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Academic literature on the topic 'Myositi'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Myositi"

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Berg, Jonathan S., Bradford C. Powell, and Richard E. Cheney. "A Millennial Myosin Census." Molecular Biology of the Cell 12, no. 4 (April 2001): 780–94. http://dx.doi.org/10.1091/mbc.12.4.780.

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The past decade has seen a remarkable explosion in our knowledge of the size and diversity of the myosin superfamily. Since these actin-based motors are candidates to provide the molecular basis for many cellular movements, it is essential that motility researchers be aware of the complete set of myosins in a given organism. The availability of cDNA and/or draft genomic sequences from humans,Drosophila melanogaster, Caenorhabditis elegans, Arabidopsis thaliana,Saccharomyces cerevisiae, Schizosaccharomyces pombe, andDictyostelium discoideum has allowed us to tentatively define and compare the sets of myosin genes in these organisms. This analysis has also led to the identification of several putative myosin genes that may be of general interest. In humans, for example, we find a total of 40 known or predicted myosin genes including two new myosins-I, three new class II (conventional) myosins, a second member of the class III/ninaC myosins, a gene similar to the class XV deafness myosin, and a novel myosin sharing at most 33% identity with other members of the superfamily. These myosins are in addition to the recently discovered class XVI myosin with N-terminal ankyrin repeats and two human genes with similarity to the class XVIII PDZ-myosin from mouse. We briefly describe these newly recognized myosins and extend our previous phylogenetic analysis of the myosin superfamily to include a comparison of the complete or nearly complete inventories of myosin genes from several experimentally important organisms.
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Hammer, J. A., B. Bowers, B. M. Paterson, and E. D. Korn. "Complete nucleotide sequence and deduced polypeptide sequence of a nonmuscle myosin heavy chain gene from Acanthamoeba: evidence of a hinge in the rodlike tail." Journal of Cell Biology 105, no. 2 (August 1, 1987): 913–25. http://dx.doi.org/10.1083/jcb.105.2.913.

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We have completely sequenced a gene encoding the heavy chain of myosin II, a nonmuscle myosin from the soil ameba Acanthamoeba castellanii. The gene spans 6 kb, is split by three small introns, and encodes a 1,509-residue heavy chain polypeptide. The positions of the three introns are largely conserved relative to characterized vertebrate and invertebrate muscle myosin genes. The deduced myosin II globular head amino acid sequence shows a high degree of similarity with the globular head sequences of the rat embryonic skeletal muscle and nematode unc 54 muscle myosins. By contrast, there is no unique way to align the deduced myosin II rod amino acid sequence with the rod sequence of these muscle myosins. Nevertheless, the periodicities of hydrophobic and charged residues in the myosin II rod sequence, which dictate the coiled-coil structure of the rod and its associations within the myosin filament, are very similar to those of the muscle myosins. We conclude that this ameba nonmuscle myosin shares with the muscle myosins of vertebrates and invertebrates an ancestral heavy chain gene. The low level of direct sequence similarity between the rod sequences of myosin II and muscle myosins probably reflects a general tolerance for residue changes in the rod domain (as long as the periodicities of hydrophobic and charged residues are largely maintained), the relative evolutionary "ages" of these myosins, and specific differences between the filament properties of myosin II and muscle myosins. Finally, sequence analysis and electron microscopy reveal the presence within the myosin II rodlike tail of a well-defined hinge region where sharp bending can occur. We speculate that this hinge may play a key role in mediating the effect of heavy chain phosphorylation on enzymatic activity.
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Siththanandan, Verl B., and James R. Sellers. "Regulation of myosin 5a and myosin 7a." Biochemical Society Transactions 39, no. 5 (September 21, 2011): 1136–41. http://dx.doi.org/10.1042/bst0391136.

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The myosin superfamily is diverse in its structure, kinetic mechanisms and cellular function. The enzymatic activities of most myosins are regulated by some means such as Ca2+ ion binding, phosphorylation or binding of other proteins. In the present review, we discuss the structural basis for the regulation of mammalian myosin 5a and Drosophila myosin 7a. We show that, although both myosins have a folded inactive state in which domains in the myosin tail interact with the motor domain, the details of the regulation of these two myosins differ greatly.
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Baines, I. C., H. Brzeska, and E. D. Korn. "Differential localization of Acanthamoeba myosin I isoforms." Journal of Cell Biology 119, no. 5 (December 1, 1992): 1193–203. http://dx.doi.org/10.1083/jcb.119.5.1193.

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Acanthamoeba myosins IA and IB were localized by immunofluorescence and immunoelectron microscopy in vegetative and phagocytosing cells and the total cell contents of myosins IA, IB, and IC were quantified by immunoprecipitation. The quantitative distributions of the three myosin I isoforms were then calculated from these data and the previously determined localization of myosin IC. Myosin IA occurs almost exclusively in the cytoplasm, where it accounts for approximately 50% of the total myosin I, in the cortex beneath phagocytic cups and in association with small cytoplasmic vesicles. Myosin IB is the predominant isoform associated with the plasma membrane, large vacuole membranes and phagocytic membranes and accounts for almost half of the total myosin I in the cytoplasm. Myosin IC accounts for a significant fraction of the total myosin I associated with the plasma membrane and large vacuole membranes and is the only myosin I isoform associated with the contractile vacuole membrane. These data suggest that myosin IA may function in cytoplasmic vesicle transport and myosin I-mediated cortical contraction, myosin IB in pseudopod extension and phagocytosis, and myosin IC in contractile vacuole function. In addition, endogenous and exogenously added myosins IA and IB appeared to be associated with the cytoplasmic surface of different subpopulations of purified plasma membranes implying that the different myosin I isoforms are targeted to specific membrane domains through a mechanism that involves more than the affinity of the myosins for anionic phospholipids.
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Heintzelman, M. B., T. Hasson, and M. S. Mooseker. "Multiple unconventional myosin domains of the intestinal brush border cytoskeleton." Journal of Cell Science 107, no. 12 (December 1, 1994): 3535–43. http://dx.doi.org/10.1242/jcs.107.12.3535.

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Representatives of class V and class VI unconventional myosins are identified as components of the intestinal brush border cytoskeleton. With brush border myosin-I and myosin-II, this brings to four the number of myosin classes associated with this one subcellular domain and represents the first characterization of four classes of myosins expressed in a single metazoan cell type. The distribution and cytoskeletal association of each myosin is distinct as assessed by both biochemical fractionation and immunofluorescence localization. Myosin-VI exists in both the microvillus and terminal web although the terminal web is the predominant site of concentration. Myosin-V is present in the terminal web and, most notably, at the distal ends of the microvilli, thus becoming the first actin-binding protein to be localized to this domain as assessed by both immunohistochemical and biochemical methods. In the undifferentiated enterocytes of the intestinal crypts, myosin-VI is expressed but not yet localized to the brush border, in contrast to myosin-V, which does demonstrate an apical distribution in these cells. An assessment of myosin abundance indicates that while myosin-II is the most abundant in the cell and in the brush border, brush border myosin-I is only slightly less abundant in contrast to myosins-V and -VI, both of which are two orders of magnitude less abundant than the others. Extraction studies indicate that of these four myosins, myosin-V is the most tightly associated with the brush border membrane, as detergent, in addition to ATP, is required for efficient solubilization.
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Yumura, Shigehiko, and Taro Q. P. Uyeda. "Transport of Myosin II to the Equatorial Region without Its Own Motor Activity in Mitotic Dictyostelium Cells." Molecular Biology of the Cell 8, no. 10 (October 1997): 2089–99. http://dx.doi.org/10.1091/mbc.8.10.2089.

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Fluorescently labeled myosin moved and accumulated circumferentially in the equatorial region of dividingDictyostelium cells within a time course of 4 min, followed by contraction of the contractile ring. To investigate the mechanism of this transport process, we have expressed three mutant myosins that cannot hydrolyze ATP in myosin null cells. Immunofluorescence staining showed that these mutant myosins were also correctly transported to the equatorial region, although no contraction followed. The rates of transport, measured using green fluorescent protein-fused myosins, were indistinguishable between wild-type and mutant myosins. These observations demonstrate that myosin is passively transported toward the equatorial region and incorporated into the forming contractile ring without its own motor activity.
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Shu, S., R. J. Lee, J. M. LeBlanc-Straceski, and T. Q. Uyeda. "Role of myosin II tail sequences in its function and localization at the cleavage furrow in Dictyostelium." Journal of Cell Science 112, no. 13 (July 1, 1999): 2195–201. http://dx.doi.org/10.1242/jcs.112.13.2195.

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Cytoplasmic myosin II accumulates in the cleavage furrow and provides the force for cytokinesis in animal and amoeboid cells. One model proposes that a specific domain in the myosin II tail is responsible for its localization, possibly by interacting with a factor concentrated in the equatorial region. To test this possibility, we have expressed myosins carrying mutations in the tail domain in a strain of Dictyostelium cells from which the endogenous myosin heavy chain gene has been deleted. The mutations used in this study include four internal tail deletions: Mydelta824-941, Mydelta943-1464, Mydelta943-1194 and Mydelta1156-1464. Contrary to the prediction of the hypothesis, immunofluorescence staining demonstrated that all mutant myosins were able to move toward the furrow region. Chimeric myosins, which consisted of a Dictyostelium myosin head and chicken skeletal myosin tail, also efficiently localized to the cleavage furrow. All these deletion and chimeric mutant myosins, except for Mydelta943-1464, the largest deletion mutant, were able to support cytokinesis in suspension. Our data suggest that there is no single specific domain in the tail of Dictyostelium myosin II that is required for its functioning at and localization to the cleavage furrow.
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Berg, J. S., B. H. Derfler, C. M. Pennisi, D. P. Corey, and R. E. Cheney. "Myosin-X, a novel myosin with pleckstrin homology domains, associates with regions of dynamic actin." Journal of Cell Science 113, no. 19 (October 1, 2000): 3439–51. http://dx.doi.org/10.1242/jcs.113.19.3439.

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Myosin-X is the founding member of a novel class of unconventional myosins characterized by a tail domain containing multiple pleckstrin homology domains. We report here the full-length cDNA sequences of human and bovine myosin-X as well as the first characterization of this protein's distribution and biochemical properties. The 235 kDa myosin-X contains a head domain with <45% protein sequence identity to other myosins, three IQ motifs, and a predicted stalk of coiled coil. Like several other unconventional myosins and a plant kinesin, myosin-X contains both a myosin tail homology 4 (MyTH4) domain and a FERM (band 4.1/ezrin/radixin/moesin) domain. The unique tail domain also includes three pleckstrin homology domains, which have been implicated in phosphatidylinositol phospholipid signaling, and three PEST sites, which may allow cleavage of the myosin tail. Most intriguingly, myosin-X in cultured cells is present at the edges of lamellipodia, membrane ruffles, and the tips of filopodial actin bundles. The tail domain structure, biochemical features, and localization of myosin-X suggest that this novel unconventional myosin plays a role in regions of dynamic actin.
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Tappe, Dennis, Günther Slesak, José Vicente Pérez-Girón, Johannes Schäfer, Andreas Langeheinecke, Gudrun Just-Nübling, César Muñoz-Fontela, and Kerstin Püllmann. "Human Invasive Muscular Sarcocystosis Induces Th2 Cytokine Polarization and Biphasic Cytokine Changes, Based on an Investigation among Travelers Returning from Tioman Island, Malaysia." Clinical and Vaccine Immunology 22, no. 6 (April 22, 2015): 674–77. http://dx.doi.org/10.1128/cvi.00042-15.

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ABSTRACTSarcocystis nesbittiis a parasite responsible for a biphasic eosinophilic febrile myositis syndrome in two recent outbreaks in Malaysia. We demonstrate Th2 cytokine polarization in infected travelers, an overall cytokine production decrease in the early phase of the disease suggestive of initial immunosuppression, and elevated levels of proinflammatory and chemotactic cytokines in the later myositic phase.
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Post, P. L., G. M. Bokoch, and M. S. Mooseker. "Human myosin-IXb is a mechanochemically active motor and a GAP for rho." Journal of Cell Science 111, no. 7 (April 1, 1998): 941–50. http://dx.doi.org/10.1242/jcs.111.7.941.

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The heavy chains of the class IX myosins, rat myr5 and human myosin-IXb, contain within their tail domains a region with sequence homology to GTPase activating proteins for the rho family of G proteins. Because low levels of myosin-IXb expression preclude purification by conventional means, we have employed an immunoadsorption strategy to purify myosin-IXb, enabling us to characterize the mechanochemical and rho-GTPase activation properties of the native protein. In this report we have examined the light chain content, actin binding properties, in vitro motility and rho-GTPase activity of human myosin-IXb purified from leukocytes. The results presented here indicate that myosin-IXb contains calmodulin as a light chain and that it binds to actin with high affinity in both the absence and presence of ATP. Myosin-IXb is an active motor which, like other calmodulin-containing myosins, exhibits maximal velocity of actin filaments (15 nm/second) in the absence of Ca2+. Native myosin-IXb exhibits GAP activity on rho. Class IX myosins may be an important link between rho and rho-dependent remodeling of the actin cytoskeleton.
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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.

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Les myopathies inflammatoires sont des maladies auto-immunes rares dont le dénominateur commun est la faiblesse musculaire et l'inflammation. Leur origine n’est pas connue et les traitements sont conventionnels partiellement efficaces. Par une approche épidémiologique, nous avons montré que l’étude de l’incidence et de la prévalence est un outil utile pour mettre en évidence des déterminants des myopathies inflammatoires. Une meilleure identification et une meilleure classification des patients atteints de ces maladies sont cependant nécessaires pour préciser l’épidémiologie des myopathies inflammatoires.Par une approche translationnelle, nous avons montré que, par rapport aux autres myopathies inflammatoires, des dysfonctions mitochondriales périfasciculaires sont une caractéristique des dermatomyosites, qui jouent un rôle dans l’intolérance à l’effort et le maintien de l’inflammation. Ces résultats ouvrent des nouvelles voies pour mieux comprendre et traités les myopathies inflammatoires
Inflammatory 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
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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.

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Serum autoantibodies play a key role in systemic autoimmune rheumatic diseases for diagnostic, classification and prognostic purposes. Research of new autoantibodies has been very active in the last decade in rare connective tissue diseases such as systemic sclerosis and poly/dermatomyositis, with new biomarkers entering the clinical practice. Immunoprecipitation of protein and/or RNA components of the target autoantigens constitutes the gold standard method for the discovery of new autoantibodies in a screening setting but is considered time- and labor-intensive and, accordingly, is performed only in a few laboratories worldwide. As a result, alternative techniques such as ELISA and immunoblotting are often preferred for large-scale testing, despite the lack of standardization. The aims of the present project are (1) to set up protein- and RNA- immunoprecipitation in our laboratory and (2) to describe serum autoantibodies identified in our series of patients affected by systemic autoimmune rheumatic diseases. During the PhD program we were able to perform correctly protein-and RNA-immunoprecipitation in our laboratory as demonstrated by positive reference sera, and then by the identification of known but also new and rare autoantibodies, as represented by two new patterns immunoprecipitated in systemic sclerosis, corresponding to serum anti-hnRNP-L and anti-mitochondrial antibodies. In psoriatic arthritis we also analyzed the concentration of circulating levels of LL37, a recently established target of autoimmune response at the skin level, and we identified an increased production in a subset of patients. In conclusion, performing protein- and RNA-immunoprecipitation as a screening method in our laboratory allows a more complete and specific autoantibody analysis that cannot be performed by the commercial techniques available nowadays, and further analysis of the role of LL37 in psoriatic arthritis patients may help in the identification of a new biomarker in this condition.
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Zhu, Jing. "The role of nonmuscle myosin IIA in endothelial cell." Morgantown, W. Va. : [West Virginia University Libraries], 2010. http://hdl.handle.net/10450/11006.

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Thesis (M.S.)--West Virginia University, 2010.
Title from document title page. Document formatted into pages; contains viii, 37 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 33-37).
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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.

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Les myopathies inflammatoires idiopathiques (MII) sont hétérogènes dans leurs physiopathologies et pronostics. L'émergence d'auto-anticorps spécifiques de myosites (ASM) suggère des sous-groupes plus homogènes de patients. Notre but est de trouver une nouvelle classification des MII fondée des critères phénotypiques, biologiques et immunologiques. Une étude observationnelle, rétrospective, multicentrique a été conduite à partir de la base de données du réseau français des myosites. Nous avons inclus 260 myosites, définies selon les classifications historiques pour la polymyosite (PM), la dermatomyosite (DM) et la myosite à inclusions (MI). Tous les patients ont eu au moins un dot myosite testant les anti-Jo1, anti-PL7, anti-PL12, anti-Mi-2, anti-Ku, anti-PMScl, anti-Scl70 and anti-SRP. Nous avons utilisé l'analyse des correspondances multiples suivie d'une classification hiérarchique ascendante afin d'agréger les patients dans des sous-groupes plus homogènes. Quatre clusters émergent. Le premier cluster (n=77) regroupe principalement des MI, avec des vacuoles bordées, des anomalies mitochondriales et de l'inflammation avec des fibres envahies. Le second cluster (n=91) était caractérisé par des myopathies nécrosantes auto-immunes (MNAi) en majorité, avec des anticorps anti-SRP et anti-HMGCR. Le troisième cluster (n=52) regroupe essentiellement des DM avec des anticorps anti-Mi-2, anti-MDA5, ou anti-TiF1 gamma. Le quatrième cluster (n=40) était défini par le SAS (n=36), avec notamment la présence des anti-Jo1 ou anti-PL7. Les critères histologiques sont dispensables pour la prédiction des clusters, soulignant l'importance d'une classification clinico-sérologique
Idiopathic 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
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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.

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Les myopathies auto-immunes (MAI), classiquement appelées myosites ou myopathies inflammatoires idiopathiques, représentent un groupe de maladies définies par des caractéristiques cliniques, histopathologiques et biologiques. Une des caractéristiques les plus notables est la présence d’auto-anticorps (aAc) chez environ 60% des patients. Les MAI regroupent : les dermatomyosites, les polymyosites, les myosites à inclusion, les myosites de chevauchement incluant le syndrome des anti-synthétases et les myopathies nécrosantes auto-immunes (MNAI). Les MNAI ont été récemment individualisées parmi les MAI comme des maladies graves fréquemment associées à la présence d’aAc dirigés contre la Signal Recognition Particle (SRP) ou la 3-Hydroxy-3-MéthylGlutaryl-CoA Réductase (HMGCR). La localisation de SRP et HMGCR étant intracellulaire, le rôle des aAc dans la physiopathologie des MNAI reste mal compris. La pathogénicité des aAc anti-SRP et anti-HMGCR envers des cellules musculaires cultivées in vitro a récemment été mise en évidence mais leurs effets in vivo demeurent inconnus.Au cours de cette thèse, j’ai étudié le rôle physiopathologique des aAc anti-SRP et anti-HMGCR in vivo chez la souris. Le transfert passif d’IgG de patients atteints de MNAI, positifs pour les aAc anti-SRP ou anti-HMGCR, à la souris sauvage entraîne un déficit musculaire. Ce déficit était prolongé chez la souris immunodéficiente Rag2-/-, et limité chez la souris déficiente pour la fraction C3 du complément. Chez les souris recevant les IgG anti-SRP+, le déficit musculaire était important et accompagné de quelques signes de nécrose myocytaire. Les IgG anti-HMGCR+ induisaient une faiblesse musculaire moindre, et des signes histopathologiques rares ou absents. Ces résultats sont en accord avec l’observation chez l’homme d’une maladie plus grave chez les patients anti-SRP+ par rapport aux patients anti-HMGCR+. La supplémentation en complément humain des souris augmentait le déficit musculaire induit par les IgG anti-HMGCR+ et de façon moindre pour les IgG anti-SRP+. En collaboration avec l’INSERM UMRS974, nous avons montré que les cibles SRP et HMGCR peuvent être détectées à la surface des fibres musculaires in vitro, suggérant qu’elles puissent être accessibles aux aAc in vivo.Ces résultats démontrent pour la première fois le rôle pathogène des aAc anti-SRP et anti-HMGCR in vivo et l’implication du complément, contribuant à une avancée dans la compréhension de la physiopathologie des MNAI
Autoimmune 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
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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.

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Cunningham, 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.

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Ennomani, Hajer. "Contractile response of biomimetic actomyosin systems." Thesis, Université Grenoble Alpes (ComUE), 2015. http://www.theses.fr/2015GREAY054/document.

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La contractilité cellulaire, un phénomène orchestrée par le système d'actomyosine, est un régulateur critique d'une large gamme de processus cellulaires, y compris l'établissement de la polarité cellulaire, la migration cellulaire, l'intégrité des tissus au cours de la morphogenèse ou du développement. Une simple perturbation de la génération de la force et des propriétés mécaniques des cellules peut affecter leurs fonctions physiologiques et par conséquent peut conduire à des défauts pathologiques y compris le cancer.Cependant, les mécanismes qui contrôlent la production de la force par le système acto-myosine et leurs modes de régulation dans les cellules ne sont pas pleinement compris. Au cours de ma thèse, j'ai utilisé un système biomimétique fait d'un ensemble minimal de protéines purifiées pour étudier les propriétés contractiles du système actomyosin.L'objectif était de comprendre comment l'architecture des filaments d'actine peut modifier la réponse contractile. A cet effet, j'étais d'abord intéressée par la construction d'une variété d'organisation de l'actine qui servira après comme substrat pour les moteurs moléculaires (la myosine) lors de la contraction.Afin de comprendre les principes généraux qui dictent l'assemblage de l'actine, nous avons développé un modèle numérique qui nous a permis d'identifier les paramètres clés, y compris l'interaction entre les filaments d'actine, les propriétés mécaniques de ces filaments et l'activation par contact entre une région de nucléation et les filaments d'actine qui poussent à partir d'un motif adjacent. Ce modèle a été utilisé en premier lieu pour implémenter les propriétés reliées à l'actine et en second lieu pour évaluer la réponse contractile des structures d'actine induite par la myosine.Durant ma thèse, j'ai pu démontrer que le niveau de connectivité module la déformation du réseau d'actine induite par la myosine, selon leur architecture. J'ai montré aussi que les protéines de pontages des filaments d'actine sont nécessaires pour effectuer une déformation et générer des forces au niveau des réseaux d'actine dynamiques en présence de la myosine. De plus, nous avons développé les simulations numériques dans le but de relier la déformation macroscopique des structures d'actines due à la myosine avec le mécanisme microscopique sous-jacent.Ce travail a révélé comment la variété des réseaux d'actine contracte d'une façon différente même en respectant les mêmes conditions biochimiques et a démontré l'importance de l'effet du réarrangement dynamique des structures d'actine sur la modulation de sa contractilité
Cellular 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
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Ripoll, Léa. "Role of myosin VI and actin dynamics in membrane remodeling during pigmentation." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB102.

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Le trafic intracellulaire consiste en la formation et le transport de vésicules ou tubules qui acheminent des composants protéiques et lipidiques entre les différents organites ou avec la membrane plasmique. L’élaboration de ces tubulo-vésicules est initiée par le remodelage local d’une membrane, tout d’abord en générant une courbure puis un bourgeon qui, s’allongeant, forme la tubulo-vésicule. Enfin, la rupture de la membrane, ou scission, libère le transporteur nouvellement formé. Ces étapes repose sur un sculptage profond de la membrane. Ceci requière des forces générées par des moteurs moléculaires, lesquels s’associent aux cytosquelettes comme les microtubules ou les filaments d’actine. Afin de mieux comprendre comment le cytosquelette et leurs moteurs façonnent ces transporteurs, nous avons examiné le rôle de l’actine et de la myosine VI dans la formation de tubules membranaires aux mélanosomes. Les mélanosomes sont des organites apparentés aux lysosomes, générés dans les mélanocytes de la peau et de la choroïde de l’œil, et qui sont le lieu de synthèse et de stockage d’un pigment, la mélanine. Dans l’épiderme, ces compartiments spécialisés évoluent par différentes étapes de maturation qui aboutissent à leurs transferts aux cellules voisines, les kératinocytes. Les mélanosomes sont des organites dynamiques qui reçoivent et recyclent constamment des composants membranaires, comme la SNARE VAMP7. Nous résultats montrent que la myosine VI et son adapteur optineurine se localisent à un sous-domaine spécifique de la membrane des mélanosomes, ou elles contrôlent la scission de tubules. En effet, l’activité motrice de la myosine VI et le réseau d’actine branchée, dépendant des complexes Arp2/3 et WASH, permettent la constriction des membranes du tubule et son détachement du mélanosome. Un défaut de scission de ces tubes engendre des mélanosomes plus pigmentés, enrichis en cargos et au pH plus acide. L’altération de l’homéostasie du mélanosome affecte sa fonction, comme sa capacité à être sécrété et transféré aux kératinocytes. Nos résultats démontrent que la myosine VI en coopération avec le cytosquelette d’actine permet la constriction et fission de membranes aux mélanosomes. Les intermédiaires de transport ainsi formés recyclent des protéines cargos pour leur possible réutilisation, et participent ainsi au maintien de l’homéostasie et de la fonction de ces organites
Intracellular 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
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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.

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Books on the topic "Myositi"

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Aggarwal, Rohit, and Chester V. Oddis, eds. Managing Myositis. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-15820-0.

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J, Staiger C., ed. Actin: A dynamic framework for multiple plant cell functions. Dordrecht: Kluwer Academic Publishers, 2000.

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Coluccio, Lynne M., ed. Myosins. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-38062-5.

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Coluccio, Lynne M. Myosins. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6519-4.

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Melica, Elisa. Myosotis. Nardò (LE), i.e. Lecce: Besa Editrice, 2000.

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Myosins. 2nd ed. Oxford: Oxford University Press, 1999.

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Betina, Begong-Bodoli. Myosotis: Roman. Saint-Louis, Sénégal: Xamal, 1997.

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Hương, Dương Thu. Myosotis: Roman. Arles: Picquier, 2003.

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Askanas, Valerie, and W. King Engel. Muscle aging: Inclusion-body myositis and myopathies. Oxford: Wiley-Blackwell, 2012.

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1933-, Sugi Haruo, and Pollack Gerald H, eds. Mechanism of myofilament sliding in muscle contraction. New York: Plenum Press, 1993.

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Book chapters on the topic "Myositi"

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Schiffenbauer, Adam, and Frederick W. Miller. "Introduction to Myositis." In Managing Myositis, 1–6. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-15820-0_1.

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Huber, Adam M. "Clinical Features of Myositis: Juvenile Dermatomyositis." In Managing Myositis, 81–89. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-15820-0_10.

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Leclair, Valérie, and Ingrid E. Lundberg. "Making the Diagnosis of Myositis: Definition and Classification of Myositis." In Managing Myositis, 91–98. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-15820-0_11.

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Lacomis, David. "Making the Diagnosis of Myositis: Electrodiagnostic Testing." In Managing Myositis, 99–108. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-15820-0_12.

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Lacomis, David. "Making the Diagnosis of Myositis: Muscle Biopsy and Interpretation." In Managing Myositis, 109–24. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-15820-0_13.

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Sander, Inbal. "Making the Diagnosis of Myositis: Skin Biopsy and Interpretation." In Managing Myositis, 125–30. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-15820-0_14.

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Schneider, Frank, and Patty Chen. "Making the Diagnosis of Myositis: Lung Biopsy and Interpretation." In Managing Myositis, 131–44. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-15820-0_15.

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Lötscher, Jonas, Balazs K. Kovacs, and Ulrich A. Walker. "Making the Diagnosis of Myositis: Muscle MRI." In Managing Myositis, 145–60. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-15820-0_16.

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Benveniste, Olivier, and Lucile Musset. "Making the Diagnosis of Myositis: Laboratory Testing in Myositis." In Managing Myositis, 161–66. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-15820-0_17.

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McHugh, Neil J., and Ira N. Targoff. "Role of ANA and Myositis Autoantibodies in Diagnosis." In Managing Myositis, 167–74. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-15820-0_18.

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Conference papers on the topic "Myositi"

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Egan, Paul F., Philip R. LeDuc, Jonathan Cagan, and Christian Schunn. "A Design Exploration of Genetically Engineered Myosin Motors." In ASME 2011 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2011. http://dx.doi.org/10.1115/detc2011-48568.

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As technology advances, there is an increasing need to reliably output mechanical work at smaller scales. At the nanoscale, one of the most promising routes is utilizing biomolecular motors such as myosin proteins commonly found in cells. Myosins convert chemical energy into mechanical energy and are strong candidates for use as components of artificial nanodevices and multi-scale systems. Isoforms of the myosin superfamily of proteins are fine-tuned for specific cellular tasks such as intracellular transport, cell division, and muscle contraction. The modular structure that all myosins share makes it possible to genetically engineer them for fine-tuned performance in specific applications. In this study, a parametric analysis is conducted in order to explore the design space of Myosin II isoforms. The crossbridge model for myosin mechanics is used as a basis for a parametric study. The study sweeps commonly manipulated myosin performance variables and explores novel ways of tuning their performance. The analysis demonstrates the extent that myosin designs are alterable. Additionally, the study informs the biological community of gaps in experimentally tabulated myosin design parameters. The study lays the foundation for further progressing the design and optimization of individual myosins, a pivotal step in the eventual utilization of custom-built biomotors for a broad range of innovative nanotechnological devices.
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Egan, Paul F., Jonathan Cagan, Christian Schunn, and Philip R. LeDuc. "Design of Complex Nano-Scale Systems Using Multi-Agent Simulations and Structure-Behavior-Function Representations." In ASME 2012 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/detc2012-70291.

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Recent trends in technology are challenging engineers to configure products at ever smaller scales. At the nano-scale, biological protein machines are commonly chosen as a power-source for a broad-range of nano-devices. This paper explores the challenges in designing these and similar systems, such as improving the emergent system performance that arises from the interactions of many stochastic components. We develop a domain-independent methodology, using multi-agent simulations as a means of modeling and predicting emergent system behavior across scales and structure-behavior-function representations for understanding and navigating the resulting design space. This methodology is validated with an application of synthetic myosin motor design at the nanoscale, with simulation results aligning well with the macroscopic performance of myosin-powered muscular contractions. The multi-agent simulation is implemented with myosins modeled as agents, allowing for the virtual design and experimentation of synthetic myosins with altered structures and mechanochemical behaviors. Four myosin populations are designed and simulated, with their emergent system performance determined by aggregating the contributions of each myosin agent over time. Although the multi-agent simulation successfully recreates the emergent behaviors of the myosins, it is difficult to draw conclusions about how each structural variation influences aggregate performance. SBF representations of the system are then developed to describe how the aggregate performance of the system is explainable in terms of myosin behaviors, which map directly to altered myosin structures. It is then demonstrated how an engineer may utilize these representations and experimental results to reason about, and configure a myosin system with optimal performance. The methodology is domain-independent, ensuring its extendibility to similar complex systems while aiding a designer in simplifying a complex physical phenomenon to a design space consisting of only a few critical parameters. The methodology is particularly suited for complex systems with many parts operating stochastically across scales, and should prove invaluable for engineers facing the challenges of biological nanoscale design, where designs with unique properties require novel approaches or useful configurations in nature await discovery.
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Alves, Laura Da Silva, Leonado André Denti, Luciana Machado Kurtz Gonçalves, Bruno Collins Matheus De Melo, Carolina Vieira Tavares, Maria Paula Costamilan Da Cunha, Jennifer Bayona Gazabon, et al. "Myositis Ossificans." In XXXIX Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2022. http://dx.doi.org/10.47660/cbr.2022.1958.

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Joven, B. E., F. Lozano, L. Nuño, F. J. López-Longo, O. Toldos, E. Rabadán, A. Hernández, et al. "FRI0435 Clinicopathological correlation in inflammatory myositis: analysis of the remicam cohort (REGISTRY OF INFLAMMATORY MYOSITYS FROM MADRID, SPAIN)." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5795.

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Schara, U. "Myositis im Kindesalter." In 24. Kongress des Medizinisch-Wissenschaftlichen Beirates der Deutschen Gesellschaft für Muskelkranke (DGM) e.V. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1684982.

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Nuño, L., B. E. Joven, P. E. Carreira, J. Martínez Barrio, V. Maldonado-Romero, C. Larena-Grijalba, I. Llorente Cubas, et al. "FRI0449 Overlap myositis and primary myositis: clinical outcomes and prognosis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.7066.

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Silva, CA, and DA Isenberg. "OP0132 Myositis and pregnancy." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.582.

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MENDES, VANESSA FRAGA, GUSTAVO DE PAIVA COSTA, RAVENA FONTENELE BELCHIOR CABRAL, and MARINA FERNANDES OLIVEIRA. "MYOSITIS OSSIFICANS: CASE REPORT." In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-185.

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Ferreira, Raul S., Carlos G. de Oliveira, and Alexandre A. B. Lima. "Myosotis." In the XIV Brazilian Symposium. New York, New York, USA: ACM Press, 2018. http://dx.doi.org/10.1145/3229345.3229379.

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Zhang, Qian, Dong Wang, Run Zhao, and Yinggang Yu. "MyoSign." In IUI '19: 24th International Conference on Intelligent User Interfaces. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3301275.3302296.

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Reports on the topic "Myositi"

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Sadot, Einat, Christopher Staiger, and Mohamad Abu-Abied. Studies of Novel Cytoskeletal Regulatory Proteins that are Involved in Abiotic Stress Signaling. United States Department of Agriculture, September 2011. http://dx.doi.org/10.32747/2011.7592652.bard.

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In the original proposal we planned to focus on two proteins related to the actin cytoskeleton: TCH2, a touch-induced calmodulin-like protein which was found by us to interact with the IQ domain of myosin VIII, ATM1; and ERD10, a dehydrin which was found to associate with actin filaments. As reported previously, no other dehydrins were found to interact with actin filaments. In addition so far we were unsuccessful in confirming the interaction of TCH2 with myosin VIII using other methods. In addition, no other myosin light chain candidates were found in a yeast two hybrid survey. Nevertheless we have made a significant progress in our studies of the role of myosins in plant cells. Plant myosins have been implicated in various cellular activities, such as cytoplasmic streaming (1, 2), plasmodesmata function (3-5), organelle movement (6-10), cytokinesis (4, 11, 12), endocytosis (4, 5, 13-15) and targeted RNA transport (16). Plant myosins belong to two main groups of unconventional myosins: myosin XI and myosin VIII, both closely related to myosin V (17-19). The Arabidopsis myosin family contains 17 members: 13 myosin XI and four myosin VIII (19, 20). The data obtained from our research of myosins was published in two papers acknowledging BARD funding. To address whether specific myosins are involved with the motility of specific organelles, we cloned the cDNAs from neck to tail of all 17 Arabidopsis myosins. These were fused to GFP and used as dominant negative mutants that interact with their cargo but are unable to walk along actin filaments. Therefore arrested organelle movement in the presence of such a construct shows that a particular myosin is involved with the movement of that particular organelle. While no mutually exclusive connections between specific myosins and organelles were found, based on overexpression of dominant negative tail constructs, a group of six myosins (XIC, XIE, XIK, XI-I, MYA1 and MYA2) were found to be more important for the motility of Golgi bodies and mitochondria in Nicotiana benthamiana and Nicotiana tabacum (8). Further deep and thorough analysis of myosin XIK revealed a potential regulation by head and tail interaction (Avisar et al., 2011). A similar regulatory mechanism has been reported for animal myosin V and VIIa (21, 22). In was shown that myosin V in the inhibited state is in a folded conformation such that the tail domain interacts with the head domain, inhibiting its ATPase and actinbinding activities. Cargo binding, high Ca2+, and/or phosphorylation may reduce the interaction between the head and tail domains, thus restoring its activity (23). Our collaborative work focuses on the characterization of the head tail interaction of myosin XIK. For this purpose the Israeli group built yeast expression vectors encoding the myosin XIK head. In addition, GST fusions of the wild-type tail as well as a tail mutated in the amino acids that mediate head to tail interaction. These were sent to the US group who is working on the isolation of recombinant proteins and performing the in vitro assays. While stress signals involve changes in Ca2+ levels in plants cells, the cytoplasmic streaming is sensitive to Ca2+. Therefore plant myosin activity is possibly regulated by stress. This finding is directly related to the goal of the original proposal.
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Goldberg, Robert. Potential Environmental Triggers of Myositis. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada613036.

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Sanders, Luraynne. Cell Adhesion, Signaling and Myosin in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2000. http://dx.doi.org/10.21236/ada392857.

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Sanders, Luraynne C. Cell Adhesion, Signaling and Myosin in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada382496.

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Chew, Teng-Leong. Regulation of Actin-Myosin Cytoskeletal Changes Involved in Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396798.

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Hofmann, Wilma A. The Role of a Novel Myosin Isoform in Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada593300.

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Zhang, John Q. Post-Myocardial Infarction and Exercise Training on Myosin Heavy Chain and Cardiac Function. Science Repository, April 2019. http://dx.doi.org/10.31487/j.jicoa.2019.01.08.

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Schiefelbein, J. Molecular genetics of myosin motors in Arabidopsis. Final report, July 1, 1992--June 30, 1996. Office of Scientific and Technical Information (OSTI), February 1997. http://dx.doi.org/10.2172/486111.

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Staiger, Christopher. Regulation of Cell Wall Assembly: Myosin and Exocyst Involvement in Cellulose Synthase Delivery to the Plasma Membrane. Office of Scientific and Technical Information (OSTI), January 2022. http://dx.doi.org/10.2172/1840725.

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Philosoph-Hadas, Sonia, Peter B. Kaufman, Shimon Meir, and Abraham H. Halevy. Inhibition of the Gravitropic Shoot Bending in Stored Cut Flowers Through Control of Their Graviperception: Involvement of the Cytoskeleton and Cytosolic Calcium. United States Department of Agriculture, December 2005. http://dx.doi.org/10.32747/2005.7586533.bard.

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Original objectives: The basic goal of the present project was to study the mechanism involved in shoot graviperception and early transduction, in order to determine the sequence of events operating in this process. This will enable to control the entire process of gravity-induced differential growth without affecting vertical growth processes essential for development. Thus, several new postulated interactions, operating at the perception and early transduction stages of the signaling cascade leading to auxin-mediated bending, were proposed to be examined in snapdragon spikes and oat shoot pulvini, according to the following research goals: 1) Establish the role of amyloplasts as gravireceptors in shoots; 2) Investigate gravity-induced changes in the integrity of shoot actin cytoskeleton (CK); 3) Study the cellular interactions among actin CK, statoliths and cell membranes (endoplasmic reticulum - ER, plasma membrane - PM) during shoot graviperception; 4) Examine mediation of graviperception by modulations of cytosolic calcium - [Ca2+]cyt, and other second messengers (protein phosphorylation, inositol 1,4,5-trisphosphate - IP3). Revisions: 1) Model system: in addition to snapdragon (Antirrhinum majus L.) spikes and oat (Avena sativa) shoot pulvini, the model system of maize (Zea mays) primary roots was targeted to confirm a more general mechanism for graviperception. 2) Research topic: brassinolide, which were not included in the original plan, were examined for their regulatory role in gravity perception and signal transduction in roots, in relation to auxin and ethylene. Background to the topic: The negative gravitropic response of shoots is a complex multi-step process that requires the participation of various cellular components acting in succession or in parallel. Most of the long-lasting studies regarding the link between graviperception and cellular components were focused mainly on roots, and there are relatively few reports on shoot graviperception. Our previous project has successfully characterized several key events occurring during shoot bending of cut flowers and oat pulvini, including amyloplast displacement, hormonal interactions and differential growth analysis. Based on this evidence, the present project has focused on studying the initial graviperception process in flowering stems and cereal shoots. Major conclusions and achievements: 1) The actin and not the microtubule (MT) CK is involved in the graviperception of snapdragon shoots. 2) Gravisensing, exhibited by amyloplast displacement, and early transduction events (auxin redistribution) in the gravitropic response of snapdragon spikes are mediated by the acto-myosin complex. 3) MTs are involved in stem directional growth, which occurs during gravitropism of cut snapdragon spikes, but they are not necessary for the gravity-induced differential growth. 4) The role of amyloplasts as gravisensors in the shoot endodermis was demonstrated for both plant systems. 5) A gravity-induced increase in IP.
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