Academic literature on the topic 'Actin cytoskeleton modulation'
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Journal articles on the topic "Actin cytoskeleton modulation"
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Uray, Karen, Evelin Major, and Beata Lontay. "MicroRNA Regulatory Pathways in the Control of the Actin–Myosin Cytoskeleton." Cells 9, no. 7 (July 9, 2020): 1649. http://dx.doi.org/10.3390/cells9071649.
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MicroRNAs (miRNAs) are key modulators of post-transcriptional gene regulation in a plethora of processes, including actin–myosin cytoskeleton dynamics. Recent evidence points to the widespread effects of miRNAs on actin–myosin cytoskeleton dynamics, either directly on the expression of actin and myosin genes or indirectly on the diverse signaling cascades modulating cytoskeletal arrangement. Furthermore, studies from various human models indicate that miRNAs contribute to the development of various human disorders. The potentially huge impact of miRNA-based mechanisms on cytoskeletal elements is just starting to be recognized. In this review, we summarize recent knowledge about the importance of microRNA modulation of the actin–myosin cytoskeleton affecting physiological processes, including cardiovascular function, hematopoiesis, podocyte physiology, and osteogenesis.
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Ganusova, Elena E., Laura N. Ozolins, Srishti Bhagat, Gary P. Newnam, Renee D. Wegrzyn, Michael Y. Sherman, and Yury O. Chernoff. "Modulation of Prion Formation, Aggregation, and Toxicity by the Actin Cytoskeleton in Yeast." Molecular and Cellular Biology 26, no. 2 (January 15, 2006): 617–29. http://dx.doi.org/10.1128/mcb.26.2.617-629.2006.
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ABSTRACT Self-perpetuating protein aggregates transmit prion diseases in mammals and heritable traits in yeast. De novo prion formation can be induced by transient overproduction of the corresponding prion-forming protein or its prion domain. Here, we demonstrate that the yeast prion protein Sup35 interacts with various proteins of the actin cortical cytoskeleton that are involved in endocytosis. Sup35-derived aggregates, generated in the process of prion induction, are associated with the components of the endocytic/vacuolar pathway. Mutational alterations of the cortical actin cytoskeleton decrease aggregation of overproduced Sup35 and de novo prion induction and increase prion-related toxicity in yeast. Deletion of the gene coding for the actin assembly protein Sla2 is lethal in cells containing the prion isoforms of both Sup35 and Rnq1 proteins simultaneously. Our data are consistent with a model in which cytoskeletal structures provide a scaffold for generation of large aggregates, resembling mammalian aggresomes. These aggregates promote prion formation. Moreover, it appears that the actin cytoskeleton also plays a certain role in counteracting the toxicity of the overproduced potentially aggregating proteins.
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Morachevskaya, Elena A., and Anastasia V. Sudarikova. "Actin dynamics as critical ion channel regulator: ENaC and Piezo in focus." American Journal of Physiology-Cell Physiology 320, no. 5 (May 1, 2021): C696—C702. http://dx.doi.org/10.1152/ajpcell.00368.2020.
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Ion channels in plasma membrane play a principal role in different physiological processes, including cell volume regulation, signal transduction, and modulation of membrane potential in living cells. Actin-based cytoskeleton, which exists in a dynamic balance between monomeric and polymeric forms (globular and fibrillar actin), can be directly or indirectly involved in various cellular responses including modulation of ion channel activity. In this mini-review, we present an overview of the role of submembranous actin dynamics in the regulation of ion channels in excitable and nonexcitable cells. Special attention is focused on the important data about the involvement of actin assembly/disassembly and some actin-binding proteins in the control of the epithelial Na+ channel (ENaC) and mechanosensitive Piezo channels whose integral activity has a potential impact on membrane transport and multiple coupled cellular reactions. Growing evidence suggests that actin elements of the cytoskeleton can represent a “converging point” of various signaling pathways modulating the activity of ion transport proteins in cell membranes.
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Gokina, Natalia I., and George Osol. "Actin cytoskeletal modulation of pressure-induced depolarization and Ca2+ influx in cerebral arteries." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 4 (April 1, 2002): H1410—H1420. http://dx.doi.org/10.1152/ajpheart.00441.2001.
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The objective of this study was to examine the role of the actin cytoskeleton in the development of pressure-induced membrane depolarization and Ca2+ influx underlying myogenic constriction in cerebral arteries. Elevating intraluminal pressure from 10 to 60 mmHg induced membrane depolarization, increased intracellular cytosolic Ca2+ concentration ([Ca2+]i) and elicited myogenic constriction in both intact and denuded rat posterior cerebral arteries. Pretreatment with cytochalasin D (5 μM) or latrunculin A (3 μM) abolished constriction but enhanced the [Ca2+]i response; similarly, acute application of cytochalasin D to vessels with tone, or in the presence of 60 mM K+, elicited relaxation accompanied by an increase in [Ca2+]i. The effects of cytochalasin D were inhibited by nifedipine (3 μM), demonstrating that actin cytoskeletal disruption augments Ca2+ influx through voltage-sensitive L-type Ca2+ channels. Finally, pressure-induced depolarization was enhanced in the presence of cytochalasin D, further substantiating a role for the actin cytoskeleton in the modulation of ion channel function. Together, these results implicate vascular smooth muscle actin cytoskeletal dynamics in the control of cerebral artery diameter through their influence on membrane potential as well as via a direct effect on L-type Ca2+ channels.
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Ebstrup, Malene Laage, Catarina Dias, Anne Sofie Busk Heitmann, Stine Lauritzen Sønder, and Jesper Nylandsted. "Actin Cytoskeletal Dynamics in Single-Cell Wound Repair." International Journal of Molecular Sciences 22, no. 19 (October 8, 2021): 10886. http://dx.doi.org/10.3390/ijms221910886.
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The plasma membrane protects the eukaryotic cell from its surroundings and is essential for cell viability; thus, it is crucial that membrane disruptions are repaired quickly to prevent immediate dyshomeostasis and cell death. Accordingly, cells have developed efficient repair mechanisms to rapidly reseal ruptures and reestablish membrane integrity. The cortical actin cytoskeleton plays an instrumental role in both plasma membrane resealing and restructuring in response to damage. Actin directly aids membrane repair or indirectly assists auxiliary repair mechanisms. Studies investigating single-cell wound repair have often focused on the recruitment and activation of specialized repair machinery, despite the undeniable need for rapid and dynamic cortical actin modulation; thus, the role of the cortical actin cytoskeleton during wound repair has received limited attention. This review aims to provide a comprehensive overview of membrane repair mechanisms directly or indirectly involving cortical actin cytoskeletal remodeling.
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Radhakrishnan, Girish K., and Gary A. Splitter. "Modulation of host microtubule dynamics by pathogenic bacteria." BioMolecular Concepts 3, no. 6 (December 1, 2012): 571–80. http://dx.doi.org/10.1515/bmc-2012-0030.
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AbstractThe eukaryotic cytoskeleton is a vulnerable target of many microbial pathogens during the course of infection. Rearrangements of host cytoskeleton benefit microbes in various stages of their infection cycle such as invasion, motility, and persistence. Bacterial pathogens deliver a number of effector proteins into host cells for modulating the dynamics of actin and microtubule cytoskeleton. Alteration of the actin cytoskeleton is generally achieved by bacterial effectors that target the small GTPases of the host. Modulation of microtubule dynamics involves direct interaction of effector proteins with the subunits of microtubules or recruiting cellular proteins that affect microtubule dynamics. This review will discuss effector proteins from animal and human bacterial pathogens that either destabilize or stabilize host microtubules to advance the infectious process. A compilation of these research findings will provide an overview of known and unknown strategies used by various bacterial effectors to modulate the host microtubule dynamics. The present review will undoubtedly help direct future research to determine the mechanisms of action of many bacterial effector proteins and contribute to understanding the survival strategies of diverse adherent and invasive bacterial pathogens.
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Danninger, C., and M. Gimona. "Live dynamics of GFP-calponin: isoform-specific modulation of the actin cytoskeleton and autoregulation by C-terminal sequences." Journal of Cell Science 113, no. 21 (November 1, 2000): 3725–36. http://dx.doi.org/10.1242/jcs.113.21.3725.
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The calponin family of F-actin-, tropomyosin- and calmodulin-binding proteins currently comprises three genetic variants. Their functional roles implicated from in vitro studies include the regulation of actomyosin interactions in smooth muscle cells (h1 calponin), cytoskeletal organisation in non-muscle cells (h2 calponin) and the control of neurite outgrowth (acidic calponin). We have now investigated the effects of calponin (CaP) isoforms and their C-terminal deletion mutants on the actin cytoskeleton by time lapse video microscopy of GFP fusion proteins in living smooth muscle cells and fibroblasts. It is shown that h1 CaP associates with the actin stress fibers in the more central part of the cell, whereas h2 CaP localizes to the ends of stress fibres and in the motile lamellipodial protrusions of spreading cells. Cells expressing h2 CaP spread more efficiently than those expressing h1 CaP and expression of GFP h1 CaP resulted in reduced cell motility in wound healing experiments. Notably, expression of GFP h1 CaP, but not GFP h2 CaP, conferred increased resistance of the actin cytoskeleton to the actin polymerization antagonists cytochalasin B and latrunculin B, as well as to the protein kinase inhibitors H7-dihydrochloride and rho-kinase inhibitor Y-27632. These data point towards a dual role of CaP in the stabilization and regulation of the actin cytoskeleton in vivo. Deletion studies further identify an autoregulatory role for the unique C-terminal tail sequences in the respective CaP isoforms.
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Chifflet, Silvia, and Julio A. Hernández. "The Plasma Membrane Potential and the Organization of the Actin Cytoskeleton of Epithelial Cells." International Journal of Cell Biology 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/121424.
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The establishment and maintenance of the polarized epithelial phenotype require a characteristic organization of the cytoskeletal components. There are many cellular effectors involved in the regulation of the cytoskeleton of epithelial cells. Recently, modifications in the plasma membrane potential (PMP) have been suggested to participate in the modulation of the cytoskeletal organization of epithelia. Here, we review evidence showing that changes in the PMP of diverse epithelial cells promote characteristic modifications in the cytoskeletal organization, with a focus on the actin cytoskeleton. The molecular paths mediating these effects may include voltage-sensitive integral membrane proteins and/or peripheral proteins sensitive to surface potentials. The voltage dependence of the cytoskeletal organization seems to have implications in several physiological processes, including epithelial wound healing and apoptosis.
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Müller, Thorsten, Caoimhin G. Concannon, Manus W. Ward, Ciara M. Walsh, Anca L. Tirniceriu, Florian Tribl, Donat Kögel, Jochen H. M. Prehn, and Rupert Egensperger. "Modulation of Gene Expression and Cytoskeletal Dynamics by the Amyloid Precursor Protein Intracellular Domain (AICD)." Molecular Biology of the Cell 18, no. 1 (January 2007): 201–10. http://dx.doi.org/10.1091/mbc.e06-04-0283.
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Amyloidogenic processing of the amyloid precursor protein (APP) results in the generation of β-amyloid, the main constituent of Alzheimer plaques, and the APP intracellular domain (AICD). Recently, it has been demonstrated that AICD has transactivation potential; however, the targets of AICD-dependent gene regulation and hence the physiological role of AICD remain largely unknown. We analyzed transcriptome changes during AICD-dependent gene regulation by using a human neural cell culture system inducible for expression of AICD, its coactivator FE65, or the combination of both. Induction of AICD was associated with increased expression of genes with known function in the organization and dynamics of the actin cytoskeleton, including α2-Actin and Transgelin (SM22). AICD target genes were also found to be differentially regulated in the frontal cortex of Alzheimer's disease patients compared with controls as well as in AICD/FE65 transiently transfected murine cortical neurons. Confocal image analysis of neural cells and cortical neurons expressing both AICD and FE65 confirmed pronounced changes in the organization of the actin cytoskeleton, including the destabilization of actin fibers and clumping of actin at the sites of cellular outgrowth. Our data point to a role of AICD in developmental and injury-related cytoskeletal dynamics in the nervous system.
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Pagliaro, L., and D. L. Taylor. "2-Deoxyglucose and cytochalasin D modulate aldolase mobility in living 3T3 cells." Journal of Cell Biology 118, no. 4 (August 15, 1992): 859–63. http://dx.doi.org/10.1083/jcb.118.4.859.
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Approximately 23% of the glycolytic enzyme aldolase in the perinuclear region of Swiss 3T3 cells is immobile as measured by FRAP. Previous studies suggest that the immobile fraction may be associated with the actin cytoskeleton (Pagliaro, L. and D. L. Taylor. 1988. J. Cell Biol. 107:981-991), and it has been proposed that the association of some glycolytic enzymes with the cytoskeleton could have functional significance, perhaps involving a fundamental relationship between glycolysis, cytoplasmic organization, and cell motility. We have tested the effect of a key glycolytic inhibitor and an actin cytoskeletal modulator on the mobility of aldolase in living cells directly, using fluorescent analog cytochemistry and FRAP. We report here that the competitive hexokinase inhibitor 2-deoxyglucose releases the bound fraction of aldolase in 3T3 cells within 10 min, and that this process is reversible upon washout of the inhibitor. A similar result is produced with the actin-binding agent, cytochalasin D. These results are consistent with models in which glycolytic enzymes are not exclusively diffusion-limited, soluble proteins, but may exist partially in the solid phase of cytoplasm. Such organization has significant implications for both the modulation of cytoplasmic structure and for cellular metabolism.
Dissertations / Theses on the topic "Actin cytoskeleton modulation"
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Caution, Kyle J. "Legionella pneumophila and caspases: modulation of the actin cytoskeleton." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1449147516.
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Ip, Wency Wan Sze. "Collagen triple helix repeat containing 1 increases melanoma cell migration, adhesion and survival through modulation of the actin cytoskeleton." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/8929.
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Background: Collagen Triple Helix Repeat Containing 1 (CTHRC1) is a recently discovered extracellular protein that can bind and activate Wnt signaling pathway. In previous gene expression profiling experiments, it was found to be aberrantly upregulated in metastatic melanoma and its expression level was correlated with melanoma progression and metastasis.
Objective: The purpose of this study is to understand the functional impact of CTHRC1 on cancer using melanoma cell lines as a model.
Experimental Methods: We transfected two melanoma cell lines, MMAN and MMRU, with plasmid vectors to create stable clones with high and low CTHRC1 expression to study the functional effects of CTHRC1 in vitro. Using these two cell lines, we assayed for melanoma migration, adhesion and survival using scratch wound healing assay, attachment assay and cell cycle analysis, respectively. In addition, the cells were stained for F-actin with AlexaFluor 594 labeled phalloidin to observe for actin organization.
Results: Using these two pairs of cell lines, we have found that CTHRC1 expression increased melanoma cell migration, enhanced melanoma cell adhesion to both tissue culture plastic and matrigel, and protected melanoma cells from serum deprivation induced apoptosis. Further, it was demonstrated that CTHRC1’s pro-survival effect was dependent on cell adhesion, as the protection effect was lost when melanoma cells were cultured in suspension. Immunofluorescent staining of F-actin revealed that CTHRC1 expression increased the formation structures such as focal complexes, lamellipodia and filopodia.
Discussion: The increased formation of the adhesion structures may be the key to CTHRC1 associated cell migration, adhesion and survival. These structures are likely regulated by the Rho family of proteins that act downstream of the Wnt/PCP pathway, with which CTHRC1 has been previously demonstrated to be involved as a co-receptor.
Conclusion: Results from this study suggest that CTHRC1 expression promotes cellular behaviours associated with tumour metastases. Therefore, inhibition of this protein may be able to block melanoma metastasis and may have value as a potential therapeutic.
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Del, Río Iñiguez Iratxe. "Intracellular vesicle traffic, immunological synapse and T cell activation. Modulation by Human Immunodeficiency Virus type 1 Rac1-Rab11-FIP3 regulatory hub coordinates vesicle traffic with actin remodeling and T cell activation Rab11-FIP3 regulation of Lck endosomal traffic controls TCR signal transduction." Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS561.
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La formation et les fonctions de la synapse immunologique sont le résultat d’un processus de polarisation cellulaire du lymphocyte T. Ce processus dépend de l’action coordonnée du cytosquelette d’actine et de microtubules, et du trafic vésiculaire intracellulaire. Le récepteur T ainsi que des protéines impliquées dans sa signalisation intracellulaire sont associés à la membrane plasmique et à des compartiments vésiculaires endosomiaux, et circulent en continu entre ces deux localisations. Je montre dans cette thèse que la tyrosine kinase Lck et la GTPase Rac1 sont associés aux endosomes exprimant Rab11. Leur localisation intracellulaire et leurs fonctions dans la formation de la synapse immune, l’activation des lymphocytes T et les remaniements du cytosquelette d’actine dépendent de Rab11 et de son effecteur FIP3. Je me suis intéressée également à la protéine Nef du VIH-1, importante pour la réplication du virus et pour la pathogénèse associée au SIDA. Nef affecte le trafic endosomial, l’activation et le cytosquelette des lymphocytes T infectés. Nous avons mis en évidence que Nef concentre de façon spécifique des formes actives des protéines de signalisation dans le compartiment endosomial Rab11. Ceci conduit à une activation de certains gènes associés aux réponses précoces et tardives des lymphocytes T. Ce processus est contrecarré par la déplétion de FIP3, qui disperse le compartiment concentrant ces protéines. En conclusion, nos données révèlent de nouveaux mécanismes impliquant le trafic vésiculaire intracellulaire dans le contrôle de l’activation et du cytosquelette des lymphocytes T et leur détournement par le virus du SIDAThe immunological synapse is the result of a T cell polarization process that depends on the orchestrated action of the actin and microtubule cytoskeleton and of intracellular vesicle traffic. The T cell antigen receptor (TCR) and various components of its proximal signaling machinery are associated with the plasma membrane and vesicular endosomal compartments, continuously trafficking between the two locations. I show in this thesis that the subcellular localization and function of the tyrosine kinase Lck and the actin cytoskeleton regulator Rac1, depend on the Rab11 recycling endosomal compartment, and more in particular, on the Rab11 effector FIP3. Importantly, FIP3-dependent Lck and Rac1 localization controls early TCR signaling, intracellular calcium concentration, IL-2 gene expression and morphological events, like T cell spreading and synapse symmetry. Moreover, I investigated how the HIV-1 accessory protein Nef, which is crucial for virus replication in vivo and AIDS pathogenesis, specifically hijacks several active signaling molecules, concentrating them in the Rab11 endosomal compartment, and concomitantly inducing the upregulation of some early and late T cell activation genes. Interestingly, dispersion of this concentration by depleting Rab11-FIP3, counteracted Nef-induced gene expression upregulation. Therefore, by modifying their endosomal traffic, Nef hijacks signaling and actin cytoskeleton regulators to dually modulate their functional outputs. In conclusion, our data shed new light into the molecular mechanisms orchestrating endosomal traffic with T cell activation and cytoskeletal rearrangements, and their subversion during HIV-1 infection
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(5930000), Yao Liu. "MODULATION OF HOST ACTIN CYTOSKELETON BY A LEGIONELLA PNEUMOPHILA EFFECTOR." Thesis, 2019.
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Legionella
pneumophila, the etiological
agent of Legionnaires’ disease, replicates intracellularly in protozoan and
human hosts. Successful colonization and replication of this pathogen in host
cells requires the Dot/Icm type IVB secretion system, which translocates over 330
effector proteins into the host cell to modulate various cellular processes. In
this study, we identified RavK (Lpg0969) as a Dot/Icm substrate that targets
the host cytoskeleton and reduces actin filament abundance in mammalian cells
upon ectopic expression. RavK harbors an H95EXXH99 (x, any amino acid)
motif associated with diverse metalloproteases, which is essential for the
inhibition of yeast growth and for the induction of cell rounding in HEK293T
cells. We demonstrate that the actin is the cellular target of RavK and that
this effector cleaves actin at a site between residues Thr351 and Phe352. Importantly,
RavK-mediated actin cleavage occurs during L.
pneumophila infection. Cleavage by RavK abolishes the ability of actin to
form polymers. Furthermore, an F352A mutation renders actin resistant to
RavK-mediated cleavage; expression of the mutant in mammalian cells suppresses
the cell rounding phenotype caused by RavK, further establishing that actin is
the physiological substrate of RavK. Thus, L. pneumophila exploits
components of the host cytoskeleton by multiple effectors with distinct
mechanisms, highlighting the importance of modulating cellular processes
governed by the actin cytoskeleton in the intracellular life cycle of this
pathogen.
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Zheng, Guifu. "Modulation of the actin cytoskeleton in the folliculo-stellate cell line TtT/GF by serum factors." Thèse, 2005. http://hdl.handle.net/1866/15739.
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Saal, Kim Ann. "Modulation of the ROCK pathway in models of Parkinson´s disease." Doctoral thesis, 2015. http://hdl.handle.net/11858/00-1735-0000-0028-8665-9.
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Bivona, Dario Antonio. "Modulation allostérique de la fonction des récepteurs FP et PAF." Thèse, 2009. http://hdl.handle.net/1866/3215.
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Les récepteurs couplés aux protéines-G (RCPGs) constituent la première étape d’une série de cascades signalétiques menant à la régulation d’une multitude de processus physiologiques. Dans le modèle classique connu, la liaison du ligand induit un changement de conformation du récepteur qui mène à sa forme active. Une fois activés, les RCPGs vont réguler l’activité d’une protéine membranaire cible qui peut être tant une enzyme qu’un canal ionique. L’interaction entre le récepteur et la cible nécessite l’intermédiaire d’une protéine hétérotrimérique appelée « protéine G », qui est activée pour favoriser l’échange du GDP (guanosine diphosphate) pour un GTP (guanosine triphosphate) et assurer la transduction du signal du récepteur à l’effecteur. Les mécanismes moléculaires menant à l’activation des effecteurs spécifiques via l’activation des RCPGs par les protéines G hétérotrimériques sont encore plutôt méconnus.
Dans notre étude nous nous sommes intéressés aux récepteurs FP et PAF, à leurs ligands naturels, la PGF2α et le Carbamyl-PAF respectivement, et à des ligands à action antagoniste sur ces récepteurs. Des ligands considérés comme agonistes, sont des molécules qui interagissent avec le récepteur et induisent les mêmes effets que le ligand naturel. Les antagonistes, par contre, sont des molécules qui interagissent avec le récepteur et bloquent l’action du ligand naturel en prévenant le changement conformationnel du complexe, et ils peuvent avoir une action compétitive ou non-compétitive.
Nous avons étudié aussi des ligands orthostériques et allostériques du récepteur FP des prostaglandines et du récepteur PAF. Un ligand orthostérique peut se comporter comme agoniste ou antagoniste en se fixant au site de liaison du ligand (agoniste) naturel. Un ligand allostérique est un agoniste ou antagoniste se fixant à un site autre que celui du ligand naturel entraînant un changement de conformation ayant pour conséquence soit une augmentation (effecteur positif), soit une diminution (effecteur négatif) de l'activité du ligand naturel.G protein coupled receptors (GPCRs) are involved in the first step of most signalling pathways that regulate a variety of physiological events. The classical view of GPCR activation suggests that ligand binding to the inactive receptor will trigger a conformational change leading to an active conformation of the receptor. The GPCRs activated regulate the activity of a target membrane protein which can then activate other signalling proteins such as enzymes and ionic channels. The interaction between the receptor and the target requires an intermediary, in this case an heterotrimeric protein named « G protein », which is activated in order to facilitate the exchange of GDP (guanosine diphospate) for a GTP (guanosine triphosphate) and allow the transduction of the signal from the receptor to the effector. The molecular mechanisms leading to the activation of signalling effectors via the activation of GPCRs by its heterotrimeric G protein have not yet been well characterized. We focused our study on two GPCRs, the FP and PAF receptors, their natural ligands, PGF2α and Carbamyl-PAF respectively, and their antagonist ligands. Agonists are ligands that bind to the target receptor and trigger the same effects as the natural ligand of the GPCR. In contrast with agonists, antagonist ligands are molecules that prevent the effects of the natural ligand by keeping the GPCR from changing to its active conformation and can be competitive or non-competitive. We have also studied orthosteric and allosteric ligands of the FP and PAF receptors. An orthosteric ligand binds the same site as the natural ligand of the receptor and can act as an agonist or an antagonist. In the contrary, an allosteric ligand will rather have a different binding site then the natural ligand (agonist) and can positively or negatively modulate the effects of the natural ligand.
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Zrieq, Rafat [Verfasser]. "The dual function of the chlamydia pneumoniae Cpn0572 protein in modulating the host actin cytoskeleton / vorgelegt von Rafat Zrieq." 2010. http://d-nb.info/1000217000/34.
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Li, Xiaodong. "Modulation of epidermal growth factor receptor protein tyrosine kinase activity influence of the receptor carboxy terminus and the cytoskeletal protein actin /." 1997. http://catalog.hathitrust.org/api/volumes/oclc/40058799.html.
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"The transforming Rho family GTPase, Wrch-1, regulates epithelial cell morphogenesis through modulating cell junctions and actin cytoskeletal dynamics." THE UNIVERSITY OF NORTH CAROLINA AT CHAPEL HILL, 2008. http://pqdtopen.proquest.com/#viewpdf?dispub=3304310.
Full textBook chapters on the topic "Actin cytoskeleton modulation"
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Okeyo, Kennedy Omondi, Hiromi Miyoshi, and Taiji Adachi. "Design Concept of Topographical and Mechanical Properties of Synthetic Extracellular Matrix to Control Cell Functions and Fates Through Actin Cytoskeletal Modulation." In Frontiers of Biomechanics, 159–86. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-55163-8_11.
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Galan, Jorge E., and Yixin Fu. "Modulation of actin cytoskeleton by Salmonella GTPase activating protein SptP." In Methods in Enzymology, 496–504. Elsevier, 2000. http://dx.doi.org/10.1016/s0076-6879(00)25469-4.
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Andersson, Tommy, Carina Hellberg, Ragnhild Löfgren, Janet Ng-Sikorski, Anita Sjölander, Maria Fällman, and Eva Särndahl. "Dynamic modulations and functional importance of the actin network in human neutrophils." In Cytoskeleton in Specialized Tissues and in Pathological States, 43–69. Elsevier, 1996. http://dx.doi.org/10.1016/s1874-6020(96)80004-8.
Full textConference papers on the topic "Actin cytoskeleton modulation"
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Dangaria, Jhanvi H., and Peter J. Butler. "Interaction of Shear Stress, Myosin II, and Actin in Dynamic Modulation of Endothelial Cell Microrheology." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192947.
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The endothelial cell (EC) cytoskeleton mediates several biological functions such as adhesion, migration, phagocytosis, cell division, and mechanosensitivity. These functions are carried out in part through dynamic cytoskeletal polymerization, modulation of crosslinking, and development of tension between intracellular organelles and the extracellular matrix via focal adhesion plaques. One important component of the cytoskeleton is actin which polymerizes into filaments and is thought to be prestressed by virtue of crosslinking proteins such as α-actinin, filamin and myosin II molecular motors. Additionally, actomyosin interaction has been hypothesized to act as a stress dissipation mechanism by virtue of dynamic crossbridging which facilitates actin diffusion through the polymer network of the cytoplasm (Humphrey et al., 2002).
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Imaoka, T., and T. Asaji. "FUNCTION OF PLATELET 47K PHOSPHOPROTEIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644634.
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Secretion of platelet granule constituents is closely associated with the phosphorylation of a cytosol polypeptide that we called P47 of Mr 47,000 (Imaoka, T. and Haslam, R.J., J. Biol. Chem. 258, 11404, 1983), by protein kinase C. Since the identity and function remains to be known, we purified protein kinase C, unphosphorylated and phosphorylated P47 to homogeneity from human platelets. Then precise phosphorylation reaction of P47 in vitro and a biological function of P47 were studied. Protein kinase C catalysed the phosphorylation reaction of P47 protein, platelet myosin light chain, histone III-S with Km of 0.8±0.2, 4.2±0.5, 4.7±0.7μM, and Vmax of 0.312, 0.189, 0.874 nmole/min/mg, respectively. Some data previously obtained in this laboratory and others utilizing histone III-S as substrate are consistent with the synergistic effect by diacylglycerol (DG) in the presence of Ca++ , phosphatidylserine (PS). Using P47 as substrate, the enzyme required both Ca++ and PS, but not DG for activity. 125I labelled unphosphorylated P47 had an ability to bind with platelet membrane fraction in the presense of phosphatidylserine. Effect of diacylglycerol was inhibitory in this PS dependent P47 binding with membrane. Unphosphorylated P47 had a inhibitory activity in platelet actin polymerization. Molar ratio to inhibit actin polymerization was 1:8(P47:actin). These activities were Ca++ independent. Purified 32P-labelled P47 lost the binding ability with membrane, also the inhibitory activity in actin polymerization.Therefore, we propose the hypothesis that unphosphorylated P47 may loosely bind with the inside of plasma membrane of platelet and inhibit actin polymerization as a modulator, when stimulated, protein Kinase C rapidly phosphorylate P47 and induce the activation of cytoskeletal network and subsequently release reaction. On the other hand, whether DG in fact can act as a second messenger remain uncertain, (supported by MESC of Japan)
Reports on the topic "Actin cytoskeleton modulation"
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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.
Full textAbstract:
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.