Academic literature on the topic 'Membrane implicite'

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Journal articles on the topic "Membrane implicite"

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Amrouche, Fethia, Bouziane Mahmah, Maiouf Belhamel, and Hocine Benmoussa. "Modélisation d’une pile à combustible PEMFC alimentée directement en hydrogène-oxygène et validation expérimentale." Journal of Renewable Energies 8, no. 2 (December 31, 2005): 109–21. http://dx.doi.org/10.54966/jreen.v8i2.856.

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La pile à combustible (PAC) est connue depuis longtemps comme un convertisseur d’hydrogène en énergie (électrique + thermique) possédant de très bons rendements, les recherches sur cette technologie se développent partout dans le monde de manière considérable. Les raisons sont bien connues: la réponse aux contraintes environnementales, aux problèmes posés par la production centralisée d’électricité, la nécessité d’avoir des alternatives énergétiques (vecteur hydrogène) et certaines exigences technologiques spécifiques telles que les applications spatiales, sous-marines, électroniques portables, alimentation électrique de sites isolés et de microsystèmes. Il est certain que nous assisterons dans les prochaines décennies à l’émergence de la filière hydrogène dans notre vie quotidienne comme vecteur énergétique. Le choix de la technologie des piles à combustible à membrane échangeuse de protons (PEMFC) est implicite vu les performances intéressantes (faible poids, robuste, électrolyte solide, démarrage rapide, large gamme de puissance de 1 W à10 MW, etc.). Il est donc important de pousser encore plus loin les efforts de recherche/développement autour de cette technologie pour pouvoir la maîtriser et étendre son application. Cet article présente les résultats de la modélisation de la cinétique électrochimique et la production électrique des piles à combustible PEMFC alimentée directement en gaz pur (hydrogène et oxygène) et la validation expérimentale grâce à une base de données établie au niveau du ‘’Laboratoire d’Hydrogène en Réseau – CDER‘’, dans le but d’exploiter et d’améliorer les modèles électrochimiques existants.
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Tian, Ye, Charles Schwieters, Stanley Opella, and Francesca Marassi. "NMR-Restrained Structure Calculations of Membrane Proteins in Implicit Lipid Bilayer Membranes." Biophysical Journal 108, no. 2 (January 2015): 251a. http://dx.doi.org/10.1016/j.bpj.2014.11.1389.

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Sáenz, James P., Daniel Grosser, Alexander S. Bradley, Thibaut J. Lagny, Oksana Lavrynenko, Martyna Broda, and Kai Simons. "Hopanoids as functional analogues of cholesterol in bacterial membranes." Proceedings of the National Academy of Sciences 112, no. 38 (September 8, 2015): 11971–76. http://dx.doi.org/10.1073/pnas.1515607112.

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The functionality of cellular membranes relies on the molecular order imparted by lipids. In eukaryotes, sterols such as cholesterol modulate membrane order, yet they are not typically found in prokaryotes. The structurally similar bacterial hopanoids exhibit similar ordering properties as sterols in vitro, but their exact physiological role in living bacteria is relatively uncharted. We present evidence that hopanoids interact with glycolipids in bacterial outer membranes to form a highly ordered bilayer in a manner analogous to the interaction of sterols with sphingolipids in eukaryotic plasma membranes. Furthermore, multidrug transport is impaired in a hopanoid-deficient mutant of the gram-negativeMethylobacterium extorquens, which introduces a link between membrane order and an energy-dependent, membrane-associated function in prokaryotes. Thus, we reveal a convergence in the architecture of bacterial and eukaryotic membranes and implicate the biosynthetic pathways of hopanoids and other order-modulating lipids as potential targets to fight pathogenic multidrug resistance.
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Petrie, Emma J., Richard W. Birkinshaw, Akiko Koide, Eric Denbaum, Joanne M. Hildebrand, Sarah E. Garnish, Katherine A. Davies, et al. "Identification of MLKL membrane translocation as a checkpoint in necroptotic cell death using Monobodies." Proceedings of the National Academy of Sciences 117, no. 15 (March 31, 2020): 8468–75. http://dx.doi.org/10.1073/pnas.1919960117.

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The necroptosis cell death pathway has been implicated in host defense and in the pathology of inflammatory diseases. While phosphorylation of the necroptotic effector pseudokinase Mixed Lineage Kinase Domain-Like (MLKL) by the upstream protein kinase RIPK3 is a hallmark of pathway activation, the precise checkpoints in necroptosis signaling are still unclear. Here we have developed monobodies, synthetic binding proteins, that bind the N-terminal four-helix bundle (4HB) “killer” domain and neighboring first brace helix of human MLKL with nanomolar affinity. When expressed as genetically encoded reagents in cells, these monobodies potently block necroptotic cell death. However, they did not prevent MLKL recruitment to the “necrosome” and phosphorylation by RIPK3, nor the assembly of MLKL into oligomers, but did block MLKL translocation to membranes where activated MLKL normally disrupts membranes to kill cells. An X-ray crystal structure revealed a monobody-binding site centered on the α4 helix of the MLKL 4HB domain, which mutational analyses showed was crucial for reconstitution of necroptosis signaling. These data implicate the α4 helix of its 4HB domain as a crucial site for recruitment of adaptor proteins that mediate membrane translocation, distinct from known phospholipid binding sites.
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Zelhof, Andrew C., Hong Bao, Robert W. Hardy, Azam Razzaq, Bing Zhang, and Chris Q. Doe. "DrosophilaAmphiphysin is implicated in protein localization and membrane morphogenesis but not in synaptic vesicle endocytosis." Development 128, no. 24 (December 15, 2001): 5005–15. http://dx.doi.org/10.1242/dev.128.24.5005.

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Amphiphysin family members are implicated in synaptic vesicle endocytosis, actin localization and one isoform is an autoantigen in neurological autoimmune disorder; however, there has been no genetic analysis of Amphiphysin function in higher eukaryotes. We show that Drosophila Amphiphysin is localized to actin-rich membrane domains in many cell types, including apical epithelial membranes, the intricately folded apical rhabdomere membranes of photoreceptor neurons and the postsynaptic density of glutamatergic neuromuscular junctions. Flies that lack all Amphiphysin function are viable, lack any observable endocytic defects, but have abnormal localization of the postsynaptic proteins Discs large, Lethal giant larvae and Scribble, altered synaptic physiology, and behavioral defects. Misexpression of Amphiphysin outside its normal membrane domain in photoreceptor neurons results in striking morphological defects. The strong misexpression phenotype coupled with the mild mutant and lack of phenotypes suggests that Amphiphysin acts redundantly with other proteins to organize specialized membrane domains within a diverse array of cell types.
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Mc Dermott, Ray, Umit Ziylan, Danièle Spehner, Huguette Bausinger, Dan Lipsker, Mieke Mommaas, Jean-Pierre Cazenave, et al. "Birbeck Granules Are Subdomains of Endosomal Recycling Compartment in Human Epidermal Langerhans Cells, Which Form Where Langerin Accumulates." Molecular Biology of the Cell 13, no. 1 (January 2002): 317–35. http://dx.doi.org/10.1091/mbc.01-06-0300.

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Birbeck granules are unusual rod-shaped structures specific to epidermal Langerhans cells, whose origin and function remain undetermined. We investigated the intracellular location and fate of Langerin, a protein implicated in Birbeck granule biogenesis, in human epidermal Langerhans cells. In the steady state, Langerin is predominantly found in the endosomal recycling compartment and in Birbeck granules. Langerin internalizes by classical receptor-mediated endocytosis and the first Birbeck granules accessible to endocytosed Langerin are those connected to recycling endosomes in the pericentriolar area, where Langerin accumulates. Drug-induced inhibition of endocytosis results in the appearance of abundant open-ended Birbeck granule-like structures appended to the plasma membrane, whereas inhibition of recycling induces Birbeck granules to merge with a tubular endosomal network. In mature Langerhans cells, Langerin traffic is abolished and the loss of internal Langerin is associated with a concomitant depletion of Birbeck granules. Our results demonstrate an exchange of Langerin between early endosomal compartments and the plasma membrane, with dynamic retention in the endosomal recycling compartment. They show that Birbeck granules are not endocytotic structures, rather they are subdomains of the endosomal recycling compartment that form where Langerin accumulates. Finally, our results implicate ADP-ribosylation factor proteins in Langerin trafficking and the exchange between Birbeck granules and other endosomal membranes.
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Wilson, D. W., S. W. Whiteheart, M. Wiedmann, M. Brunner, and J. E. Rothman. "A multisubunit particle implicated in membrane fusion." Journal of Cell Biology 117, no. 3 (May 1, 1992): 531–38. http://dx.doi.org/10.1083/jcb.117.3.531.

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The N-ethylmaleimide sensitive fusion protein (NSF) is required for fusion of lipid bilayers at many locations within eukaryotic cells. Binding of NSF to Golgi membranes is known to require an integral membrane receptor and one or more members of a family of related soluble NSF attachment proteins (alpha-, beta-, and gamma-SNAPs). Here we demonstrate the direct interaction of NSF, SNAPs and an integral membrane component in a detergent solubilized system. We show that NSF only binds to SNAPs in the presence of the integral receptor, resulting in the formation of a multisubunit protein complex with a sedimentation coefficient of 20S. Particle assembly reveals striking differences between members of the SNAP protein family; gamma-SNAP associates with the complex via a binding site distinct from that used by alpha- and beta-SNAPs, which are themselves equivalent, alternative subunits of the particle. Once formed, the 20S particle is subsequently able to disassemble in a process coupled to the hydrolysis of ATP. We suggest how cycles of complex assembly and disassembly could help confer specificity to the generalized NSF-dependent fusion apparatus.
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Parodi, Emily M., Crystal S. Baker, Cayla Tetzlaff, Sasha Villahermosa, and Linda S. Huang. "SPO71 Mediates Prospore Membrane Size and Maturation in Saccharomyces cerevisiae." Eukaryotic Cell 11, no. 10 (May 18, 2012): 1191–200. http://dx.doi.org/10.1128/ec.00076-12.

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ABSTRACT The mechanisms that control the size and shape of membranes are not well understood, despite the importance of these structures in determining organelle and cell morphology. The prospore membrane, a double lipid bilayer that is synthesized de novo during sporulation in S. cerevisiae , grows to surround the four meiotic products. This membrane determines the shape of the newly formed spores and serves as the template for spore wall deposition. Ultimately, the inner leaflet of the prospore membrane will become the new plasma membrane of the cell upon germination. Here we show that Spo71, a pleckstrin homology domain protein whose expression is induced during sporulation, is critical for the appropriate growth of the prospore membrane. Without SPO71 , prospore membranes surround the nuclei but are abnormally small, and spore wall deposition is disrupted. Sporulating spo71 Δ cells have prospore membranes that properly localize components to their growing leading edges yet cannot properly localize septin structures. We also found that SPO71 genetically interacts with SPO1 , a gene with homology to the phospholipase B gene that has been previously implicated in determining the shape of the prospore membrane. Together, these results show that SPO71 plays a critical role in prospore membrane development.
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He, Yi, Lidia Prieto, and Themis Lazaridis. "Electrostatic Interactions between Antimicrobial Peptides and Anionic Membranes: Insights from an Implicit Membrane Model." Biophysical Journal 100, no. 3 (February 2011): 497a. http://dx.doi.org/10.1016/j.bpj.2010.12.2914.

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Boyd, RB, JP Burke, J. Atkin, VW Thompson, and JF Nugent. "Significance of capillary basement membrane changes in diabetes mellitus." Journal of the American Podiatric Medical Association 80, no. 6 (June 1, 1990): 307–13. http://dx.doi.org/10.7547/87507315-80-6-307.

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Diabetes mellitus is a disease in which the capillary basement membranes are substantially altered. This diabetic microangiopathy is characterized by a thickening of the basement membrane and changes in its permeability characteristic due to a disturbance in the production and distribution of its functional components. Glucose metabolism and insulin imbalance have been implicated in these basement membrane modifications. The authors describe normal capillary basement membrane architecture and then discuss how pathologic changes caused by diabetes mellitus are related to diabetic foot pathology.
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Dissertations / Theses on the topic "Membrane implicite"

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Lanrezac, André. "Interprétation de données expérimentales par simulation et visualisation moléculaire interactive." Electronic Thesis or Diss., Université Paris Cité, 2023. http://www.theses.fr/2023UNIP7133.

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L'objectif de l'approche des simulations moléculaires interactive (Interactive Molecular Simulations - IMS) est d'observer en direct la dynamique conformationnelle d'une simulation moléculaire en cours. Le retour visuel instantané permet un suivi instructif ainsi que l'observation des changements structurels imposés par la manipulation de l'IMS par l'utilisateur. J'ai mené une étude approfondie des connaissances pour rassembler et synthétiser l'ensemble des recherches qui ont développé l'IMS. La dynamique moléculaire interactive (Interactive Molecular Dynamics - IMD) est l'un des premiers protocoles IMS qui a posé les bases du développement de cette approche. Mon laboratoire de thèse s'est inspirée de celle-ci pour développer le moteur de simulation BioSpring basé sur le modèle de réseaux élastique. Ce modèle permet de simuler la flexibilité de grands ensembles biomoléculaires et ainsi potentiellement révéler des changements à longue échelle de temps qui ne seraient pas facilement saisis par la dynamique moléculaire. Ce moteur de simulation ainsi que le logiciel de visualisation UnityMol, développé par le biais du moteur de jeu Unity3D, et liés par l'interface de communication MDDriver ont été étendus pour les faire converger vers une suite logicielle complète. Le but est de fournir à un expérimentateur, qu'il soit expert ou profane, une boîte à outils complète pour modéliser, afficher et contrôler interactivement l'ensemble des paramètres d'une simulation. L'implémentation particulière d'un tel protocole, basé sur une communication formalisée et extensible entre les différents composants, a été pensée pour pouvoir facilement intégrer de nouvelles possibilités de manipulation interactive et des jeux de données expérimentales qui s'ajouteront aux contraintes imposées à la simulation. L'utilisateur peut donc manipuler la molécule d'intérêt sous le contrôle des propriétés biophysiques intégrés dans le modèle simulé, tout en ayant la possibilité de piloter à la volée les paramètres de simulation. Aussi, un des objectifs initiaux de cette thèse était d'intégrer la gestion des contraintes d'interaction ambigües du logiciel d'amarrage biomoléculaire HADDOCK directement dans UnityMol, rendant possible l'utilisation de ces mêmes contraintes à une variété de moteurs de simulations. Un axe principal de ces recherches était de développer un algorithme de positionnement rapide et interactif de protéines dans des membranes implicite tiré d'un modèle appelé Integrative Membrane Protein and Lipid Association Method (IMPALA) développée par l'équipe de Robert Brasseur en 1998. La première étape consistait à effectuer une recherche approfondie des conditions dans lesquelles les expériences ont été réalisées à l'époque, afin de vérifier la méthode et de valider notre propre implémentation. Nous verrons qu'elle ouvre des questions intéressantes sur la manière dont on peut reproduire les expériences scientifiques. L'étape finale qui conclue cette thèse était le développement d'une nouvelle méthode universelle d'interaction lipide-protéine, UNILIPID, qui est un modèle d'incorporation interactif de protéines dans les membranes implicites. Elle est indépendante de l'échelle de représentation, peut être appliquée à des niveaux tout atomes, gros-grains jusqu'au niveau d'un grain par acide aminé. La représentation de la dernière version Martini3[6] ainsi qu'une méthode d'échantillonnage Monte-Carlo et de simulation de dynamique des corps rigides ont été spécialement intégrés à la méthode, en plus de divers outils de préparation de systèmes. En outre, UNILIPID est une approche versatile qui reproduit précisément des termes d'hydrophobicité expérimentaux pour chaque acide aminé. En plus de membranes implicites simples, je décrirai une implémentation analytique de membranes doubles ainsi qu'une généralisation à des membranes de forme arbitraire, toutes deux s'appuyant sur des applications inédites
The goal of Interactive Molecular Simulations (IMS) is to observe the conformational dynamics of a molecular simulation in real-time. Instant visual feedback enables informative monitoring and observation of structural changes imposed by the user's manipulation of the IMS. I conducted an in-depth study of knowledge to gather and synthesize all the research that has developed IMS. Interactive Molecular Dynamics (IMD) is one of the first IMS protocols that laid the foundation for the development of this approach. My thesis laboratory was inspired by IMD to develop the BioSpring simulation engine based on the elastic network model. This model allows for the simulation of the flexibility of large biomolecular ensembles, potentially revealing long-timescale changes that would not be easily captured by molecular dynamics. This simulation engine, along with the UnityMol visualization software, developed through the Unity3D game engine, and linked by the MDDriver communication interface, has been extended to converge towards a complete software suite. The goal is to provide an experimenter, whether an expert or novice, with a complete toolbox for modeling, displaying, and interactively controlling all parameters of a simulation. The particular implementation of such a protocol, based on formalized and extensible communication between the different components, was designed to easily integrate new possibilities for interactive manipulation and sets of experimental data that will be added to the restraints imposed on the simulation. Therefore, the user can manipulate the molecule of interest under the control of biophysical properties integrated into the simulated model, while also having the ability to dynamically adjust simulation parameters. Furthermore, one of the initial objectives of this thesis was to integrate the management of ambiguous interaction constraints from the HADDOCK biomolecular docking software directly into UnityMol, making it possible to use these same restraints with a variety of simulation engines. A primary focus of this research was to develop a fast and interactive protein positioning algorithm in implicit membranes using a model called the Integrative Membrane Protein and Lipid Association Method (IMPALA), developed by Robert Brasseur's team in 1998. The first step was to conduct an in-depth search of the conditions under which the experiments were performed at the time to verify the method and validate our own implementation. We will see that this opens up interesting questions about how scientific experiments can be reproduced. The final step that concluded this thesis was the development of a new universal lipid-protein interaction method, UNILIPID, which is an interactive protein incorporation model in implicit membranes. It is independent of the representation scale and can be applied at the all-atom, coarse-grain, or grain-by-grain level. The latest Martini3 representation, as well as a Monte Carlo sampling method and rigid body dynamics simulation, have been specially integrated into the method, in addition to various system preparation tools. Furthermore, UNILIPID is a versatile approach that precisely reproduces experimental hydrophobicity terms for each amino acid. In addition to simple implicit membranes, I will describe an analytical implementation of double membranes as well as a generalization to arbitrarily shaped membranes, both of which rely on novel applications
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Lekostaj, Jacqueline K. "Molecular analysis of membrane transporters implicated in drug resistance." Connect to Electronic Thesis (ProQuest) Connect to Electronic Thesis (CONTENTdm), 2008. http://worldcat.org/oclc/436214303/viewonline.

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Mesquita, Arthur Dias. "Uma formulação do Método dos Elementos Finitos aplicada à análise elastoplástica de cascas." Universidade de São Paulo, 1998. http://www.teses.usp.br/teses/disponiveis/18/18134/tde-22032018-120500/.

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Um elemento finito para análises elastoplásticas de placas (em flexão ou não) e cascas é descrito. Este elemento apresenta geometria triangular e é o resultado do acoplamento entre um elemento de flexão de placas (DKT) e um elemento de tensão plana, baseado na formulação livre (FF). O elemento DKT é um elemento finito bem conhecido, considerado por muitos autores como um dos melhores de sua classe. O elemento FF apresenta o grau de liberdade rotacional normal, que é essencial quando se trabalha com cascas aproximadamente planas. Além disso, sua convergência é garantida devido à imposição do \'Teste do Elemento Individual\'. O comportamento elastoplástico é aproximado por meio de técnicas de integração implícita. Plasticidade associativa é considerada com encruamento isotrópico e critério de von Mises. Afim de preservar a taxa assintótica de convergência quadrática do método de Newton-Raphson, a matriz tangente elastoplástica consistente é aplicada. Resultados demonstram a precisão e eficiência da formulação proposta.
A finite element for elastoplastic analysis of plates (in bending or not) and shells is described. This element presents triangular geometry and is the result of a coupling between a plate in bending element (DKT) and a plane stress elernent, based on the free formulation (FF). The DKT element is a well-known finite element, considered by many authors as one of the best of its class. The FF element presents the normal rotation degree of freedom, what is essential when working with near planar shells. Beyond this, its convergence is guaranteed due to the imposition of the \'Individual Element Test\'. The elastoplastic behaviour is approached by means of implicit integration techniques. Associative plasticity is considered with isotropic hardening and the von Mises criteria. In order to preserve the quadratic rate of asymptotic convergence of Newton-Raphson method, the consistent elastoplastic tangent matrix is applied. Results demonstrates the accuracy and efficiency of the proposed formulation.
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Gouguet, Paul. "Deciphering the proteic partners of REMORIN, a membrane-raft phosphoprotein implicated in plant cell-to-cell communication." Thesis, Bordeaux, 2018. http://www.theses.fr/2018BORD0418.

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Les REMORINES du groupe 1 sont des protéines spécifiques des plantes, localisées dans la membrane plasmique. Nous avons montré que StREM1.3 (REM) constitue un marqueur des radeaux lipidiques, des domaines membranaires du plasmalemme enrichis en stérols et sphingolipides. De plus, REM se trouve enrichie dans les plasmodesmes (PD), des canaux ancrés dans la paroi qui assurent les communications intercellulaires. Nous avons mis en évidence pour la première fois le rôle physiologique de REM dans la plante, cette protéine est capable de ralentir la propagation virale du Potato Virus X (PVX) et d’autres virus. Par ailleurs, l’activité antivirale de REM est régulée par phosphorylation et conduit à une modification de la taille du pore des PD par dépôt de callose. Des candidats protéiques ont été sélectionnées et leur validation fonctionnelle a été initiée in planta par des approches de transgénèse, en expression transitoire et sur des plantes transgéniques soumises à des infections virales pour étudier la propagation des virus. Des approches de biochimie d’interaction des protéines, et d’imagerie ont également été envisagés. Le sujet de cette thèse vise à appréhender les mécanismes de l’interaction de REM avec ses partenaires dans la membrane lors de l’infection virale, en se focalisant sur les interactions protéines-protéines lors de la réponse au PVX. Nous nous intéresserons plus particulièrement aux protéines des PD et des radeaux membranaires qui sont très probablement ciblées lors de cette interaction avec les virus
Group 1 REMORINs are plant-specific proteins located at the plasma membrane. We have shown that StREM1.3 (REM) is a marker of lipid rafts, plasma membrane domains enriched in sterols and sphingolipids. In addition, REM is enriched in plasmodesmata channels (PD) which are anchored within the cell wall and enable intercellular communication between virtually all plant cells. We have demonstrated for the first time the physiological role of REM in plants, this protein is able to reduce the viral cell-to-cell movement of Potato Virus X (PVX) and other viruses. Moreover, the antiviral activity of REM is regulated by phosphorylation and leads to a modification of the pore size of PD via the accumulation of callose, a sugar polymer, around the neck regions of PD. In order to understand how REM is able to induce the accumulation of callose in these specific regions, a large set of proteins have been selected and the deciphering of their functions have been initiated in planta by transgenic approaches, in transient expression and on transgenic plants, which will be subjected to viral infections to study the spread of viruses. Protein interaction, biochemistry and imaging approaches were also used to study this question. This thesis aims at understanding the mechanisms of the REM interaction with its membrane partners during viral infection, focusing on the protein-protein interactions during the response to PVX. We will focus more particularly on PD proteins and membrane rafts that are most likely targeted during this interaction with viruses
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Liu, Yi. "Calcium-related fungal genes implicated in arbuscular mycorrhiza." Phd thesis, Université de Bourgogne, 2012. http://tel.archives-ouvertes.fr/tel-00985826.

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Fluctuations in intracellular (Ca2+) calcium levels generate signaling events and regulate different cellular processes. Whilst the implication of Ca2+ in plant cell responses during arbuscular mycorrhiza (AM) interactions is well documented, nothing is known about the regulation or role of this secondary meesenger in the fungal symbiont. The molecular basis of fungal calcium homeostasis in the AM symbiosis was analyzed by investigating the expression of Ca2+-related fungal genes. In a first study, G. mosseae genes putatively encoding a MAP3k-like protein kinase (Gm2) and a P-type ATPase (Gm152) were investigated. Both Ca2+-related genes were up-regulated by A. sinicum root exudates, suggesting a role in early interactions prior to symbiosis establishment. The full-length cDNA sequence of Gm152 obtained from germinating spores of G. mosseae confirmed its identity. The role of Ca2+ in fungal processes leading to establishment of an AM symbiosis was investigated in more detail in G. intraradices-M. truncatula interactions. Enhanced expression of genes encoding six membrane transport proteins and one nuclear protein kinase, selected from the G. intraradices transcriptome database, was related to colonization of wild-type M. truncatula (line J5) roots and not observed with the mycorrhiza-resistant mutant dmi3/Mtsym13. Laser microdissection mapping of transcripts indicated that the Ca2+-related G. intraradices genes were differentially up-regulated in arbuscules and/or in intercellular hyphae. The tempo-spatial variations in fungal gene expression suggest different roles in the development or functioning of the AM symbiosis. Full-length cDNA of three G. intraradices genes putatively encoding a PMR-like endoplasmic reticulum P-type ATPase, a VCX1-like vacuolar Ca2+ ion transporter and a nuclear CCaMK were obtained for functional analyses in yeast mutants to gain insight into their role in the mycorrhizal symbiosis. Possible mechanisms are discussed in which Ca2+-related proteins of G. intraradices may play a role in the mobilization and perception of the intracellular messenger by the AM fungus during symbiotic interactions with host roots
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Canu, Stéphane. "La continuation appliquée aux modèles biologiques." Compiègne, 1986. http://www.theses.fr/1986COMPI237.

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Silva, Nancy Fonseca. "The characterization of PERK1 a novel receptor kinase implicated in plant defense and development /." 2003. http://wwwlib.umi.com/cr/yorku/fullcit?pNQ82822.

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Thesis (Ph. D.)--York University, 2003. Graduate Programme in Biology.
Typescript. Includes bibliographical references (leaves 192-219). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://wwwlib.umi.com/cr/yorku/fullcit?pNQ82822.
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Books on the topic "Membrane implicite"

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Shier, Peter. Purification of a plasma membrane glycoprotein implicated in cell sorting in dictyostelium discoideum. 1987.

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Johnson, Elizabeth M. Hyaline moulds. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0017.

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Hyaline moulds are fungi that grow predominantly in a filamentous form with colourless hyphae. This is not a taxonomic grouping and encompasses many thousands of different fungal genera. However, there is a small subset of environmental saprobes or plant pathogenic moulds, currently comprising at least 75 species from 30 different genera, that are opportunistic human pathogens and have been implicated in invasive infections referred to as hyalohyphomycosis. In addition they may cause less invasive cutaneous, subcutaneous, mucous membrane, and corneal infections. This group of organisms includes Fusarium, Sarocladium, Paecilomyces, Purpureocillium, Scedosporium, Rasamsonia, and Scopulariopsis spp., and it is these that form the focus of this chapter. Aspects of taxonomy, cell biology, pathogenesis, epidemiology, incidence, risk factors, presentation, diagnosis, and treatment are discussed with particular reference to those features that are specific to hyaline moulds.
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Heidet, Laurence, Bertrand Knebelmann, and Marie Claire Gubler. Alport syndrome. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0323.

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The diagnosis of Alport syndrome is suspected from the clinical features and confirmed by identifying the almost pathognomonic ultrastructural changes to the basement membrane in a family member with early disease (so that glomeruli are not too sclerosed), or in modern times by identifying a causative mutation in one or more of the three implicated COL4 genes. Genetic testing is becoming simpler and cheaper, but is still out of the reach of many. Eighty-five per cent of cases are caused by COL4A5 mutations and 10–15% by autosomal recessive disease. A significant proportion of morbidity in X-linked disease occurs in female ‘carriers’ heterozygous for the disease. Changes by light microscopy are non-specific, and can be misleading unless accompanied by electron microscopy. Immunohistology can be helpful but may not be definitive as some causative mutations are not associated with absence of protein product. As COL4A5 is expressed in skin, skin studies are theoretically useful, but they are technically challenging and only a definite negative result is helpful. It is important to distinguish other disorders causing renal disease with deafness, and other causes of glomerular haematuria. Two rare syndromes are caused by extended deletions beyond the COL4A5 gene: X-linked Alport syndrome with diffuse oesophageal leiomyomatosis in which smooth muscle leoimyomas is transmitted in a dominant fashion, and X-linked Alport syndrome with mental retardation.
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Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0064_update_001.

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It has been clear for several decades from comparison with the rodent model disease Heymann nephritis that membranous glomerulonephritis (MGN) is an immune condition in which antibodies, usually autoantibodies, bind to targets on the surface of podocytes. However, the antigen in Heymann nephritis, megalin, is not present on human podocytes. The first potential antigen was identified by studying rare examples of maternal alloimmunization, leading to congenital membranous nephropathy in the infant caused by antibodies to neutral endopeptidase. More recently, the target of autoantibody formation in most patients with primary MGN has been identified to be the phospholipase A2 receptor, PLA2R. Genome-wide association studies identify predisposing genetic loci at HLADQ and at the locus encoding the autoantigen itself. So antibodies to at least two different molecular targets can cause MGN, and it seems likely that there may be other targets in secondary types of MGN, and possibly haptenized or otherwise modified molecules are implicated in drug- and toxin-induced MGN. Once antibodies are fixed, animal models and human observations suggest that complement is involved in mediating tissue damage. However, immunoglobulin G4, not thought to fix complement, is the predominant isotype in human MGN, and the mechanisms are not fully unravelled. Podocyte injury is known to cause proteinuria. In MGN, antibody fixation or cell damage may stimulate production of extracellular matrix to account for the increased GBM thickness with ‘podocyte type’ basement membrane collagen isoforms, and ultimately cell death and glomerulosclerosis.
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Book chapters on the topic "Membrane implicite"

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Feig, Michael. "Implicit Membrane Models for Membrane Protein Simulation." In Methods in Molecular Biology, 181–96. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-177-2_10.

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Auger, Denise, Pam Bounelis, and Richard B. Marchase. "Phosphoglucomutase is a Cytoplasmic Glycoprotein Implicated in the Regulated Secretory Pathway." In Molecular Mechanisms of Membrane Traffic, 289–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02928-2_52.

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Park, Joshua K., Nathan J. Coffey, Aaron Limoges, and Anne Le. "The Heterogeneity of Lipid Metabolism in Cancer." In The Heterogeneity of Cancer Metabolism, 39–56. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_3.

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AbstractThe study of cancer cell metabolism has traditionally focused on glycolysis and glutaminolysis. However, lipidomic technologies have matured considerably over the last decade and broadened our understanding of how lipid metabolism is relevant to cancer biology [1–3]. Studies now suggest that the reprogramming of cellular lipid metabolism contributes directly to malignant transformation and progression [4, 5]. For example, de novo lipid synthesis can supply proliferating tumor cells with phospholipid components that comprise the plasma and organelle membranes of new daughter cells [6, 7]. Moreover, the upregulation of mitochondrial β-oxidation can support tumor cell energetics and redox homeostasis [8], while lipid-derived messengers can regulate major signaling pathways or coordinate immunosuppressive mechanisms [9–11]. Lipid metabolism has, therefore, become implicated in a variety of oncogenic processes, including metastatic colonization, drug resistance, and cell differentiation [10, 12–16]. However, whether we can safely and effectively modulate the underlying mechanisms of lipid metabolism for cancer therapy is still an open question.
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Ventura, Raúl, and María Isabel Hernández-Alvarez. "Endoplasmic Reticulum: A Hub in Lipid Homeostasis." In Updates on Endoplasmic Reticulum [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105450.

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Endoplasmic Reticulum (ER) is the largest and one of the most complex cellular structures, indicating its widespread importance and variety of functions, including synthesis of membrane and secreted proteins, protein folding, calcium storage, and membrane lipid biogenesis. Moreover, the ER is implicated in cholesterol, plasmalogen, phospholipid, and sphingomyelin biosynthesis. Furthermore, the ER is in contact with most cellular organelles, such as mitochondria, peroxisomes, Golgi apparatus, lipid droplets, plasma membrane, etc. Peroxisomes are synthesized from a specific ER section, and they are related to very-long-chain fatty acid metabolism. Similarly, lipid droplets are vital structures in lipid homeostasis that are formed from the ER membrane. Additionally, there is a specific region between the ER-mitochondria interface called Mitochondria-Associated Membranes (MAMs). This small cytosolic gap plays a key role in several crucial mechanisms from autophagosome synthesis to phospholipid transfer. Due to the importance of the ER in a variety of biological processes, alterations in its functionality have relevant implications for multiple diseases. Nowadays, a plethora of pathologies like non-alcoholic steatohepatitis (NASH), cancer, and neurological alterations have been associated with ER malfunctions.
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Grossfield, Alan. "Chapter 5 Implicit Modeling of Membranes." In Current Topics in Membranes, 131–57. Elsevier, 2008. http://dx.doi.org/10.1016/s1063-5823(08)00005-7.

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Robinson, Margaret S. "Adaptor proteins (AP-1-AP-3)." In Guidebook to the Cytoskeletal and Motor Proteins, 494–97. Oxford University PressOxford, 1999. http://dx.doi.org/10.1093/oso/9780198599579.003.00147.

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Abstract The ADP-ribosylation factors (Arf) are a family of 21 kDa GTP binding proteins which have been implicated as regulators of a wide variety of vesicular transport steps, as structural components of non-clathrin (COP!) coated vesicles and as direct activators of phospholipase D (PLD1). Activation of Arfs, coincident with the binding of GTP, causes a translocation of the otherwise soluble protein to membranes and is proposed to result in the nucleation of coat protein assembly and vesicular budding. Apparently conflicting data currently lead to uncertainty regarding the role of (Arf sensitive) PLO in vesicular transport, the role of Arf proteins in transport in general, and the view of Arf as a structural component of vesicle or membrane coated structures.
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Carraway, Coralie A. Carothers, and Kermjt I. Carraway. "Signalling complexes: association of signalling proteins with the cytoskeleton." In Cytoskeleton: signalling and cell regulation, 51–78. Oxford University PressOxford, 1999. http://dx.doi.org/10.1093/oso/9780199637829.003.0004.

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Abstract A plethora of studies in the areas of membranes, cytoskeleton and. more recently. signal transduction have contributed to both concepts and technologies for the study of interactions of signalling proteins with the cytoskeleton (for overviews. see refs 1 and 2). These studies have implicated association of signalling proteins with the membrane and with the cytoskeleton in targeting these proteins to appropriate cellular loc,11ions for their participation in signal transduction events. Appropriate cellular localization is requisite for activation processes (3) and can occur reversibly. to turn off signal. The approaches used historically are diverse, ranging from tissue and cell localization by microscopy, to protein sequence analyses for the identification of domains for structure-function determinations to genetic perturbations. The recent explosion in genomics/proteomics and informatics is beginning to contribute in a major way to design and interpretation of cxpcrimenb based on sequence similarities, structural and functional domains. Further, these areas arc expected to play signilicant roles in crossfertilization of concepts among major areas of technology and of hiological investigation.
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Cheney, Richard E. "Myosin V." In Guidebook to the Cytoskeletal and Motor Proteins, 440–44. Oxford University PressOxford, 1999. http://dx.doi.org/10.1093/oso/9780198599579.003.00133.

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Abstract The class V myosins are an abundant and widely distributed group of motor proteins implicated in organelle trafficking and membrane targeting. They appear to form two-headed dimers that are joined by a stalk to a globular tail domain of unknown function. A combination of biochemical and molecular genetic studies has led to the hypothesis that class V myosins may function as actin-based motors for organelle transport.
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Gu, Anyu, Chikezie O. Madu, and Yi Lu. "Perspective Chapter: Role of Cancer-Associated Fibroblasts in Oncogenesis." In Tumor Microenvironment - New Insights [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.108832.

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The tumor microenvironment consists of multiple types of cells, including endothelial cells, pericytes, neutrophil macrophage mast cells, lymphatic cells, basement membrane extracellular matrix, as well as fibroblasts. Fibroblasts populations found in cancers, also known as cancer-associated fibroblasts, have been implicated in the initiation, progression, and metastasis of tumors. This chapter will focus on the roles of cancer-associated fibroblasts in the progression of cancer and the studies of use of cancer-associated fibroblasts as a therapeutic target for cancer intervention.
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Hasson, Tama. "Myosin VII." In Guidebook to the Cytoskeletal and Motor Proteins, 448–50. Oxford University PressOxford, 1999. http://dx.doi.org/10.1093/oso/9780198599579.003.00135.

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Abstract Myosin Vila is an unconventional myosin implicated in deafness syndromes in mouse and human. It has a conserved N-terminal motor domain, a light chain-binding neck region, which may associate with five calmodulin light chains, and a C-terminal tail comprised of coiled coil and a direct repeat of two motifs termed the Myth domain and the talin-like domain. These structural domains target myosin Vila to the actin cytoskeleton and to membrane domains in inner ear hair cells, retina, and testis.
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Conference papers on the topic "Membrane implicite"

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Gordnier, Raymond E., and Peter J. Attar. "Implicit LES Simulations for an Aspect Ratio Two Flexible Membrane Wing." In ASME-JSME-KSME 2011 Joint Fluids Engineering Conference. ASMEDC, 2011. http://dx.doi.org/10.1115/ajk2011-08008.

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Development of an aeroelastic solver with application to flexible membrane wings for micro air vehicle applications is presented. A high-order (up to 6th order) Navier-Stokes solver is coupled with a geometrically nonlinear p-version Reissner-Mindlin finite element plate model to simulate the highly flexible elastic membrane. An implicit LES approach is employed to compute the mixed laminar/transitional/turbulent flowfields present for the low Reynolds number flows associated with micro air vehicles. Intitial computations for a baseline rigid membrane wing are presented to understand the complex vortex dynamics associated with these flows before proceeding with the more challenging flexible cases.
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Gordnier, Raymond, and Peter Attar. "Implicit LES Simulations of a Low Reynolds Number Flexible Membrane Wing Airfoil." In 47th AIAA Aerospace Sciences Meeting including The New Horizons Forum and Aerospace Exposition. Reston, Virigina: American Institute of Aeronautics and Astronautics, 2009. http://dx.doi.org/10.2514/6.2009-579.

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Eaton, Brandon, Michael R. von Spakovsky, Michael W. Ellis, Douglas J. Nelson, Benoit Olsommer, and Nathan Siegel. "One-Dimensional, Transient Model of Heat, Mass, and Charge Transfer in a Proton Exchange Membrane." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/aes-23652.

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Abstract A transient, one-dimensional, model of the membrane of a proton exchange membrane fuel cell is presented. The role of the membrane is to transport protons from the anode to cathode of the fuel cell while preventing the transport of other reactants. The membrane is modeled assuming mono-phase, multi-species flow. For water transport, the principle driving forces modeled are a convective force, an osmotic force (i.e. diffusion), and an electric force. The first of these results from a pressure gradient, the second from a concentration gradient, and the third from the migration of protons from anode to cathode and their effect (drag) on the dipole water molecules. Equations are developed for the conservation of protons and water, the conservation of thermal energy, and the variation of proton potential within the membrane. The model is solved using a fully implicit finite difference approach. Results showing the effects of current density, pressure gradients, water and heat fluxes, and fuel cell start-up on water concentration, temperature, and proton potential across the membrane are presented.
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Li, He, and George Lykotrafitis. "Modeling Diffusion and Vesiculation in Defective Human Erythrocyte Membrane." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14203.

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The hemolytic disorders of hereditary spherocytosis (HS) and hereditary elliptocytosis (HE) affect the lives of millions of individuals worldwide. In HS and HE, connections in the vertical and horizontal directions between components of the RBC membrane (see Fig. 1(a)), are disrupted due to defective proteins, leading to loss of the structural and functional integrity of the membrane (1–2). Moreover, disruptions of either the vertical interactions or horizontal interactions affect the lateral diffusivity of the mobile band 3 proteins, as the motion of band 3 in the RBC membrane is confined by the cytoskeleton (3). Although a number of coarse-grained molecular dynamics (CGMD) RBC membrane models have been developed in the past two decades, very few RBC membrane models have been used to study the disordered band 3 diffusion and membrane vesiculation in HS and HE. The implicit representations of either the lipid bilayer or the cytoskeleton in these membrane models limit their applications in the membrane instability problems in HS and HE. In this extended abstract, we develop a two-component CGMD human RBC membrane model that explicitly comprises both the lipid bilayer and the cytoskeleton. In this way, the interactions between the cytoskeleton and the proteins embedded in the lipid bilayer can be simulated. The proposed model allows us to measure the band 3 lateral mobility and simulate the process of membrane vesiculation in the membrane with protein defects.
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Gorski, J., L. Van Hove, F. Vanlangendonck, M. A. Boogaerts, R. L. Verwilghen, and J. Vermylen. "PLATELET MEMBRANE GLYCOPROTEINS ABNORMALITIES IN PATIENTS WITH ACUTE LEUKEMIAS AND MALIGNANT LYMPHOMAS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643201.

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Membrane glycoproteins are implicated in platelet functions.In myeloproliferative disorders some of the platelet functions are known to be perturbated and an abnormal glycoproteins pattern was demonstrated ear-lier.In this study flow cytometry analysis of human platelet membrane glycoproteins IIa and IIIa in patients with acute leukemias and malignant lymphomas has been performed using monoclonal antibodies against these glycoproteins.A reduction in number of glycoproteins receptors on platelet membrane was demonstrated in patients with acute leukemias and malignant lymphomas in comparison with platelets of healthy donors.In patients with leukemias the positive correlation of percentage of platelets recovered in various density receptor regions to bleeding time and negative correlation to platelet number for both glycoproteins have been found.The study demonstrated that flow cytometry can be a useful method of analysis of platelet membrane glycoproteins, and that the patients with acute leukemias and malignant lymphomas have the number of glycoproteins reduced.
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Morss, Alisa, Michael Jonas, and Elazer R. Edelman. "Elevated Basement Membrane Fibroblast Growth Factor-2 Protects Endothelial Cells in High Glucose." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176187.

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Vascular disease is the primary cause of morbidity and mortality in diabetics. Diabetic vascular disease is disseminated and includes renal capillary hypertrophy, reduced wound repair, impaired angiogenesis, and rapid and excessive hyperplasia after endovascular intervention [1, 2]. No single biochemical aberration unifies the diffuse nature of diabetic vascular disease. Hyperglycemia has been implicated, and yet glucose effects persist long after restoration of euglycemia. It is possible that acute fluctuations in glucose concentration have prolonged cell and tissue effects.
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Gordnier, Raymond E., and Peter J. Attar. "Impact of Flexibility on the Aerodynamics of an Aspect Ratio Two Membrane Wing." In ASME 2012 Fluids Engineering Division Summer Meeting collocated with the ASME 2012 Heat Transfer Summer Conference and the ASME 2012 10th International Conference on Nanochannels, Microchannels, and Minichannels. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/fedsm2012-72296.

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Development of an aeroelastic solver with application to flexible membrane wings for micro air vehicles is presented. A high-order (up to 6th order) Navier-Stokes solver is coupled with a geometrically nonlinear p-version Reissner-Mindlin finite element plate model to simulate the highly flexible elastic membrane. An implicit LES approach is employed to compute the mixed laminar/transitional/turbulent flowfields present for the low Reynolds number flows associated with micro air vehicles. Computations are performed for an aspect ratio two membrane wing at angles of attack α = 10°, 16° and 23° for a Reynolds number, Re = 24,300. Comparisons of the computational results with experimental PIV and surface deflection measurements demonstrated reasonable agreement. Reduced separation and enhanced lift are obtained due to favorable interactions between the flexible membrane wing and the unsteady flow over the wing. The impact of flexibility on the aerodynamic performance comes primarily from the development of mean camber with some further effects arising from the interaction between the dynamic motion of the membrane and the unsteady flowfield above. At lower angles of attack this lift enhancement comes at the cost of reduced L/D. The nose-down pitching moment increases with flexibility at the lowest angle of attack but is reduced for the higher two angles of attack. These results suggest that membrane flexibility might provide a means to reduce the impact of strong gust encounter by maintaining lift and reducing the effect of the gust on pitching moment.
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Asijee, G. M., T. Bruin, A. Sturk, J. E. ten Cate, and L. Muszbek. "VINCULIN ISOFORMS IN HUMAN BLOOD PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643902.

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In several cells vinculin has been implicated in the interaction between the cytoskeleton and the outer ceil membrane. We have recently demonstrated that vinculin becomes associated with the Triton X-100 insoluble cytoskeleton of blood platelets upon thrombin-induced activation (Asijee et al, Exp Cell Res, 1987, in press). In the present study we demonstrate by SDS-PAGE and immunoblotting that vinculin is also present in the membrane skeleton of both non-activated and activated human blood platelets. The membrane skeleton was prepared by the method of Fox (J Clin Invest, 1985: 76, 1673), and platelets were stimulated 5 min at 37 °c with 0.1 U/ml thrombin. The association was specifically inhibited by DNase I-induced depolymerization of the actin filaments.Protein analysis by the O’Farrell technique (first dimension IEF, second dimension SDS-PAGE) and subsequent immunoblotting demonstrated purified vinculin to consist of 4 major isoforms (pI 6.8 - 7.2). These isoforms differed in subcellular distribution. Upon thrombin-induced platelet activation, cytoskeletal vinculin consisted of the 2 most acidic isoforms, and cytoplasmic vinculin of 2 more basic isoforms. The membrane skeleton-associated vinculin contained all 4 isoforms.We conclude that: 1. vinculin is a component of the membrane skeleton of both non-activated and activated human blood platelets, 2. similar to chicken gizzard smooth muscle cells, human blood platelet vinculin consists of several isoforms with differing subcellular distribution.
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Ball, J., M. Greaves, C. Jackson, J. Peel, and F. E. Preston. "DN-9693: A PHOSPHODIESTERASE INHIBITOR WITH A PLATELET MEMBRANE EFFECT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643583.

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We have examined the effect of DN-9693 (piperidinyl - imidazo - quinazoline: Daiichi Seiyaku, Japan) a water soluble phosphodiesterase inhibitor on platelet aggregation, secretion and thromboxane B2 (TXB2) production. In platelet rich plasma and at concentrations of 2uM and 5uM the drug significantly inhibited aggregation induced by adenosine diphosphate, collagen and sodium arachidonate. TXB2 production and release of adenosine tri-phosphate and 14C 5-hydroxytryptamine were also significantly inhibited by the drug. Cyclic adenosine mono-phosphate accumulation was enhanced. Inhibition of ristocetin induced platelet agglutination was an unexpected finding and further experiments were undertaken to explore this. These suggested no specific effect against a plasma factor (von Willebrand factor) and reduced expression of the platelet membrane glycoprotein Ib was implicated. To investigate this further we examined the effect of DN-9693 on the binding of a monoclonal antibody (McAb) to platelet membrane glycoprotein lb (AN51). This was assessed by a FACS IV flow cytofluorimeter utilising a goat anti-mouse fluorescein isothiocyanate (FITC) labelled secondary antibody. Similar experiments were also performed with McAbs to the membrane glycoprotein complex IIb/IIIa (M148) and also to glycoprotein IIIa (C17). In platelet rich plasma, at concentrations which have been shown to inhibit aggregation, DN-9693 significantly reduced the mean fluorescence intensity of the cells coated with McAb AN51 in a dose related manner. This strongly suggested a drug effect against the glycoprotein Ib receptor site. Also, the drug appeared to enhance the binding of McAb C17 to glycoprotein IIIa. This study indicates that in addition to potent phosphodiesterase inhibitor activity, DN-9693 causes a platelet surface membrane change which is associated with reduced expression of membrane glycoprotein Ib.
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Giltay, J. C., O. C. Leeksma, A. E. G. Kr v. d. Borne, and J. A. van Mourik. "THE PLATELET ALLOANTIGEN Zwa (P1A1) IS EXPRESSED BY CULTURED ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642812.

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Zwa (P1A1) is a platelet specific alloantigen, located on glycoprotein (GP) IIIa, and is of pathogenic importance in alloimmunologic disorders such as neonatal alloimmune thrombocytopenia and post transfusion purpura. As endothelial cells synthesize a plasma membrane protein complex which is structurally closely related to the platelet membrane GP IIb/IIIa complex, we examined whether these cells also express Zwa. Employing a variety of immunochemical techniques, our studies show that endothelial cells indeed can express this antigen at the plasma membrane surface.We also compared the expression of Zwa on platelets, isolated from umbilical cord blood, with the expression of Zwa on cultured endothelial cells, isolated from the same umbilical cord, of a number of neonates. Both platelets and endothelial cells obtained from the same individual, either expressed Zwa (Zwa positive individuals) or lacked expression of Zwa (Zwa negative individuals). These findings strongly suggest that endothelial-and platelet Zwa are encoded by the same genes.Thus, Zwa is not exclusively expressed by platelets, also endothelial cells express this alloantigen.An important consequence could be, that in alloimmunologic disorders in which the Zwa antigen is implicated, not only the platelets, but also the vessel wall is involved.
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Reports on the topic "Membrane implicite"

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Chen, Junping, Zach Adam, and Arie Admon. The Role of FtsH11 Protease in Chloroplast Biogenesis and Maintenance at Elevated Temperatures in Model and Crop Plants. United States Department of Agriculture, May 2013. http://dx.doi.org/10.32747/2013.7699845.bard.

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specific objectives of this proposal were to: 1) determine the location, topology, and oligomerization of FtsH11 protease; 2) identify the substrate/s of FtsH11 and the downstream components involved in maintaining thermostability of chloroplasts; 3) identify new elements involved in FtsH11 protease regulatory network related to HT adaptation processes in chloroplast; 4) Study the role of FtsH11 homologs from crop species in HT tolerance. Background to the topic: HT-tolerant varieties that maintain high photosynthetic efficiency at HT, and cope better with daily and seasonal temperature fluctuations are in great need to alleviate the effect of global warming on food production. Photosynthesis is a very complex process requiring accurate coordination of many complex systems and constant adjustments to the changing environments. Proteolytic activities mediated by various proteases in chloroplast are essential part of this process and critical for maintaining normal chloroplast functions under HT. However, little is known about mechanisms that contribute to adaptation of photosynthetic processes to HT. Our study has shown that a chloroplast-targeted Arabidopsis FtsH11 protease plays an essential and specific role in maintaining thermostability of thylakoids and normal photosynthesis at moderate HT. We hypothesized that FtsH11 homologs recently identified in other plant species might have roles similarly to that of AtFtsH1. Thus, dissecting the underlying mechanisms of FtsH11 in the adaptation mechanisms in chloroplasts to HT stress and other elements involved will aid our effort to produce more agricultural products in less favorable environments. Major conclusions, solutions, achievements - Identified the chloroplast inner envelope membrane localization of FtsH11. - Revealed a specific association of FtsH11 with the a and b subunits of CPN60. - Identified the involvement of ARC6, a protein coordinates chloroplast division machineries in plants, in FtsH11 mediated HT adaptation process in chloroplast. -Reveal possible association of a polyribonucleotide nucleotidyltransferase (cpPNPase), coded by At3G03710, with FtsH11 mediated HT adaptation process in chloroplast. - Mapped 4 additional loci in FtsH11 mediated HT adaptation network in chloroplast. - Demonstrated importance of the proteolytic activity of FtsH11 for thermotolerance, in addition to the ATPase activity. - Demonstrated a conserved role of plant FtsH11 proteases in chloroplast biogenesis and in maintaining structural and functional thermostability of chloroplast at elevated temperatures. Implications, both scientific and agricultural:Three different components interacting with FtsH11 were identified during the course of this study. At present, it is not known whether these proteins are directly involved in FtsH11mediated thermotolerance network in chloroplast and/or how these elements are interrelated. Studies aiming to connect the dot among biological functions of these networks are underway in both labs. Nevertheless, in bacteria where it was first studied, FtsH functions in heat shock response by regulating transcription level of σ32, a heat chock factor regulates HSPsexpression. FtsH also involves in control of biosynthesis of membrane components and quality control of membrane proteins etc. In plants, both Arc 6 and CPN60 identified in this study are essential in chloroplast division and developments as mutation of either one impairs chloroplast division in Arabidopsis. The facts that we have found the specific association of both α and β CPN60 with FtsH11 protein biochemically, the suppression/ enhancement of ftsh11 thermosensitive phenotype by arc6 /pnp allele genetically, implicate inter-connection of these networks via FtsH11 mediated network(s) in regulating the dynamic adaptation processes of chloroplast to temperature increases at transcriptional, translational and post-translational levels. The conserved role of FtsH11 proteases in maintaining thermostability of chloroplast at HT demonstrated here provides a foundation for improving crop photosynthetic performance at high temperatures.
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Christopher, David A., and Avihai Danon. Plant Adaptation to Light Stress: Genetic Regulatory Mechanisms. United States Department of Agriculture, May 2004. http://dx.doi.org/10.32747/2004.7586534.bard.

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Original Objectives: 1. Purify and biochemically characterize RB60 orthologs in higher plant chloroplasts; 2. Clone the gene(s) encoding plant RB60 orthologs and determine their structure and expression; 3. Manipulate the expression of RB60; 4. Assay the effects of altered RB60 expression on thylakoid biogenesis and photosynthetic function in plants exposed to different light conditions. In addition, we also examined the gene structure and expression of RB60 orthologs in the non-vascular plant, Physcomitrella patens and cloned the poly(A)-binding protein orthologue (43 kDa RB47-like protein). This protein is believed to a partner that interacts with RB60 to bind to the psbA5' UTR. Thus, to obtain a comprehensive view of RB60 function requires analysis of its biochemical partners such as RB43. Background & Achievements: High levels of sunlight reduce photosynthesis in plants by damaging the photo system II reaction center (PSII) subunits, such as D1 (encoded by the chloroplast tpsbAgene). When the rate of D1 synthesis is less than the rate of photo damage, photo inhibition occurs and plant growth is decreased. Plants use light-activated translation and enhanced psbAmRNA stability to maintain D1 synthesis and replace the photo damaged 01. Despite the importance to photosynthetic capacity, these mechanisms are poorly understood in plants. One intriguing model derived from the algal chloroplast system, Chlamydomonas, implicates the role of three proteins (RB60, RB47, RB38) that bind to the psbAmRNA 5' untranslated leader (5' UTR) in the light to activate translation or enhance mRNA stability. RB60 is the key enzyme, protein D1sulfide isomerase (Pill), that regulates the psbA-RN :Binding proteins (RB's) by way of light-mediated redox potentials generated by the photosystems. However, proteins with these functions have not been described from higher plants. We provided compelling evidence for the existence of RB60, RB47 and RB38 orthologs in the vascular plant, Arabidopsis. Using gel mobility shift, Rnase protection and UV-crosslinking assays, we have shown that a dithiol redox mechanism which resembles a Pill (RB60) activity regulates the interaction of 43- and 30-kDa proteins with a thermolabile stem-loop in the 5' UTR of the psbAmRNA from Arabidopsis. We discovered, in Arabidopsis, the PD1 gene family consists of II members that differ in polypeptide length from 361 to 566 amino acids, presence of signal peptides, KDEL motifs, and the number and positions of thioredoxin domains. PD1's catalyze the reversible formation an disomerization of disulfide bonds necessary for the proper folding, assembly, activity, and secretion of numerous enzymes and structural proteins. PD1's have also evolved novel cellular redox functions, as single enzymes and as subunits of protein complexes in organelles. We provide evidence that at least one Pill is localized to the chloroplast. We have used PDI-specific polyclonal and monoclonal antisera to characterize the PD1 (55 kDa) in the chloroplast that is unevenly distributed between the stroma and pellet (containing membranes, DNA, polysomes, starch), being three-fold more abundant in the pellet phase. PD1-55 levels increase with light intensity and it assembles into a high molecular weight complex of ~230 kDa as determined on native blue gels. In vitro translation of all 11 different Pill's followed by microsomal membrane processing reactions were used to differentiate among PD1's localized in the endoplasmic reticulum or other organelles. These results will provide.1e insights into redox regulatory mechanisms involved in adaptation of the photosynthetic apparatus to light stress. Elucidating the genetic mechanisms and factors regulating chloroplast photosynthetic genes is important for developing strategies to improve photosynthetic efficiency, crop productivity and adaptation to high light environments.
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Wisniewski, Michael, Samir Droby, John Norelli, Dov Prusky, and Vera Hershkovitz. Genetic and transcriptomic analysis of postharvest decay resistance in Malus sieversii and the identification of pathogenicity effectors in Penicillium expansum. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7597928.bard.

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Use of Lqh2 mutants (produced at TAU) and rNav1.2a mutants (produced at the US side) for identifying receptor site-3: Based on the fact that binding of scorpion alpha-toxins is voltage-dependent, which suggests toxin binding at the mobile voltage-sensing region, we analyzed which of the toxin bioactive domains (Core-domain or NC-domain) interacts with the DIV Gating-module of rNav1.2a. This analysis was based on the assumption that the dissociation of toxin mutants upon depolarization would vary from that of the unmodified toxin should the substitutions affect a site of interaction with the channel Gating-module. Using a series of toxin mutants (mutations at both domains) and two channel mutants that were shown to reduce the sensitivity to scorpion alpha-toxins, and by comparison of depolarization-driven dissociation of Lqh2 derivatives off their binding site at rNav1.2a mutant channels we found that the toxin Core-domain interacts with the Gating-module of DIV. Details of the experiments and results appear in Guret al (2011). Mapping receptor site 3 at Nav1.2a by extensive channel mutagenesis (Seattle): Since previous studies with photoaffinity labeling and antibody mapping implicated domains I and IV in scorpion alpha-toxin binding, Nav1.2 channel mutants containing substitutions at these extracellular regions were expressed and tested for receptor function by whole-cell voltage clamp. Of a large number of channel mutants, T1560A, F1610A, and E1613A in domain IV had ~5.9-, ~10.7-, and ~3.9-fold lower affinities for the scorpion toxin Lqh2, respectively, and mutant E1613R had 73-fold lower affinity. Toxin dissociation was accelerated by depolarization for both wild-type and mutants, and the rates of dissociation were also increased by mutations T1560A, F1610A and E1613A. In contrast, association rates for these three mutant channels at negative membrane potentials were not significantly changed and were not voltage-dependent. These results indicated that Thr1560 in the S1-S2 loop, Phe1610 in the S3 segment, and Glu1613 in the S3-S4 loop in domain IV participate in toxin binding. T393A in the SS2-S6 loop in domain I also showed a ~3.4-fold lower affinity for Lqh2, indicating that this extracellular loop may form a secondary component of the toxin binding site. Analysis with the Rosetta-Membrane algorithm revealed a three-dimensional model of Lqh2 binding to the voltage sensor in a resting state. In this model, amino acid residues in an extracellular cleft formed by the S1-S2 and S3-S4 loops in domain IV that are important for toxin binding interact with amino acid residues on two faces of the wedge-shaped Lqh2 molecule that are important for toxin action. The conserved gating charges in the S4 transmembrane segment are in an inward position and likely form ion pairs with negatively charged amino acid residues in the S2 and S3 segments (Wang et al 2011; Gurevitz 2012; Gurevitzet al 2013).
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