Dissertations / Theses on the topic 'Myositi'
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Meyer, Alain. "Rôle de la mitochondrie et du stress oxydant au cours des myopathies inflammatoires." Thesis, Strasbourg, 2017. http://www.theses.fr/2017STRAJ118/document.
Full textInflammatory myopathies are rare autoimmune diseases whose common denominator is muscle weakness and inflammation. Their origin is not known and conventional treatments are partially effective. Using an epidemiological approach, we have shown that the study of incidence and prevalence is an useful tool for identifying determinants of inflammatory myopathies. However, better identification and classification of patients is mandatory to refine the epidemiology of inflammatory myopathies. Using a translational approach, we have shown that, compared with other inflammatory myopathies, perifascicular mitochondrial dysfunctions are a characteristic of dermatomyositis, which play a role in exercise intolerance and in the maintenance of inflammation. These results open up new avenues to better understand and treat inflammatory myopathies
Ceribelli, A. "PROTEIN AND RNA IMMUNOPRECIPITATION FOR THE IDENTIFICATION OF SPECIFIC SERUM AUTOANTIBODIES IN SYSTEMIC AUTOIMMUNE RHEUMATIC DISEASES." Doctoral thesis, Università degli Studi di Milano, 2016. http://hdl.handle.net/2434/365538.
Full textZhu, Jing. "The role of nonmuscle myosin IIA in endothelial cell." Morgantown, W. Va. : [West Virginia University Libraries], 2010. http://hdl.handle.net/10450/11006.
Full textTitle from document title page. Document formatted into pages; contains viii, 37 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 33-37).
Mariampillai, Kubéraka. "Une nouvelle classification des myopathies inflammatoires fondée sur des manifestations cliniques et la présence d'auto-anticorps spécifiques par analyses multidimensionnelles." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066501.
Full textIdiopathic inflammatory myopathies (IIM or myositis) are heterogeneous in their pathophysiology and prognosis. The emergence of myositis-specific autoantibodies (MSA) suggests homogenous subgroups of patients. Our aim was to find a new classification of IIM based on phenotypic, biological and immunological criteria. An observational, retrospective, multicentre study was led from the database of the myositis French network. We included 260 adult myositis, defined according to historical classifications for polymyositis (PM), dermatomyositis (DM) and inclusion body myositis (IBM). All patients did at least a screening with a line blot assays testing anti-Jo1, anti-PL7, anti-PL12, anti-Mi-2, anti-Ku, anti-PMScl, anti-Scl70 and anti-SRP. We performed multiple correspondence analysis and hierarchical clustering analysis to aggregate patients in homogenous subgroups. Four clusters emerged. The first cluster (n=77) regrouped primarily IBM patients with vacuolated fibres, mitochondrial abnormalities and inflammation with invaded fibres. The second cluster (n=91) was characterized by immune-mediated necrotizing myopathy (IMNM) in the majority of patients, with anti-SRP and anti-HMGCR antibodies. The third cluster (n=52) regrouped mainly DM patients with anti-Mi-2, anti-MDA5, or anti-TiF1 gamma antibodies. The fourth cluster (n=40) was defined by anti-synthetase syndrome (ASS), with the notable presence of anti-Jo1 or anti-PL7 antibodies. The histological criteria are dispensable for the prediction of the clusters, underlining the importance of a clinico-serological classification
Bergua, Cecile. "Pathogénicité des auto-anticorps anti-SRP et anti-HMGCR au cours des myopathies nécrosantes auto-immunes." Thesis, Normandie, 2017. http://www.theses.fr/2017NORMR067/document.
Full textAutoimmune myopathies (AIM), classically called myositis or idiopathic inflammatory myopathies, represent a group of diseases characterized by clinical, histopathologic and biologic properties. One of the most notable properties is the presence of autoantibodies (aAb) in approximately 60% of patients. AIM includes five principal entities: dermatomyositis, polymyositis, inclusion body myositis, overlap myositis including the anti-synthetase syndrome and immune-mediated necrotizing myopathies (IMNM). IMNM have recently been individualized among AIM as severe diseases frequently associated with aAb directed against Signal Recognition Particle (SRP) or 3-Hydroxy-3-MethylGlutaryl-CoA Reductase (HMGCR). Since SRP and HMGCR have an intracellular localization, the role of anti-SRP and anti-HMGCR aAb in the pathophysiology of IMNM remains unclear. Anti-SRP and anti-HMGCR aAb were recently shown to be pathogenic to muscle cells in vitro but in vivo effects remain unknown.During this thesis, I studied the pathophysiological role of anti-SRP and anti-HMGCR aAb in vivo in mice. Passive transfer of IgG purified from plasma of IMNM patients positive for anti-SRP and anti-HMGCR aAb to wild-type mice elicited a muscle weakness. Immune-deficient Rag2-/- mice presented a prolonged muscle deficit, whereas complement component C3 deficient mice had limited signs. Mice injected with anti-SRP+ IgG displayed a strong muscle weakness with mild myocytic necrosis. The muscle deficit was milder and histopathologic findings were not always present in mice receiving anti-HMGCR+ IgG. This is in accordance with clinical findings in anti-SRP+ patients which present a more severe disease than anti-HMGCR+ patients. When supplemented with human complement, mice receiving anti-HMGCR+ IgG showed a more severe muscle deficit. This supplementation increased the deficit induced by anti-SRP IgG in a milder way. In collaboration with INSERM UMRS974, we showed that the targets SRP and HMGCR can be detected on the surface of myofibres in vitro, suggesting that they could be accessible to aAb in vivo.Together, these results demonstrate for the first time the pathogenic role of anti-SRP and anti-HMGCR aAb in vivo and the implication of complement, contributing to a progress in the comprehension of MNAI pathophysiology
Stevens, Richard. "Two light chains of the unconventional myosin Myo2p /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/9226.
Full textCunningham, Cynthia A. "Induction of myosin cross-reactive antibody and cytolytic T cell responses in mice with Streptococcus pyogenes." Morgantown, W. Va. : [West Virginia University Libraries], 2000. http://etd.wvu.edu/templates/showETD.cfm?recnum=1530.
Full textEnnomani, Hajer. "Contractile response of biomimetic actomyosin systems." Thesis, Université Grenoble Alpes (ComUE), 2015. http://www.theses.fr/2015GREAY054/document.
Full textCellular contractility – the internal generation of force by a cell orchestrated by theactomyosin machinery – is a critical regulator of a wide range of cellular processes includingthe establishment of cell polarity, cell migration, tissue integrity or morphogenesis duringdevelopment. Disruptions of the force generation and of mechanical properties of living cellsaffect their physiological functions and consequently can lead to pathological defectsincluding cancer. However, the parameters or mechanisms that drive force production by theactin-myosin system and their mode of regulation in cells are not fully understood. During myPhD, I used biomimetic system made of a minimum set of proteins to study the properties ofactomyosin contractile systems. The goal was to understand how/if the actin architecture canmediate the contractile response. For this purpose, I was first interested in building a varietyof actin organization that will serve next as substrate for myosin during contraction. Tounderstand the general principles that dictate geometrically-controlled actin assembly, wedeveloped a model that allowed us to identify key parameters including filaments/filamentsinteraction, filament mechanical property and contact activation between actin filamentsgrowing from the adjacent pattern and the nucleation area. These actin templates were usedthen to evaluate the response of oriented actin structures to myosin-induced contractility. Idemonstrated that crosslinking level modulates the myosin-induced deformation of actinnetworks according to their architecture. I showed also that crosslinkers are necessary tosustain myosin-driven deformation and force production of dynamic actin networks. Inaddition, we developed numerical simulation in order to relate the observed myosin-drivenactin deformation with the underlying microscopic mechanism. This work revealed howdiverse cellular actin networks contract differently to a define set of biochemical conditionsand hence how dynamic rearrangements can modulate network contractility
Ripoll, Léa. "Role of myosin VI and actin dynamics in membrane remodeling during pigmentation." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB102.
Full textIntracellular transport among organelles and the plasma membrane occurs through the formation and transport of vesicular and tubular membrane carriers. The formation of these carriers requires first the bending of membrane and the generation of a bud, followed by its elongation to form the tubule-vesicle. Lastly, the carrier is released from the membrane source by the scission of the membrane. Importantly, all these different steps need an accurate orchestration to properly deform the membrane. The actions exerted by molecular motors onto microtubule and actin cytoskeletons provide forces onto membrane that contribute to its remodeling during the biogenesis of carrier. Actin filaments (F-actin) and myosins are thought to participate in the initiation and the fission of carriers. However, the role of actin machinery during carrier biogenesis remains elusive. We thus decided to address the role of F-actin and the actin-based motor myosin VI in the formation of tubular intermediates at melanosome. Melanosomes are lysosome-related organelles of skin melanocytes and eye pigment cells that function in the synthesis and storage of the melanin pigment. Melanosomes originate from endosomes and progressively mature into fully pigmented compartments, which fate is to be secreted and transferred to neighboring keratinocytes. Melanosomes are dynamic organelles that constantly receive, but also recycle proteins such as the SNARE VAMP7 through the formation and release of tubular intermediates. Our work reveals that myosin VI, together with Arp2/3- and WASH-mediated branched actin localize at specific melanosomal subdomains where they promote the constriction and scission of tubular intermediates. This fission event allows the export of components such as VAMP7 from melanosomes and promotes their maturation and subsequent transfer to keratinocytes. Altogether, our results uncover a new role for myosin VI and F-actin in the constriction and scission of membrane tubules at melanosome that is required for organelle homeostasis and function
Guimard, Laurent. "Modélisation et synthèse de peptides interagissant avec une protéine cible : application au complexe calmoduline-RS20." Montpellier 1, 1995. http://www.theses.fr/1995MON1T037.
Full textDzangué, Tchoupou Gaëlle. "Caractérisation des réponses immunitaires chez les patients atteints de myopathies auto-immunes idiopathiques." Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS171/document.
Full textMyositis is an autoimmune disease characterized by muscular and extra-muscular disorders. In the early stages of the disease, the diagnosis of myositis can be misleading and requires expertise, in order to avoid the administration of inappropriate treatment. The mechanisms involved in these diseases are poorly understood. Our aim was to describe the immune profile specific to each patient group, in order to identify biomarkers that may be useful for diagnosis and management of patients. We used a panel of 36 markers by mass cytometry to characterize PBMCs derived from active patients (sIBM, anti-Jo1 ASyS, anti-SRP and anti-HMGCR myopathies) and healthy subjects. First, we developed and optimized a technical procedure for the simultaneous detection of extracellular and intracellular targets by mass cytometry. Using different bioinformatics tools, we isolated a frequency of CD8 +T-bet + cells > 51.5% as a specific biomarker for sIBM compared to other myositis, with a sensitivity of 94.74% and a specificity of 88. , 46%. In addition, we identified an activated CD8 + T-bet + CD57- immune profile, potentially capable of proliferation and the maintenance of autoimmune mechanisms in patients with sIBM. In anti-Jo1 patients, we observed a dysregulation of B cell homeostasis, characterized by a decrease in circulating memory B cells. The presence of the latter in the muscle of patients suggests that they nest in the muscle to avoid immunosuppressants. This work allowed the identification of a biomarker that could enhance the diagnosis of MIs compared to other myositis and the identification of cells potentially involved during sIBM and anti-Jo1 ASyS
Wu, Hau-sze, and 胡巧思. "Study of the myositis-specific and myositis-associated autoantibodies in Chinese patients with idiopathic inflammatory myopathies." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46579539.
Full textPhillips, Kelli R. "Characterization of myosin I in the inner ear." Morgantown, W. Va. : [West Virginia University Libraries], 2007. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5140.
Full textTitle from document title page. Document formatted into pages; contains vii, 114 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
Arnardơttir, Snjơlaug. "Studies in sporadic inclusion body myositis /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-572-7/.
Full textBhat, Alka. "Les dynamiques d'agrégats de myosine et leurs rôles dans les fermetures d'epithelia." Thesis, Strasbourg, 2019. http://www.theses.fr/2019STRAJ070.
Full textMyosin clusters have been reported in a variety of systems, such as Drosophila, C. elegans, and acto-myosin in vitro assays. However, their integration in a general framework is still lacking. In theory, actin filaments and myosin motors are predicted to follow generic rules of self-organisation. Recent findings from the laboratory reported that cluster dynamics within cytokinetic rings are associated with biological functions, i.e. stress generation when radial, and transport when tangential. In this study, we show that these simple rules hold as well for acto-myosin ring wound closure in epithelial monolayers. By using microfabrication, cell biology, quantitative imaging and theoretical physics, we report that radial and tangential clusters are related to local closures and stalled portions of rings, respectively. This conserved mechanism between single and multi-cellular system suggests that these myosin clusters dynamics could be used as generic read-out for mapping and predicting changes in shapes in developing embryos
Englund, Pernilla. "Immunopathogenic mechanisms in inflammatory myopathies /." Stockholm : [Karolinska institutets bibl.], 2002. http://diss.kib.ki.se/2002/91-7349-351-1/.
Full textBrady, Stefen. "A clinicopathological study of inclusion body myositis." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:bf7b9891-3cc1-46c5-bf96-3423a0087b6f.
Full textShabrokh, Elika. "Mitochondrial Biology in Sporadic Inclusion Body Myositis." Diss., Virginia Tech, 2014. http://hdl.handle.net/10919/47782.
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Seiberras, Serge. "Myosite à inclusions sporadique et maladies associées." Bordeaux 2, 1999. http://www.theses.fr/1999BOR23036.
Full textDulou, Renaud. "Myosite à inclusions : à propos d'une observation." Bordeaux 2, 1994. http://www.theses.fr/1994BOR2M182.
Full textVILON, PHILIPPE. "Myosites localisees : revue de la litterature a propos d'un cas." Nantes, 1989. http://www.theses.fr/1989NANT088M.
Full textFigarella-Branger, Dominique. "La myosite a inclusions : une trop grande heterogeneite : etude clinico-pathologique a propos de 21 observations." Aix-Marseille 2, 1988. http://www.theses.fr/1988AIX20527.
Full textWelsch, Marie-José. "Les myosites a inclusions." Université Louis Pasteur (Strasbourg) (1971-2008), 1985. http://www.theses.fr/1985STR1M167.
Full textMasson, d'Autume Adèle de. "Lymphocytes B régulateurs dans la GVH chronique humaine et rôle de la myosine 18A dans la cytotoxicité des lymphocytes NK." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC177/document.
Full textAllogeneic hematopoietic stem cell transplantation (HSCT) remains the only curative treatment for many patients with haematological malignancies. In almost half of the cases, it is complicated by chronic graft-versus-host disease (cGVHD). Regulatory B cells are a population of B cells secreting interleukin (IL)-10 that can inhibit the immune responses. We have shown that in patients with active cGVHD, the frequency of regulatory B cells is decreased in the peripheral blood. Regulatory B cells are enriched in the memory B cell and plasmablast B cell pools. Increased plasmablasts frequencies and decreased memory B cells frequencies were found in patients with active cGVHD, suggesting alterations in the terminal differentiation of B cells. Our work also focused on NK cells that have a cytotoxic role. We identified one surface receptor of NK cells, CD245, as myosin 18A. Myosin 18A is involved in the organization of the cytoskeleton and is a receptor of the surfactant A. We have shown that myosin 18A was a coactivating receptor of the NK cytotoxicity and that this increase in cytotoxicity could be linked to the stimulation of the expression of CD137 (4-1BB) on the surface of the NK lymphocyte. These results suggest a potential therapeutic role of the use of specific CD245 agonist antibodies
Legros, Vincent. "Atteintes du système musculo-squelettique par deux arbovirus émergents : cas des virus zika et du chikungunya." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC226/document.
Full textMusculoskeletal lesions caused by arthropod-borne-viruses (arboviruses) are invalidating for patients and remain poorly understood. In this study, we investigated the development of these manifestations after infection with two arboviruses: chikungunya virus (CHIKV) from the Togaviridae family, and Zika virus (ZIKV) from the Flaviviridae family. The first part of the study focused on arthritis following CHIKV infection. For this purpose, we developed a reporter virus expressing NanoLuciferase and performed experimental infections in a murine model. In vivo, a strong bioluminescent signal indicated viral replication and we observed persistence of the signal in the joints up to 34 days post-infection. By isolating primary murine cells from cartilage, we demonstrated the susceptibility of chondrocytes to CHIKV infection suggesting a role of reservoir of these cells. Furthermore, we investigated the consequences of the infection using in vitro models. We showed that primary human chondrocytes are also susceptible to CHIKV infection, which leads to the production of several cytokines involved in cartilage catabolism and induces apoptosis. In the second part of the study, we studied ZIKV muscular tropism and the associated lesions. Firstly, we confirmed the development of muscular lesions in a mouse model of ZIKA. Then, using human primary muscle cells we observed the infection of myoblasts but not myotubes, suggesting a differentiation-dependent tropism. We compared three viral strains and observed no significant difference in terms of replication, number of infected cells and viral production. Myoblasts infection induced a caspase-independent cells death mechanism and electronic microscope observations revealed intense vacuolization of cytoplasm, suggesting a paraptosis-like cell death. Proteomic analysis revealed that the Asian ZIKV strain modulated protein expression of infected cells with an increased effect after 48 hours. ZIKV-infection induced an important upregulation of biological processes associated with type I interferon and an inhibition of protein synthesis in the infected cells. These results provide valuable information about the mechanisms involved in the development of musculoskeletal lesions during arboviroses
Al-Nahedh, Yousra. "Analysis of MRI in the diagnosis of myositis." Thesis, University of Salford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.490219.
Full textChinoy, Hector. "A correlation of genotype and phenotype in myositis." Thesis, University of Manchester, 2007. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:141949.
Full textAlexanderson, Helene. "Exercise and outcome measures in patients with polymyositis and dermatomyositis /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-596-4/.
Full textEl, Bahloul Amel. "Caractérisation fonctionnelle et structurale de trois myosines non conventionnelles : la myosine VI, la myosine VIIa et la myosine IB d'Acanthamoeba." Paris 11, 2004. http://www.theses.fr/2004PA112138.
Full textGunawardena, Harsha. "A clinical and serological study of adult and juvenile idiopathic inflammatory myopathy." Thesis, University of Bath, 2010. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.527146.
Full textCHOPRA, SOEB. "Formes pseudo-myopathiques ou myopathiques chroniques et aigues revelatrices de la sarcoidose : trois observations ; revue de la litterature." Nantes, 1991. http://www.theses.fr/1991NANT038M.
Full textAfshar, Mohammad. "Interactions calmoduline-cibles : modélisation moléculaire et approche expérimentale." Montpellier 1, 1995. http://www.theses.fr/1995MON1T029.
Full textIuliano, Olga. "Myosin1b controls the formation of the axon and the establishment of neuronal polarity by regulating actin waves." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066649.
Full textNeurons are highly polarized cells, with a long axon and multiple short dendrites. Rearrangements of cytoskeleton, increased microtubule-based transport and coupling mechanically actin cytoskeleton to plasma membrane are required for the establishment of neuronal polarity. Class 1 Myosin, with the unique property to couple mechanically actin cytoskeleton to plasmamembrane are good candidate for regulatin axonogenesis. Myosin1b is highly expressed in developing brain where it was first identified. Thus, we investigated its role in axonogenesis. Depletion of endogenous Myo1b in cultured cortical neurons delays the neuronal differentiation and impairs the axonogenesis and the establishment of the neuronal polarity. The overexpression of Myosin1b rushes the neuronal development and promotes the formation of supernumerary axon-like structures. Myo1b requires its motor activity and its interaction with phosphoinositides via its PH motif to promote the axonogenesis. Myo1b associates and controls the formation of anterograde actin waves that cross-talk with microtubules to direct microtubules-bases transport of kinesin-1, and drive axon formation. Myo1b depletion impairs the propagation of actin waves and the translocation of KIF5560, a constitutively active version of the microtubules motor Kinesin-1. The motor activity and interaction with phosphoinositides of Myo1b are also required for the propagation of actin waves. Together our data indicate that myosin1b controls the neuronal symmetry breaking and the axogenesis by controlling the orientation of the actin polymerization to the membrane in the waves that drive the propagation of anterograde actin waves
Pinal, Fernández Iago. "Transcriptome profiling and longitudinal cohort studies of myositis subsets." Doctoral thesis, Universitat Oberta de Catalunya, 2020. http://hdl.handle.net/10803/673293.
Full textLas miopatías inflamatorias son una familia heterogénea de enfermedades autoinmunes raras que afectan a múltiples órganos y sistemas, incluidos los músculos, la piel, los pulmones y/o las articulaciones. Definir con precisión su patogenia y clasificarlas correctamente es clave para comprender y manejar estas enfermedades. En esta tesis doctoral exploramos subconjuntos específicos de miositis definidas por autoanticuerpos y comparamos cuantitativamente la capacidad de los autoanticuerpos con la clasificación EULAR/ACR de 2017 para predecir el fenotipo de pacientes con miositis. Además, realizamos la secuenciación de ARN en 119 biopsias musculares de pacientes con diferentes tipos de miositis y 20 controles. Estudiamos la expresión diferencial, realizamos análisis de vías y desarrollamos procesos de aprendizaje automático exploratorios para definir los perfiles de expresión específicos y las vías patogénicas en cada subgrupo de enfermedades. Con estos estudios determinamos que los autoanticuerpos superan los criterios clínicos actuales para predecir el fenotipo de los pacientes con miositis y descubrimos perfiles de expresión únicos en el tejido muscular de pacientes con diferentes tipos de miositis.
Les miopaties inflamatòries són una família heterogènia de malalties autoimmunes rares que afecten múltiples òrgans i sistemes, inclosos els músculs, la pell, els pulmons i/o les articulacions. Definir-ne amb precisió la patogènia i classificar-les correctament és clau per comprendre i manejar aquestes malalties. En aquesta tesi doctoral explorem subconjunts específics de miositis definides per autoanticossos i comparem quantitativament la capacitat dels autoanticossos amb la classificació EULAR/ACR de 2017 per predir el fenotip de pacients amb miositis. A més, realitzem la seqüenciació d'ARN en 119 biòpsies musculars de pacients amb diferents tipus de miositis i 20 controls. Estudiem l'expressió diferencial, fem anàlisis de vies i desenvolupem processos d'aprenentatge automàtic exploratoris per definir els perfils específics d'expressió i les vies patogèniques a cada subgrup de malalties. Amb aquests estudis determinem que els autoanticossos superen els criteris clínics actuals per predir el fenotip dels pacients amb miositis i descobrim perfils d'expressió únics al teixit muscular de pacients amb diferents tipus de miositis.
Lee, James Hoi-Fung. "Muscle and Nerve Excitability in Sporadic Inclusion Body Myositis." Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/22896.
Full textAubry, Aurélie. "Recherche d'interacteurs de Myosine II au cours de l'intercalation cellulaire chez l'embryon de Drosophila melanogaster." Thesis, Aix-Marseille 2, 2011. http://www.theses.fr/2011AIX22117/document.
Full textEpithelial tissue is composed of polarized cells, which are closely attached to each other by adherens junctions. The loss of adherens junctions is often a key step in the development of cancer in epithelial tissues. It is therefore important to understand the mechanisms of attachment between the cells. To study such epithelial plasticity, we use the Drosophila embryo as a model system, where a fine regulation of adherens junctions is required for one of the early processes of development: germ band elongation. During this process, epithelial cells change their neighbors along the anterior-posterior axis (cell cell intercalation) without loss of cell adhesion. Polarized recruitment of the molecular motor Myosin II at the junctions, that disassemble and reassemble, underlies the intercalation process. In part, intercalation relies on the normal activity of the the JAK / STAT pathway that is crucial for the spatial control of Myosin II. During my PhD, I conducted a genetic screen, in a mutant for the ligand of the JAK / STAT pathway, designed to identify second site interactors for Myosin II control. I identified several genes that appear to be involved in the intercalation process. Among these candidates, I focused on one with the strongest phenotype: the gene CG13992. The functional characterization of this gene was the second stage of my thesis (because only the nucleotide and the protein sequences were known). Preliminary results highlight the involvement of this gene in the localization of Myosin II that remain to be confirmed
Cáceres, Rodrigo. "Role of acto-myosin based force production in cell invasion during development in Caenorhabditis elegans." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB027/document.
Full textBasement membrane (BM) is a dense sheet of specialized extracellular matrix that separates epithelia from underlying tissue. The penetration of cells through BM barriers, called “invasion”, is an important process during normal tissue development and in cancer metastasis. Much has been understood concerning the genetics and signaling of how holes are formed in the BM during invasion. However less is clear about the physical forces involved: how myosin contractility participates in BM removal and how different actin polymerization factors and crosslinkers contribute to the invasive process. To address these questions, we studied an invasion event in a developmental process, anchor cell (AC) invasion in Caenorhabditis elegans. AC breaching of the BM is known to depend on an actin-rich protrusion and the activity of matrix metalloproteases (MMPs), similar to cancer cell invasion. RNAi knockdown of different actin polymerization activators and nucleators, and expression of a dominant negative form of an Arp2/3 complex activator specifically in the AC showed that AC invasion depended strongly on branched filaments formed via WASP/WSP-1 activation of the Arp2/3 complex. Super-resolution microscopy indicated that the AC invasive protrusion was densely packed with filaments, in keeping with the idea that the invasive protrusion was highly branched. We further showed that another Arp2/3 complex activator, WAVE/WVE-1, could enable invasion when WASP/WSP-1 was absent. Formins appeared not to play a major role and actin cross-linking proteins were likewise dispensable for AC invasion. In wild type worms, we observed that myosin activity was not needed for invasion. However it has been reported that cancer cells upregulate myosin contractility to invade in the absence of proteases, so we used a worm deleted for the five main MMPs of the worm genome to test the role of myosin in this context. AC invasion took place in MMP- worms, but with a time delay. RNAi knockdown of different components of the myosin machinery gave no enhancement of the invasion defect. In addition visualization of the actin cytoskeleton in MMP- worms revealed that actin was concentrated in the AC protrusion and barely detectable in the cortex, making it unlikely that myosin contraction of the cortex was helping the cell squeeze through the BM as reported in cancer cells in the absence of proteases. All together these results showed that the invasive cell adapted its branched actin filament polymerization to maintain invasion in different biochemical and environmental contexts. This plasticity is a crucial point that needs to be better understood in order to develop future treatments targeting cancer cell invasion
Biswas, Anindita. "Analysis of motor activity of recombinant myosin-1c." Morgantown, W. Va. : [West Virginia University Libraries], 2007. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5522.
Full textTitle from document title page. Document formatted into pages; contains xi, 82 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
Vigouroux, Clémence. "Regulation of actin assembly and mechanotransduction in cell-matrix adhesion complexes by the protein RIAM The PIP2-talin-RIAM-VASP pathway controls actin polymerization and organisation Talin dissociates from RIAM and associates to vinculin sequentially in response to the actomyosin force Integrin-bound talin head inhibits actin filament barbed-end elongation." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL015.
Full textDuring cell migration, adhesion complexes control the production of force and the adaptation to the mechanical properties of the environment. The aim of this project was to understand the molecular mechanisms by which these complexes control the force produced by actin assembly and encode mechanical information into biochemical reactions. The first study shows that the proteins talin, RIAM and VASP assemble on the surface of a membrane to stimulate actin assembly by a novel. mechanism The second part is based on the reconstitution of the mechanosensitive machinery of the adhesion complexes with pure proteins on a micropatterned surface observed in microscopy. The study reveals that the stretchable protein talin exchanges its partner RIAM for vinculin in response to the force transmitted by the actin cytoskeleton. Talin thus codes mechanical information by recruiting partners that correspond to its degree of stretch
MERCIER, PASQUIER PATRICIA. "Polyglobulie revelatrice d'une myosite ossifiante circonscrite : a propos d'un cas." Limoges, 1989. http://www.theses.fr/1989LIMO0140.
Full textCoffin, Allison Beth. "Unconventional myosins in fish ears." College Park, Md. : University of Maryland, 2005. http://hdl.handle.net/1903/2445.
Full textThesis research directed by: Biology. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
Chérin, Patrick. "L'immunomodulation au cours des myosites." Paris 11, 1996. http://www.theses.fr/1996PA11T027.
Full textCatalán, García Marc. "Mitochondrial profile and amyloidogenic molecules in sporadic inclusion body myositis." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/586382.
Full textLa miositis per cossos d’inclusió en la seva forma esporàdica (MCI) és la miopatia més comú en individus de més de 50 anys tot i ser una malaltia rara. Cursa amb atròfia muscular progressiva distal i proximal i actualment no es coneix cura. A nivell histopatològic presenta un component inflamatori, un component mitocondrial i un component degeneratiu. Degut al seu component degeneratiu i a la similitud de les proteïnes que formen aquests cossos d’inclusió, s’ha establert un possible paral·lelisme amb la malaltia d’Alzheimer. Els objectius d’aquesta tesi doctoral són explorar a nivell molecular les alteracions mitocondriales en la MCI en múscul, però també en cèl·lules mononuclears de sang perifèrica (CMSP), ja que és un teixit menys invasiu. A més, com a segon objectiu principal pretén d’estudiar mol·lècules relacionades amb la inflamació, amb el mitocondri i amb la degeneració en plasma d’aquests pacients per tal de demostrar la seva implicación amb la etiopatogènia i a més per establir nous marcadors menys invasius que permetin diagnosticar la malaltia i diferenciarla d’altres malalties similars com la dermatomiositis i la polimiositis. Fent referència a l’estudi mitocondrial, tant la quantitat de DNA mitocondrial com l’activitat del complex IV de la cadena mitocondrial (COX) es van trobar disminuïts en músculs dels pacients amb MCI. D’altra banda, amb l’estudi de les CMSP, també vam trobar disminuïda l’activitat de la COX, i a més una desregulación de la síntesis de proteïnes mitocondrials. Donat que un 57% dels pacients va presentar delecions múltiples al DNA mitocondrial, la presència d’aquestes delecions correlacionava amb una menor quantitat de DNA mitocondrial i a més amb un decrement de proteïna MFN-2, implicada en la dinàmica mitocondrial. Amb l’estudi de les molècul·les plasmàtiques, es van analitzar en plasma de pacients amb MCI, en controls però també en pacients amb dermatomiositis i polimiositis mol·lècules relacionades amb la inflamació (IL-6 i TNF-α), amb el mitocondri (DNA mitocondrial circulant, FGF-21 i enzim CoQ) i amb la amiloidogènesi (BACE-1, PS-1 i sAPPβ). Les mol.lècules amiloidogèniques es trobaven incrementades en els pacients amb MCI respecte controls i altres miopatíes inflamatòries, demostrant la seva impliació en la etiopatogènia i obtenint un cert valor diagnòstic. Amb aquesta tesi, s’ha demostrat la implicació mitocondrial en la etiopatogènia de la MCI, i s’han trobat alteracions en plasma de mol·lècules amiloidogèniques que, a més, tenen potencial diagnòstic per diferenciar aquesta malaltia d’altres miopatíes inflamatòries com la polimiositis.
Ahmed, M. "Investigating novel therapeutic approaches for sporadic inclusion body myositis (sIBM)." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1343623/.
Full textMiller, A. D. "Development of new therapeutic strategies for sporadic Inclusion Body Myositis." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1469260/.
Full textPutau-Poussard, Stéphanie. "La myosite ossifiante chez le paraplégique : à propos d'un cas." Bordeaux 2, 1999. http://www.theses.fr/1999BOR2M055.
Full textPetzoldt, Astrid G. "DE-cadherin regulates unconventional myosin ID through myosin IC in Drosophila melanogaster." Nice, 2009. http://www.theses.fr/2009NICE4048.
Full textThe accurate establishment of stereotyped L/R asymetry is subject to a strict genetic program and crucial for the functionality of the organism. It is only recently that the mechanism of L/R asymmetry establishment is exploited in the invertebrate species Drosphophila melanogaster (Hozumi et al. , 2006 ; Speder et al. , 2006). The unconventional type ID myosin (MyoID) has been characterised as a dextral determinant accountable for the clockwise (dextral) rotation of the male genital plate during pupae stage. In our attempt to isolate new components of the L/R mechanism, we first focussed on MyoIC, the closest homologue of genitalia, thus L/R axis inversion. We provide evidence that this situs inversus phenotype is du to an inhibition of MyoID function through MyoIC and consequently define MyoIC as an anti-dextral effector of MyoID. An interaction between MyoID and adherents junctions had been suggested by Speder et al. (2006) as the authors could show by two-hybrid screen and GST pull down that MyoID tail and beta-catenin cal physically interact. Our DE-cadherin loss and gain of function studies revealed a linear interaction between DE-cadherin zand the unconventional myosins MyoID and MyoIC. DE-cadherin controls MyoIC expression, acting as inhibitor of MyoIC. As MyoID functionality is regulated by MyoIC expression, myoIC functions as a mediator between DE-cadherin and myoID. In summary, we present in this study a new regulatory network of L/R asymmetry establishment, where DE-cadherin affects MyoID activity through regulation of MyoIC protein expression
Kuzmanovic, Deborah Allen. "The role of a myosin in yeast cytokinesis /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/10299.
Full textReymann, Anne-Cécile. "Dynamique des réseaux d'actine d'architecture contrôlée." Phd thesis, Université de Grenoble, 2011. http://tel.archives-ouvertes.fr/tel-00686015.
Full textLevayer, Romain. "Modulation of intercellular adhesion during epithelial morphogenesis." Thesis, Aix-Marseille 2, 2011. http://www.theses.fr/2011AIX22076/document.
Full textEpithelia build up strong mechanical and chemichal barriers in Metazoans. Adherens junctions, through the adhesion provided by the transmembrane protein E-cadherin (E-cad), are essential for the mechanical integrity of the tissue. Yet, epithelia can be dramatically remodeled during embryogenesis or wound healing. During gastrulation of Drosophila embryo, the ventrolateral epithelium (the germ band) undergoes a massive elongation along the anteroposterior (AP) axis, driven by cell-cell intercalation. This is based on the polarized remodeling of intercellular junctions whereby junctions parallel to the dorsoventral axis (DV) shrink and form new junctions along AP axis. This remodeling is mediated by the planar polarized enrichment of Myosin II (MyoII) in DV junctions, which generates high tension. Adhesion proteins are also planar polarized, E-cad is enriched in AP junctions, but we did not know if this polarity contributed to cell-cell intercalation and the mechanism driving this polarity. As such, I have studied the role of Clathrin mediated endocytosis (CME) during germ band extension. I have shown that E-cad CME is specifically upregulated at the junction plane in the germ band, and planar polarized (enriched in DV shrinking junctions). It is required for cell-cell intercalation and the planar polarized distribution of E-cad. E-cad CME is regulated by the concerted action of the Formin Diaphanous and Myosin-II, which accelerates CME through the lateral clustering of E-cad. They are controlled by RhoGEF2, which is also enriched in DV junctions. In the second part of my PhD, I have studied the coupling between E-cad and MyoII dynamics. Indeed, planar polarized contractile flows of MyoII are required for DV junction shrinkage, but we did not know the mechanism driving the polarity of these flows. I have shown that the transient anisotropy of anchoring forces between two facing junctions triggers flow. As such, the low steady state amount of E-cad and the high rate of CME in DV junctions trigger more anisotropy and polarize the flow. These results outline the strong crossregulation between E-cad and MyoII and their concerted action in morphogenesis