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Relevant bibliographies by topics / Cytoskeleton model

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Academic literature on the topic 'Cytoskeleton model'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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Journal articles on the topic "Cytoskeleton model"

1

Durand-Smet, Pauline, Tamsin A. Spelman, Elliot M. Meyerowitz, and Henrik Jönsson. "Cytoskeletal organization in isolated plant cells under geometry control." Proceedings of the National Academy of Sciences 117, no. 29 (2020): 17399–408. http://dx.doi.org/10.1073/pnas.2003184117.

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The cytoskeleton plays a key role in establishing robust cell shape. In animals, it is well established that cell shape can also influence cytoskeletal organization. Cytoskeletal proteins are well conserved between animal and plant kingdoms; nevertheless, because plant cells exhibit major structural differences to animal cells, the question arises whether the plant cytoskeleton also responds to geometrical cues. Recent numerical simulations predicted that a geometry-based rule is sufficient to explain the microtubule (MT) organization observed in cells. Due to their high flexural rigidity and

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Akram, Zain, Ishtiaq Ahmed, Heike Mack, et al. "Yeast as a Model to Understand Actin-Mediated Cellular Functions in Mammals—Illustrated with Four Actin Cytoskeleton Proteins." Cells 9, no. 3 (2020): 672. http://dx.doi.org/10.3390/cells9030672.

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The budding yeast Saccharomyces cerevisiae has an actin cytoskeleton that comprises a set of protein components analogous to those found in the actin cytoskeletons of higher eukaryotes. Furthermore, the actin cytoskeletons of S. cerevisiae and of higher eukaryotes have some similar physiological roles. The genetic tractability of budding yeast and the availability of a stable haploid cell type facilitates the application of molecular genetic approaches to assign functions to the various actin cytoskeleton components. This has provided information that is in general complementary to that provid

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Wang, Jizeng, and Long Li. "Coupled elasticity–diffusion model for the effects of cytoskeleton deformation on cellular uptake of cylindrical nanoparticles." Journal of The Royal Society Interface 12, no. 102 (2015): 20141023. http://dx.doi.org/10.1098/rsif.2014.1023.

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Molecular dynamic simulations and experiments have recently demonstrated how cylindrical nanoparticles (CNPs) with large aspect ratios penetrate animal cells and inevitably deform cytoskeletons. Thus, a coupled elasticity–diffusion model was adopted to elucidate this interesting biological phenomenon by considering the effects of elastic deformations of cytoskeleton and membrane, ligand–receptor binding and receptor diffusion. The mechanism by which the binding energy drives the CNPs with different orientations to enter host cells was explored. This mechanism involved overcoming the resistance

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Ning, Liang, Hani Y. Suleiman, and Jeffrey H. Miner. "Synaptopodin deficiency exacerbates kidney disease in a mouse model of Alport syndrome." American Journal of Physiology-Renal Physiology 321, no. 1 (2021): F12—F25. http://dx.doi.org/10.1152/ajprenal.00035.2021.

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Alport syndrome (AS) is a hereditary disease of the glomerular basement with hematuria and proteinuria. Podocytes eventually exhibit foot process effacement, indicating actin cytoskeletal changes. To investigate how cytoskeletal changes impact podocytes, we generated Alport mice lacking synaptopodin, an actin-binding protein in foot processes. Analysis showed a more rapid disease progression, demonstrating that synaptopodin is protective. This suggests that the actin cytoskeleton is a target for therapy in AS and perhaps other glomerular diseases.

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REDONDO, Pedro C., Ana I. LAJAS, Ginés M. SALIDO, Antonio GONZALEZ, Juan A. ROSADO, and José A. PARIENTE. "Evidence for secretion-like coupling involving pp60src in the activation and maintenance of store-mediated Ca2+ entry in mouse pancreatic acinar cells." Biochemical Journal 370, no. 1 (2003): 255–63. http://dx.doi.org/10.1042/bj20021505.

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Store-mediated Ca2+ entry (SMCE) is one of the main pathways for Ca2+ influx in non-excitable cells. Recent studies favour a secretion-like coupling mechanism to explain SMCE, where Ca2+ entry is mediated by an interaction of the endoplasmic reticulum (ER) with the plasma membrane (PM) and is modulated by the actin cytoskeleton. To explore this possibility further we have now investigated the role of the actin cytoskeleton in the activation and maintenance of SMCE in pancreatic acinar cells, a more specialized secretory cell type which might be an ideal cellular model to investigate further th

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Jean, Ronald P., Christopher S. Chen, and Alexander A. Spector. "Finite-Element Analysis of the Adhesion-Cytoskeleton-Nucleus Mechanotransduction Pathway During Endothelial Cell Rounding: Axisymmetric Model." Journal of Biomechanical Engineering 127, no. 4 (2005): 594–600. http://dx.doi.org/10.1115/1.1933997.

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Endothelial cells possess a mechanical network connecting adhesions on the basal surface, the cytoskeleton, and the nucleus. Transmission of force at adhesions via this pathway can deform the nucleus, ultimately resulting in an alteration of gene expression and other cellular changes (mechanotransduction). Previously, we measured cell adhesion area and apparent nuclear stretch during endothelial cell rounding. Here, we reconstruct the stress map of the nucleus from the observed strains using finite-element modeling. To simulate the disruption of adhesions, we prescribe displacement boundary co

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Symington, Alison L., Selma Zimmerman, and A. M. Zimmerman. "The influence of hydrostatic pressure on the distribution of histone mRNA in HeLa cells." Biochemistry and Cell Biology 71, no. 3-4 (1993): 150–55. http://dx.doi.org/10.1139/o93-024.

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Hydrostatic pressure and HeLa S3 cells were used (as a model system) to investigate the relationship of the cytoskeleton and histone gene expression. Exposure of HeLa S3 cells to hydrostatic pressure of 1000 – 10 000 psi (6.89 × 103 – 6.89 × 104 kPa) disrupts the cytoskeleton and reduces H1 and core histone mRNA and actin mRNA levels as determined by hybridization to specific DNA probes. Soluble and insoluble cell fractions were isolated from HeLa cells after lysis in Triton X-100 buffered with PIPES and being subjected to low-speed centrifugation. The insoluble fraction was designated the cyt

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Clark, J. I., J. M. Clark, L. L. David, and H. Matsushima. "Lens cytoskeleton and transparency: A model." Eye 13, no. 3 (1999): 417–24. http://dx.doi.org/10.1038/eye.1999.116.

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Liu, Fei, Dan Wu, Xiaoyong Wu, and Ken Chen. "Analyses of the cell mechanical damage during microinjection." Soft Matter 11, no. 7 (2015): 1434–42. http://dx.doi.org/10.1039/c4sm02773f.

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The structure of the cell mechanical model. The cell model contains the membrane networks, the internal cytoskeleton, ACPs, motors and their functions, including the binding/unbinding and the folding/unfolding of the proteins, the polymerization/depolymerization of cytoskeletal filaments, and the walk of motors.

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Dufort, Paul A., and Charles J. Lumsden. "Cellular automaton model of the actin cytoskeleton." Cell Motility and the Cytoskeleton 25, no. 1 (1993): 87–104. http://dx.doi.org/10.1002/cm.970250110.

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Dissertations / Theses on the topic "Cytoskeleton model"

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Lane, D. C. "A mathematical investigation of a mechanochemical model for the cytoskeleton." Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379843.

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Dewolf, Christine Elizabeth. "Properties of model biological membranes." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244082.

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Muddana, Hari Shankar. "Integrated biomechanical model of cells embedded in extracellular matrix." [College Station, Tex. : Texas A&M University, 2006. http://hdl.handle.net/1969.1/ETD-TAMU-1074.

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Monreal, Gretel. "Ventricular Remodeling in a Large Animal Model of Heart Failure." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1210007937.

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Lewis, Sara Ann. "Functions of Drosophila Pak (p21-activated kinase) in Morphogenesis: A Mechanistic Model based on Cellular, Molecular, and Genetic Studies." Diss., The University of Arizona, 2015. http://hdl.handle.net/10150/594389.

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Intellectual disability (ID) is a common phenotype of brain-development disorders and is heterogeneous in etiology with numerous genetic causes. PAK3 is one gene with multiple mutations causing ID. Affected individuals have microcephaly, and other brain-structure defects have been reported. Additionally, PAK3 is in a genetic network with eighteen other genes whose mutations cause ID, suggesting the molecular mechanisms by which PAK3 regulates of cognitive function may be shared by other genetic ID disorders. Studies in rodent models have shown that the orthologs of PAK3 are important for regul

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Bauer, David. "Využití tensegritních struktur pro modelování mechanického chování hladkých svalových buněk." Master's thesis, Vysoké učení technické v Brně. Fakulta strojního inženýrství, 2011. http://www.nusl.cz/ntk/nusl-229836.

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The master’s thesis deals with the computational modelling of the mechanical testing of isolated smooth muscle cells. The main aims are to create computational model of a cell, to simulate single-axis tensile test and to modify the model so that the model reflects real mechanical response. The model of the cell includes cytoplasm, nucleus, cell membrane and cytoskeleton which is modelled as a tensegrite structure. On this model the tensile test was simulated in case of the cell with cytoskeleton and the cell with distributed the cytoskeleton. Force-elongation curves, which were obtained from t

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Yadav, Preeti [Verfasser], and Michael [Gutachter] Sendtner. "Studying Neuronal Cytoskeleton Defects and Synaptic Defects in Mouse Model of Amyotrophic Lateral Sclerosis and Spinal Muscular Atrophy / Preeti Yadav. Gutachter: Michael Sendtner." Würzburg : Universität Würzburg, 2016. http://d-nb.info/1113535075/34.

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Kovari, Daniel T. "Investigations of the spreading and closure mechanisms of phagocytosis in J774a.1 macrophages." Diss., Georgia Institute of Technology, 2015. http://hdl.handle.net/1853/54882.

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Phagocytosis is the process by which cells engulf foreign bodies. It is the hallmark behavior of white blood cells, being the process through which those cells ingest and degrade pathogens and debris. To date a large amount of research has focused on documenting the existence and role of biochemical components involved with phagocytosis. Scores of signaling molecules have been implicated in the complex signal cascade which drives the process. These molecules are small (typically no larger than 5 nanometers) and operate in a crowded, chemically “noisy,” environment, yet they coordinate the cell

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Ganay, Thibault. "Caractérisation du modèle murin de la Neuropathie à Axones Géants : rôle de la gigaxonine dans la survie neuronale et l'organisation du cytosquelette." Thesis, Aix-Marseille 2, 2011. http://www.theses.fr/2011AIX22075.

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La Neuropathie à Axones Géants (NAG) est une maladie neurodégénérative rare et fatale caractérisée par une détérioration du système nerveux central et périphérique, impliquant les fonctions motrices et sensorielles. La détérioration massive du système nerveux est accompagnée d'une désorganisation générale des Filaments Intermédiaires ce qui la différencie de nombreuses maladies neurodégénératives où seuls les neurofilaments(NFs) sont affectés. La protéine déficiente, la gigaxonine, est la sous-unité d'une ubiquitine ligase E3, responsable de la reconnaissance spécifique des substrats MAP1B, MA

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Henninger, Nils. "Inhibiting Axon Degeneration in a Mouse Model of Acute Brain Injury Through Deletion of Sarm1." eScholarship@UMMS, 2017. http://escholarship.umassmed.edu/gsbs_diss/900.

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Traumatic brain injury (TBI) is a leading cause of disability worldwide. Annually, 150 to 200/1,000,000 people become disabled as a result of brain trauma. Axonal degeneration is a critical, early event following TBI of all severities but whether axon degeneration is a driver of TBI remains unclear. Molecular pathways underlying the pathology of TBI have not been defined and there is no efficacious treatment for TBI. Despite this significant societal impact, surprisingly little is known about the molecular mechanisms that actively drive axon degeneration in any context and particularly followi

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Books on the topic "Cytoskeleton model"

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Hameroff, Stuart R. Ultimate computing: Biomolecular consciousness and nanotechnology. North-Holland, 1987.

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Ultimatecomputing: Biomolecular consciousness and nano technology. North-Holland, 1987.

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Mofrad, Mohammad R. K., and Roger D. Kamm. Cytoskeletal Mechanics: Models and Measurements in Cell Mechanics. Cambridge University Press, 2011.

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Cytoskeletal Mechanics: Models and Measurements (Cambridge Texts in Biomedical Engineering). Cambridge University Press, 2006.

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Read, Nick D. Fungal cell structure and organization. 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/9780198755388.003.0004.

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Human pathogenic fungi produce three basic ‘cell’ types: hyphae, yeast cells, and spores. The organization and subcellular structure of these different cell types and their modes of growth and formation are reviewed. Growth and form is the consequence of how new cell surface is formed. This is generated by the delivery of vesicles to the surface which provides new membrane and the enzymes for cell wall synthesis. To generate these various cell types, the pathway of vesicle secretion to the surface has to be carefully regulated. These vesicles have to be transported through the cell by the cyto

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Book chapters on the topic "Cytoskeleton model"

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Spira, Micha E., and Hadas Erez. "From an Axon into a Growth Cone After Axotomy: A Model for Cytoskeletal Dynamics." In The Cytoskeleton. Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-266-7_10.

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Santos, Luís Carlos, Emilia Laura Munteanu, and Nicolas Biais. "An In Vitro Model System to Test Mechano-microbiological Interactions Between Bacteria and Host Cells." In Cytoskeleton Methods and Protocols. Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3124-8_10.

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Reggio, Hubert, Daniel Louvard, and Evelyne Coudrier. "Membrane Cytoskeleton Interactions, A Model System : The Intestinal Microvilli." In Cellular and Molecular Control of Direct Cell Interactions. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-5092-7_18.

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Keković, G., D. Raković, M. V. Satarić, and Dj Koruga. "A Kink-Soliton Model of Charge Transport through Microtubular Cytoskeleton." In Materials Science Forum. Trans Tech Publications Ltd., 2005. http://dx.doi.org/10.4028/0-87849-971-7.507.

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Bretschneider, Till. "Reinforcement of Cytoskeleton-Matrix Bonds and Tensiotaxis: A Cell-Based Model." In Function and Regulation of Cellular Systems. Birkhäuser Basel, 2004. http://dx.doi.org/10.1007/978-3-0348-7895-1_28.

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Woolf, Nancy J., Avner Priel, and Jack A. Tuszynski. "The Cytoskeleton as a Nanoscale Information Processor: Electrical Properties and an Actin-Microtubule Network Model." In Nanoneuroscience. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03584-5_3.

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Hufnagel, Linda A. "The Cilioprotist Cytoskeleton, a Model for Understanding How Cell Architecture and Pattern Are Specified: Recent Discoveries from Ciliates and Comparable Model Systems." In Methods in Molecular Biology. Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1661-1_13.

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Lin, Shin, Mary A. Risinger, and James A. Butler. "A Model for Protein-Protein Interactions Involved in the Linkage of the Actin Cytoskeleton to Transmembrane Receptors for Extracellular Matrix Proteins." In Springer Series in Biophysics. Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73925-5_61.

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Lindemann, Charles B., and Kathleen A. Lesich. "Detergent-Extracted Models for the Study of Cilia or Flagella." In Cytoskeleton Methods and Protocols. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-376-3_19.

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Hackney, C. M., and D. N. Furness. "Observations on the Cytoskeleton and Related Structures of Mammalian Cochlear Hair Cells." In Cochlear Mechanisms: Structure, Function, and Models. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5640-0_2.

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Conference papers on the topic "Cytoskeleton model"

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Allen, Kathleen B., and Bradley Layton. "A Mechanical Model for Cytoskeleton and Membrane Interactions in Neuronal Growth Cones." In ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-42008.

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Revealing the molecular events of neuronal growth is critical to obtaining a deeper understanding of nervous system development, neural injury response, and neural tissue engineering. Central to this is the need to understand the mechanical interactions among the cytoskeleton and the cell membrane, and how these interactions affect the overall growth mechanics of neurons. Using ANSYS, the force produced by a cytoskeletal protein acting against a deformable membrane was modeled, and the deformation, stress, and strain were computed for the membrane. Parameters to represent the flexural rigiditi

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Coghlan, Karen M., Patrick McGarry, Mohammad R. K. Mofrad, and Peter E. McHugh. "Development of a Discrete Finite Element Cell Model." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176734.

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Computational models have proven useful in the study of cell mechanics and mechanotransduction. While most finite element (FE) models of cells are commonly described in terms of the laws of continuum mechanics, a model that can accurately represent the microstructure of the filamentous network of the cytoskeleton would be required to relate mechanics to biology at the microscale level. An alternative approach to a continuum is presented here, whereby the discrete nature of the cytoskeleton of the cell is emphasized and the known structural properties of the cytoskeleton of the cell are utilize

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Mehrbod, Mehrdad, and Mohammad R. K. Mofrad. "On the Mechanics of Microtubule Filaments." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53896.

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Quantitative understanding of cell mechanics has challenged biological scientists during the past couple of decades. one of the promising attempts towards mechanical modeling of the cytoskeleton has been the “tensegrity” cytoskeletal model, which simplifies the complex network of cytoskeletal filaments as a structure merely composed of compression-bearing elements (hinge-ended struts) and tensile members (cables). This discrete model can interestingly explain many experimental observations in cell mechanics. However, evidence suggests that the simplicity of this model may undermine the accurac

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Nakamura, Masanori, Ray Noguchi, Yoshihiro Ujihara, Hiroshi Miyazaki, and Shigeo Wada. "Proposal of a Mechano-Cell Model With Membrane, Cytoskeleton and Nucleus." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192527.

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The mechanical properties of cells have been of great interest to scientists from early studies which suggested that mechanical stress-induced alterations in cell shape and structure are critical for control of many cell functions. Although various loading tests of a cell have been designed to understand the cellular mechanical properties, the heterogeneous intracellular structure such as cytoskeletons brings about difficulties in interpreting experimental data.

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Lykotrafitis, George, and He Li. "Two-Component Coarse-Grain Model for Erythrocyte Membrane." In ASME 2011 International Mechanical Engineering Congress and Exposition. ASMEDC, 2011. http://dx.doi.org/10.1115/imece2011-62133.

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Biological membranes are vital components of living cells as they function to maintain the structural integrity of the cells. Red blood cell (RBC) membrane comprises the lipid bilayer and the cytoskeleton network. The lipid bilayer consists of phospholipids, integral membrane proteins, peripheral proteins and cholesterol. It behaves as a 2D fluid. The cytoskeleton is a network of spectrin tetramers linked at the actin junctions. It is connected to the lipid bilayer primarily via Band-3 and ankyrin proteins. In this paper, we introduce a coarse-grained model with high computational efficiency f

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Kaunas, Roland. "A Theoretical Model of Stretch-Induced Stress Fiber Remodeling." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193241.

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Cyclic stretching of endothelial cells (ECs), such as occurs in arteries during the cardiac cycle, induces ECs and their actin stress fibers to orient perpendicular to the direction of maximum stretch. This perpendicular alignment response is strengthened by increasing the magnitudes of stretch and cell contractility (1). The actin cytoskeleton is a dynamic structure that regulates cell shape changes and mechanical properties. It has been shown that actin stress fibers are ‘prestretched’ under normal, non-perturbed, conditions (2), consistent with the ideas of ‘prestress’ that have motivated t

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Han, Sangyoon J., and Nathan J. Sniadecki. "Traction Forces During Cell Migration Predicted by the Multiphysics Model." In ASME 2011 International Mechanical Engineering Congress and Exposition. ASMEDC, 2011. http://dx.doi.org/10.1115/imece2011-63843.

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Cells rely on traction forces in order to crawl across a substrate. These traction forces come from dynamic changes in focal adhesions, cytoskeletal structures, and chemical and mechanical signals from the extracellular matrix. Several computational models have been developed that help explain the trajectory or accumulation of cells during migration, but little attention has been placed on traction forces during this process. Here, we investigated the spatial and temporal dynamics of traction forces by using a multiphysics model that describes the cycle of steps for a migrating cell on an arra

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Pathak, Amit, Vikram S. Deshpande, Robert M. McMeeking, and Anthony G. Evans. "Simulation of the Coupling of Cell Contractility and Focal Adhesion Formation." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176108.

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The remodeling of the cytoskeleton and focal adhesion distributions for cells on substrates with micro-patterned ligand patches is investigated using a bio-chemo-mechanical model. All the cells have approximately the same area and we investigate the effect of ligand pattern shape on the cytoskeletal arrangements and focal adhesion distributions. The model for the cytoskeleton accounts for the dynamic rearrangement of the actin/myosin stress fibers and entails the highly non-linear interactions between signaling, the kinetics of tension-dependent stress-fiber formation/dissolution and stress de

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Vernerey, Franck J. "Biophysical Model of the Coupled Mechanisms of Cell Adhesion, Contraction and Spreading." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80309.

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Recent research has shown that cell spreading is highly dependent on the contractility of its cytoskeleton and the mechanical properties of its surrounding environment. This extended abstract introduces a mathematical formulation of cell spreading and contraction that couples the processes of stress fiber formation, protrusion growth through actin polymerization at the cell edge and dynamics of cross-membrane protein (integrins) enabling cell-substrate attachment. The evolving cell’s cytoskeleton is modeled as a mixture of fluid, proteins and filaments that can exchange mass and generate contr

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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

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