreira de. "Efeitos da manutenção em ambiente enriquecido em aspectos cognitivos e nas proteínas AKT, RhoA e RhoE musculares de ratos diabéticos /". Rio Claro, 2016. http://hdl.handle.net/11449/150223.
Texto completoBanca: Julio Wilson dos Santos
Banca: Andressa Coope dos Santos
Resumo: O diabetes mellitus é um quadro patológico que traz diversas complicações como prejuízos metabólicos, endócrinos, cognitivos, sarcopenia, emagrecimento, hiperfagia e polidispia. Estudos prévios têm demonstrado que a manutenção de animais em ambiente enriquecido traz um conjunto de benefícios através dos estímulos que oferece, sendo a atividade física um desses estímulos. Apesar disso, poucos estudos investigaram os efeitos da manutenção de animais diabéticos em ambiente enriquecido. Desta forma, a presente dissertação teve por objetivos investigar os efeitos do diabetes na atividade física realizada no ambiente enriquecido e investigar os efeitos do ambiente enriquecido em parâmetros bioquímicos, morfométricos, cognitivos e nas proteínas AKT, RhoA e RhoE musculares. Para isso, na primeira etapa do desenho experimental, ratos wistar foram distribuídos em dois grupos: controle e diabetes. O diabetes foi induzido por estreptozotocina via intraperitonial (50 mg/kg) e os animais foram inseridos em gaiolas amplas contendo objetos coloridos e rodas de atividade com contador de giros. O rastreamento foi realizado pelo sistema para análises cinemáticas, Digital Video For Biomechanics - Windows 32 bits (DVIDEOW® ) e software Matlab® . Na segunda etapa do desenho experimental, os animais foram distribuídos nos seguintes grupos: controle, diabetes e diabetes gaiola enriquecida. O diabetes foi induzido por estreptozotocina via intraperitonial (50 mg/kg) e os animais foram mantidos em gaiolas padrão ou ambiente enriquecido. A massa corporal, ingestão hídrica e alimentar foram coletadas duas vezes por semana e a glicemia no início e final do experimento. Ao final do período experimental foi registrado o comprimento corporal e coletadas amostras do músculo gastrocnêmio para as análises da fosforilação da AKT e expressão de RhoA e ... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Diabetes mellitus is a pathological condition that brings several complications such as metabolic, endocrine, cognitive loss, sarcopenia, weight loss, hyperphagia and polydipsia. Previous studies have shown that keeping animals in enriched environment brings a set of benefits through the stimuli it provides, and the physical activity is one of these stimuli. Despite this, few studies have investigated the effects of the maintenance of animals in diabetic enriched environment. The present dissertation aimed to investigate the effects of diabetes on physical activity performed in the enriched environment and to investigate the effects of enriched environment on biochemical parameters, morphometric, cognitive, and AKT, RhoA and RhoE proteins in the muscle. For this, in the first step of the experimental design, wistar rats were distributed into two groups: control and diabetes. Diabetes was induced streptozotocin via intraperitoneal (50 mg/kg) and the animals were placed in large cages, containing colored objects and the wheels of activity and a counter of revolutions. The tracking was carried out by the system for analysis, kinematics, Digital Video For Biomechanics - 32-bit Windows (DVIDEOW®) and Matlab® software. In the second step of the experimental design, the animals were distributed into the following groups: control, diabetic and diabetic - enriched cage. Diabetes was induced streptozotocin via intraperitoneal (50 mg/kg) and the animals were kept in cages of standard or enriched environment. The body mass, the intake of water and food were collected twice per week and the blood glucose at the beginning and end of the experiment. At the end of the experimental period was recorded and the length of the body and collected samples of the gastrocnemius muscle for the analysis of the phosphorylation of AKT and expression of RhoA and RhoE. For these analyses, ... (Complete abstract click electronic access below)
Mestre
Leppert, Amanda Fitch. "GENETIC ANALYSIS OF RHOA SIGNALING DURING EPITHELIAL MORPHOGENESIS IN DROSOPHILA". Master's thesis, University of Central Florida, 2004. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/4430.
Texto completoM.S.
Department of Biology
Arts and Sciences
Biology
Zhou, Xuan. "RhoA GTPase Controls Cytokinesis and Programmed Necrosis of Hematopoietic Progenitors". University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1378197381.
Texto completoSchömel, Franziska [Verfasser]. "Einfluss von RhoA auf die Invasivität von Mammakarzinomzellen / Franziska Schömel". Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2021. http://d-nb.info/1234847086/34.
Texto completoMoose, Devon Lyle. "Rhoa-myosin II pathway confers resistance to fluid shear stress". Thesis, University of Iowa, 2018. https://ir.uiowa.edu/etd/6221.
Texto completoMARCHESI, STEFANO. "DEPDC-1B MODULATES RHOA-DEPENDENT CELL ADHESION DURING MITOTIC ENTRY". Doctoral thesis, Università degli Studi di Milano, 2011. http://hdl.handle.net/2434/214609.
Texto completoHowe, Grant Alexander. "Identification of Mechanisms Regulating Endothelial Cell Capillary Morphogenesis". Thesis, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/26196.
Texto completoSalo, Paul David. "Protein prenylation inhibitors reveal a novel role for rhoa and rhoc in trafficking of g protein-coupled receptors through recycling endosomes". Diss., Atlanta, Ga. : Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/26711.
Texto completoCommittee Co-Chair: Hud, Nicholas; Committee Co-Chair: Radhakrishna, Harish; Committee Member: Doyle, Donald; Committee Member: Fahrni, Christoph; Committee Member: McCarty, Nael. Part of the SMARTech Electronic Thesis and Dissertation Collection.
Loomis, Rebecca Jo Su Lishan. "The role of RhoA signaling pathways in regulating HIV-1 replication". Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2006. http://dc.lib.unc.edu/u?/etd,517.
Texto completoTitle from electronic title page (viewed Oct. 10, 2007). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Curriculum of Genetics and Molecular Biology." Discipline: Genetics and Molecular Biology; Department/School: Medicine.
Rao, Milly Yushu. "Role of the RhoA/ROCK pathway in hypertension associated with diabetes". Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/38344.
Texto completoBöhringer, Christian [Verfasser] y Carsten [Akademischer Betreuer] Culmsee. "The role of RhoA in corticogenesis / Christian Böhringer. Betreuer: Carsten Culmsee". München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2012. http://d-nb.info/1027066259/34.
Texto completoDovas, Athanassios. "Regulation of RhoA by PKCa during syndecan-4-mediated cell adhesion". Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434916.
Texto completoBetuing, Sandrine. "Regulation 2-adrenergique du cytosquelette dans les preadipocuytes : implication de rhoa". Toulouse 3, 1998. http://www.theses.fr/1998TOU30202.
Texto completoChen, Weihua. "Role of RhoA/ROCK pathway in angiogenesis and their potential values in prostate cancer treatment". Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05T047/document.
Texto completoProstate cancer remains a major cause of mortality among males in western countries. Treatment options for metastatic castration-resistant disease remain limited. There is a continuing unmet need for new systemic interventions in patients with progressive prostate cancer. RhoA/Rho-associated protein kinases (ROCK) are key regulators of the cytoskeleton and have been implicated in PCa angiogenesis and tumour invasion. In the first study (Part I), we investigated the anti-angiogenic effects of fasudil, a ROCK inhibitor, on PCa-induced angiogenesis in vitro. Proliferation of PCa-conditioned human umbilical vein endothelial cells (HUVECs) was assessed using a bromodeoxyuridine (BrdU) assay, and migration was assessed with a wound healing assay. In vitro angiogenesis of PCa-conditioned HUVECs was evaluated by tube formation and a spheroid sprouting assay. Fasudil inhibited PCa-induced endothelial cell proliferation, and also decreased PCa-induced endothelial cell migration. In the in vitro angiogenesis assay, tube formation and spheroid sprouts were significantly inhibited at fasudil in a dose dependent manner. Western blotting results showed that expression of phosphorylated myosin phosphatase target subunit 1 (MYPT-1) was significantly lower after fasudil treatment, confirming that fasudil inhibited ROCK activity in these model systems. In the second study (Part II & III), we evaluated RhoA expression and activity in a total of 34 paraffin embedded and 20 frozen prostate specimens, respectively, obtained from 45 patients treated with radical prostatectomy for clinically localized cancer. The expression patterns of RhoA were tested by immunohistochemical staining and Western blotting, and further compared between the tumour centre, tumour front and distant peritumoral tissue. RhoA activity was assessed by G-LISA. Our results showed an increasing gradient of expression from the centre to the periphery of index tumour foci. RhoA expression was indeed significantly higher at the tumour front as compared to tumour centre, using immunohistochemistry (p=0.001). Gleason score was significantly higher in the patients with higher RhoA expression in both the tumour front and tumour centre (p=0.044 and 0.039, respectively). After a median follow-up of 52 months, the rate of PSA relapse was higher in patients with a higher RhoA expression at the tumour front (62.5% vs 35%), although the difference was not significant (p=0.089). There was no association between RhoA expression and PSA, pathological stage. We also found ROCK2 expression, but not ROCK1 expression, was significantly higher in the prostate cancer tumor front. In conclusion, we found fasudil significantly inhibits the key steps of endothelial cell angiogenesis, including proliferation, migration, capillary tube formation and spheroid sprouting, in a dose-dependent manner. These effects may due to inhibition of ROCK activity induced by PCa cell secretions. We also identified higher RhoA and ROCK2 expression in human prostate tumour front. The correlation of higher RhoA expression with higher Gleason score and higher rate of cancer relapse. This indicated the association of RhoA/ROCK2 pathway with aggressiveness of prostate cancer. The insights described here may provide the foundation for novel therapeutic approaches targeting RhoA/ROCK pathway to inhibit angiogenesis and clinically aggressiveness of PCa. Fasudil may be a useful anti-angiogenic agent and should be investigated further for its potential role in PCa treatment
Rochelle, Tristan. "Signalisation des GTPases de la famille Rho dans les phénotypes migratoires induits par les différentes formes de Bcr-Abl". Thesis, Poitiers, 2012. http://www.theses.fr/2012POIT1401/document.
Texto completoBcr-Abl chimeric oncogenes (p190bcr-abl and p210bcr-abl) result from the t(9,22) chromosomal translocation that fuse the bcr and the c-abl genes. p210bcr-abl and p190bcr-abl are associated with Chronic Myelogenous Leukemia (CML) and a subset of Acute Lymphoblastic Leukemia (ALL) respectively. The only difference between these two chimeras is the presence of a specific RhoA-GEF domain in the p210bcr-abl oncogene. Bcr-Abl expression in Ba/F3 lymphoblasts induces spontaneous migration of these cells without apparent directionality. Motility triggering of Bcr-Abl-expressing Ba/F3 depends on the RhoGTPase Rac1.RhoA activity is associated with a typical amoeboid movement of Ba/F3p210 cells embedded in Matrigel™ 3D matrix, whereas the Ba/F3p190 cells, devoid of RhoA activity, display a rolling-type motility. In this work we showed that activation of the RhoA effector ROCK1 triggers two parallel pathways which are both necessary for amoeboid movement: 1) the Myosin Light chain (MLC) pathway 2) ADF family proteins (Actin Depolymerizing Factor) pathway, specifically the ADF/destrin isoform. Besides, we showed that Ba/F3p190 cells could assemble invadopodia-like structures. The formation of these structures is driven by the reduction of RhoA activity associated with the absence of the DH/PH domain in p190bcr-abl and correlates with an increase in Cdc42 activity. We finally demonstrated that the RhoA/ROCK pathway is constitutively activated in CD34+ cells isolated from CML patients while not in their normal counterparts. We also demonstrated that this activation is independent of the tyrosine Kinase activity of Bcr-Abl
Nyamandi, Vongai. "The role of RhoA/ROCK signaling in the development of diabetic cardiomyopathy". Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/64116.
Texto completoCraig, Graham Peter. "INOS mediates increased RhoA expression and altered cell signaling in diabetic cardiomyopathy". Thesis, University of British Columbia, 2006. http://hdl.handle.net/2429/32344.
Texto completoPharmaceutical Sciences, Faculty of
Graduate
Tirrell, Lee Sean. "The role of RhoA GTPase activating protein DLC2 in painful diabetic neuropathy". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/195956.
Texto completopublished_or_final_version
Anatomy
Master
Master of Philosophy
Callis, Thomas. "Characterization of genes required for RhoA signaling during epithelial morphogenesis in Drosophila". Honors in the Major Thesis, University of Central Florida, 2003. http://digital.library.ucf.edu/cdm/ref/collection/ETH/id/685.
Texto completoBachelors
Arts and Sciences
Biology
Cooper, Katherine. "Analysis of RhoA GTPase and the cytoskeleton in planar polarity of Drosophila". Thesis, University of Sheffield, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401119.
Texto completoMegrelis, Laura. "Caractérisation de Fam65b, un nouvel inhibiteur de RhoA, impliqué dans la réponse des lymphocytes T en aval de CCR7". Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCB092/document.
Texto completoThe motility of naive T lymphocytes between the blood and secondary lymphoid organs is essential to the efficiency of the adaptative immune response, and allows those cells to meet their cognate antigen. Numerous signaling pathways are involved in this phenomenon, such as Rho GTPases, modulators of the actin cytoskeleton. We have identified Fam65b as a new regulator of T lymphocytes recirculation. We have shown that a decrease of Fam65b expression in human primary T cells increases the morphological polarization, the adhesion and the in vitro migration of those cells. Looking for a more physiological model, we developed, in the lab, a Fam65b KO (Knock-Out) mouse, specific to the T lineage. In those animals, T cells showed decreased levels of F-actin, an increase in the display of L-selectin and integrins, and a slower and less straight migration, compared to WT (Wild-Type) T cells. On the other hand, we weren't able to see any significant differences in the morphological polarisation, the in vitro migration or the homing capacity of the Fam65b KO T cells. We have identified Rho GTPases as mediators of the effects of Fam65b. We showed, in flow cytometry, that the amount of RhoA-GTP and Rac-GTP are increased in the Fam65b KO cells. The RhoA-GTP levels are also increased in human primary T cells expressing low levels of Fam65b. We have identified, in in vitro experiments, that Fam65b slows down RhoA loading with GTP by its GEF proteins, thus inhibiting RhoA activity. Moreover, we showed that Fam65b dissociates from RhoA after chemokine stimulation of T cells, thus allowing RhoA activation. The phosphorylation of Fam65b is a probable cause to this phenomenon. Fam65b also dissociates from Rac1 in these conditions, although no mechanism is yet known. Furthermore, the transcription factor FOXO1 controls the expression of Fam65b. FOXO1 is also known to control the homing capacity of T cells, since it controls the expression of molecules involved in the entry of lymphocytes in the lymph nodes. Fam65b, an atypical regulator of Rho GTPases activity, thus represents a new connection between the PI3K/FOXO1 and the Rho GTPases pathways
Gluth, Markus [Verfasser], Wolfgang [Akademischer Betreuer] Uckert, Franz [Akademischer Betreuer] Theuring y Daniel C. [Akademischer Betreuer] Baumgart. "Untersuchungen zum Einfluss von RhoA und der RhoA Effektorkinase PKN auf die TNF-induzierte Barrieredysfunktion in humanen intestinalen Epithelzellen / Markus Gluth. Gutachter: Wolfgang Uckert ; Franz Theuring ; Daniel C. Baumgart". Berlin : Humboldt Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2012. http://d-nb.info/1023725754/34.
Texto completoOsaki, Juliana Harumi. "O papel de RhoA e Rac1 GTPases nas respostas celulares após danos no DNA induzidos por radiação ionizante gama". Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-22092015-075415/.
Texto completoThe mechanism by which a cell responds to DNA damage is extremely important. This occurs by a quick activation of the DNA damage repair machinery, which consists of an intricate protein signaling network culminating in DNA repair. But if the damages are irreparable occurs there is activation of cell death mechanisms. RhoA and Rac1 belong to family of small Rho GTPases, signaling proteins that act as molecular switches cycling between the active state (GTP-bound) and inactive state (GDP-bound). Members of this family are implicated in the control of diverse cellular process such as cytoskeletal remodeling, migration, adhesion, endocytosis, cell cycle progression, and oncogenesis. However, despite Rho proteins are involved in a broad spectrum of biological activities, there is just a few information about their roles in the maintenance of genomic integrity, that is, when the cells are subjected to some kinf of genotoxic agent. To investigate the involvement of the GTPases RhoA and Rac1 in cellular responses to gamma radiation, we generated from human cervix carcinoma cells - HeLa, clonal sublines of RhoA and Rac1 mutants, exogenous and stably expressing the constitutively active RhoA (HeLa-RhoA V14), the dominant negative RhoA (HeLa-RhoA N19), the constitutively active Rac1 (HeLa-Rac1 V12) and the dominant negative Rac1 (HeLa-Rac1 N17). After all these cell lines have been exposed to different doses of gamma radiation, we found that both GTPases, RhoA and Rac1, are activated in response to the radiation effects. Furthermore, the modulation of two enzymes activity, by using the mutant clones, led to a change in cellular responses to the DNA damage, as the reduction in the capacity of repairing DNA single and double strand breaksr. On the other hand, the deficiency of RhoA or Rac1 GTPase led to a reduction of Chk1 and Chk2 activation, or on the phosphorylation of histone H2AX, respectively, hindering the mechanisms of DNA damage detection and arresting cells in the G1/S and/or G2/M checkpoints of cell cycle. These factors significantly contributed to the reduction of cell proliferation and survival, leading cells to death. Finally, cellular assays of DNA damage repair of exogenous DNA by Homologous Recombination (HR) and Non-Homologous End Joining (NHEJ), demonstrated that RhoA inhibition significantly reduced the repair efficiency of both pathways. Thus, this work demonstrates and reinforces the existence of other biological functions of small GTPases RhoA and Rac1 in HeLa cells, by regulating cellular responses to DNA damage induced by exposure to gamma radiation, modulating the survival, proliferation and indirectly modulating the response to DNA damage repair pathway through the Homologous Recombination and Non-Homologous Recombination