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Articoli di riviste sul tema "Cells Motility"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 28 luglio 2024

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1

ULFENDAHL, M. "Motility in auditory sensory cells." Acta Physiologica Scandinavica 130, no. 3 (July 1987): 521–27. http://dx.doi.org/10.1111/j.1748-1716.1987.tb08171.x.

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2

Pate, Jack L. "Gliding motility in procaryotic cells." Canadian Journal of Microbiology 34, no. 4 (April 1, 1988): 459–65. http://dx.doi.org/10.1139/m88-079.

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3

Recho, Pierre, Thibaut Putelat, and Lev Truskinovsky. "Mechanics of motility initiation and motility arrest in crawling cells." Journal of the Mechanics and Physics of Solids 84 (November 2015): 469–505. http://dx.doi.org/10.1016/j.jmps.2015.08.006.

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4

Schwab, Albrecht, Peter Hanley, Anke Fabian, and Christian Stock. "Potassium Channels Keep Mobile Cells on the Go." Physiology 23, no. 4 (August 2008): 212–20. http://dx.doi.org/10.1152/physiol.00003.2008.

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Cell motility is a prerequisite for the creation of new life, and it is required for maintaining the integrity of an organism. Under pathological conditions, “too much” motility may cause premature death. Studies over the past few years have revealed that ion channels are essential for cell motility. This review highlights the importance of K+ channels in regulating cell motility.

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Sarna, Sushil K. "Are interstitial cells of Cajal plurifunction cells in the gut?" American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 2 (February 2008): G372—G390. http://dx.doi.org/10.1152/ajpgi.00344.2007.

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The proposed functions of the interstitial cells of Cajal (ICC) are to 1) pace the slow waves and regulate their propagation, 2) mediate enteric neuronal signals to smooth muscle cells, and 3) act as mechanosensors. In addition, impairments of ICC have been implicated in diverse motility disorders. This review critically examines the available evidence for these roles and offers alternate explanations. This review suggests the following: 1) The ICC may not pace the slow waves or help in their propagation. Instead, they may help in maintaining the gradient of resting membrane potential (RMP) th

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6

Coelho Neto, José, and Oscar Nassif Mesquita. "Living cell motility." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 366, no. 1864 (August 2, 2007): 319–28. http://dx.doi.org/10.1098/rsta.2007.2091.

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The motility of living eukaryotic cells is a complex process driven mainly by polymerization and depolymerization of actin filaments underneath the plasmatic membrane (actin cytoskeleton). However, the exact mechanisms through which cells are able to control and employ ‘actin-generated’ mechanical forces, in order to change shape and move in a well-organized and coordinated way, are not quite established. Here, we summarize the experimental results obtained by our research group during recent years in studying the motion of living cells, such as macrophages and erythrocytes. By using our recen

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7

Sharma, Pooja, Van K. Lam, Christopher B. Raub, and Byung Min Chung. "Tracking Single Cells Motility on Different Substrates." Methods and Protocols 3, no. 3 (August 4, 2020): 56. http://dx.doi.org/10.3390/mps3030056.

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Motility is a key property of a cell, required for several physiological processes, including embryonic development, axon guidance, tissue regeneration, gastrulation, immune response, and cancer metastasis. Therefore, the ability to examine cell motility, especially at a single cell level, is important for understanding various biological processes. Several different assays are currently available to examine cell motility. However, studying cell motility at a single cell level can be costly and/or challenging. Here, we describe a method of tracking random cell motility on different substrates

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8

Melkonian, M. "Centrin-Mediated Motility: A Novel Cell Motility Mechanism in Eukaryotic Cells." Botanica Acta 102, no. 1 (February 1989): 3–4. http://dx.doi.org/10.1111/j.1438-8677.1989.tb00059.x.

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9

Xu, X., W. E. I. Li, G. Y. Huang, R. Meyer, T. Chen, Y. Luo, M. P. Thomas, G. L. Radice, and C. W. Lo. "Modulation of mouse neural crest cell motility by N-cadherin and connexin 43 gap junctions." Journal of Cell Biology 154, no. 1 (July 9, 2001): 217–30. http://dx.doi.org/10.1083/jcb.200105047.

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Connexin 43 (Cx43α1) gap junction has been shown to have an essential role in mediating functional coupling of neural crest cells and in modulating neural crest cell migration. Here, we showed that N-cadherin and wnt1 are required for efficient dye coupling but not for the expression of Cx43α1 gap junctions in neural crest cells. Cell motility was found to be altered in the N-cadherin–deficient neural crest cells, but the alterations were different from that elicited by Cx43α1 deficiency. In contrast, wnt1-deficient neural crest cells showed no discernible change in cell motility. These observ

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10

Shea, C., J. W. Nunley, and H. E. Smith-Somerville. "Variable expression of gliding and swimming motility in Deleya marina." Canadian Journal of Microbiology 37, no. 11 (November 1, 1991): 808–14. http://dx.doi.org/10.1139/m91-140.

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Surface-associated motility has been observed in the Deleya marina type strain ATCC 25374 (strain 219). Slime tracks and a complex growth pattern, characteristic of gliding motility, developed on semisolid marine-agar motility plates. Cell movement observed by light microscopy consisted of rapid glides and flips by single cells and groups of cells. Following the development of the gliding cell growth pattern, a subpopulation of swimming cells appeared. The variation in motility was random and reversible in subculture. Electron microscopic comparisons of cells of the two motility types showed t

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11

Jing, Zhixin, Zachary L. Benet, and David R. Fooksman. "Plasma cells Dynamics in the Bone Marrow Niche." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 11.02. http://dx.doi.org/10.4049/jimmunol.206.supp.11.02.

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Abstract Plasma cells (PCs) can become long-lived with age to maintain prophylactic antibody titer for decades in the bone marrow (BM) microenvironment that are enriched in supporting chemokines and pro-survival cytokines. It has been that PCs are sessile in the BM to receive various pro-survival signals, but how they access these signals in the dynamic BM microenvironment remains unknown. Here by establishing long-term intravital imaging of the mouse tibial BM, we show that PCs are overall motile within the BM parenchyma with unique intermittent and heterogenous motility over time. Their moti

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12

Panopoulos, Andreas, Michael Howell, Rati Fotedar, and Robert L. Margolis. "Glioblastoma motility occurs in the absence of actin polymer." Molecular Biology of the Cell 22, no. 13 (July 2011): 2212–20. http://dx.doi.org/10.1091/mbc.e10-10-0849.

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In fibroblasts and keratocytes, motility is actin dependent, while microtubules play a secondary role, providing directional guidance. We demonstrate here that the motility of glioblastoma cells is exceptional, in that it occurs in cells depleted of assembled actin. Cells display persistent motility in the presence of actin inhibitors at concentrations sufficient to fully disassemble actin. Such actin independent motility is characterized by the extension of cell protrusions containing abundant microtubule polymers. Strikingly, glioblastoma cells exhibit no motility in the presence of microtub

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13

Leo, Angela, Erica Pranzini, Laura Pietrovito, Elisa Pardella, Matteo Parri, Paolo Cirri, Gennaro Bruno, et al. "Claisened Hexafluoro Inhibits Metastatic Spreading of Amoeboid Melanoma Cells." Cancers 13, no. 14 (July 15, 2021): 3551. http://dx.doi.org/10.3390/cancers13143551.

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Metastatic melanoma is characterized by poor prognosis and a low free-survival rate. Thanks to their high plasticity, melanoma cells are able to migrate exploiting different cell motility strategies, such as the rounded/amoeboid-type motility and the elongated/mesenchymal-type motility. In particular, the amoeboid motility strongly contributes to the dissemination of highly invasive melanoma cells and no treatment targeting this process is currently available for clinical application. Here, we tested Claisened Hexafluoro as a novel inhibitor of the amoeboid motility. Reported data demonstrate

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14

Koga, Hiroaki. "Study of the motility and contractility of cultured brain-tumor cells." Journal of Neurosurgery 62, no. 6 (June 1985): 906–11. http://dx.doi.org/10.3171/jns.1985.62.6.0906.

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✓ The motility of cultured cells and contractility of their cytoplasmic microfilament system were studied in benign compared with malignant brain-tumor cells. Motility of cultured cells was continuously monitored in a perfusion chamber by a computerized microscope system equipped with an autotracking device. The contractility of the microfilament system was defined by the increase in cell motility when the cell was perfused with an antimicrofilamentous agent, cytochalasin B. The motility and contractility of malignant cells were greater than those of benign cells. The increased contractility o

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15

Miyawaki, Hironori, Shuzo Arishige, Masaya Takumida, and Yasuo Harada. "Motility of Isolated Vestibular Hair Cells." Equilibrium Research 51, Suppl-8 (1992): 95–99. http://dx.doi.org/10.3757/jser.51.suppl-8_95.

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16

Tanigawa, Tohru, Hironori Miyawaki, Masaya Takumida, Katsuhiro Hirakawa, Mamoru Suzuki, Naoki Hayashi, and Koji Yajin. "Motility of Isolated Vestibular Hair Cells." Equilibrium Research 55, no. 1 (1996): 20–25. http://dx.doi.org/10.3757/jser.55.20.

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17

Xu, Ying, Ming-Zheng Xie, and Guo-Gang Liang. "Enteric glial cells and gastrointestinal motility." World Chinese Journal of Digestology 26, no. 26 (September 18, 2018): 1537–44. http://dx.doi.org/10.11569/wcjd.v26.i26.1537.

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18

Suzuki, Y., A. Mobaraki, W. Al-Jahdari, Y. Yoshida, H. Sakurai, and T. Nakano. "In Vitro, Fractionation Enhances Cells Motility." International Journal of Radiation Oncology*Biology*Physics 72, no. 1 (September 2008): S719. http://dx.doi.org/10.1016/j.ijrobp.2008.06.1588.

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19

Yilmaz, Mahmut, and Gerhard Christofori. "Mechanisms of Motility in Metastasizing Cells." Molecular Cancer Research 8, no. 5 (May 2010): 629–42. http://dx.doi.org/10.1158/1541-7786.mcr-10-0139.

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20

Leonardy, Simone, Iryna Bulyha, and Lotte Søgaard-Andersen. "Reversing cells and oscillating motility proteins." Molecular BioSystems 4, no. 10 (2008): 1009. http://dx.doi.org/10.1039/b806640j.

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21

Hotta, Ryo, Dipa Natarajan, Alan J. Burns, and Nikhil Thapar. "Stem cells for GI motility disorders." Current Opinion in Pharmacology 11, no. 6 (December 2011): 617–23. http://dx.doi.org/10.1016/j.coph.2011.09.004.

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22

Chicoine, Michael R., and Daniel L. Silbergeld. "Assessment of brain tumor cell motility in vivo and in vitro." Journal of Neurosurgery 82, no. 4 (April 1995): 615–22. http://dx.doi.org/10.3171/jns.1995.82.4.0615.

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✓ Brain tumor dispersal far from bulk tumor contributes to and, in some instances, dominates disease progression. Three methods were used to characterize brain tumor cell motility in vivo and in vitro: 1) 2 weeks after implantation in rat cerebral cortex, single C6 cells labeled with a fluorescent tag had migrated to brain sites greater than 16 mm distant from bulk tumor; 2) time-lapse videomicroscopy of human brain tumor cells revealed motility of 12.5 µm/hr. Ruffling leading edges and pseudopod formation were most elaborate in more malignant cells; 3) an in vitro assay was devised to quantit

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23

De la Fuente, Ildefonso M., and José I. López. "Cell Motility and Cancer." Cancers 12, no. 8 (August 5, 2020): 2177. http://dx.doi.org/10.3390/cancers12082177.

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Cell migration is an essential systemic behavior, tightly regulated, of all living cells endowed with directional motility that is involved in the major developmental stages of all complex organisms such as morphogenesis, embryogenesis, organogenesis, adult tissue remodeling, wound healing, immunological cell activities, angiogenesis, tissue repair, cell differentiation, tissue regeneration as well as in a myriad of pathological conditions. However, how cells efficiently regulate their locomotion movements is still unclear. Since migration is also a crucial issue in cancer development, the goa

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24

Raje, Manoj, and Karvita B. Ahluwalia. "Motility of leukemic lymphocytes." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 3 (August 12, 1990): 368–69. http://dx.doi.org/10.1017/s0424820100159382.

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In Acute Lymphocytic Leukemia motility of lymphocytes is associated with dissemination of malignancy and establishment of metastatic foci. Normal and leukemic lymphocytes in circulation reach solid tissues where due to in adequate perfusion some cells get trapped among tissue spaces. Although normal lymphocytes reenter into circulation leukemic lymphocytes are thought to remain entrapped owing to reduced mobility and form secondary metastasis. Cell surface, transmembrane interactions, cytoskeleton and level of cell differentiation are implicated in lymphocyte mobility. An attempt has been made

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25

Dragoi, Ana-Maria, Arthur M. Talman, and Hervé Agaisse. "Bruton's Tyrosine Kinase Regulates Shigella flexneri Dissemination in HT-29 Intestinal Cells." Infection and Immunity 81, no. 2 (December 10, 2012): 598–607. http://dx.doi.org/10.1128/iai.00853-12.

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ABSTRACTShigella flexneriis a Gram-negative intracellular pathogen that infects the intestinal epithelium and utilizes actin-based motility to spread from cell to cell.S. flexneriactin-based motility has been characterized in various cell lines, but studies in intestinal cells are limited. Here we characterizedS. flexneriactin-based motility in HT-29 intestinal cells. In agreement with studies conducted in various cell lines, we showed thatS. flexnerirelies on neural Wiskott-Aldrich Syndrome protein (N-WASP) in HT-29 cells. We tested the potential role of various tyrosine kinases involved in N

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Wei, Xueming, and Wolfgang D. Bauer. "Starvation-Induced Changes in Motility, Chemotaxis, and Flagellation of Rhizobium meliloti." Applied and Environmental Microbiology 64, no. 5 (May 1, 1998): 1708–14. http://dx.doi.org/10.1128/aem.64.5.1708-1714.1998.

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ABSTRACT The changes in motility, chemotactic responsiveness, and flagellation of Rhizobium meliloti RMB7201, L5-30, and JJ1c10 were analyzed after transfer of the bacteria to buffer with no available C, N, or phosphate. Cells of these three strains remained viable for weeks after transfer to starvation buffer (SB) but lost all motility within just 8 to 72 h after transfer to SB. The rates of motility loss differed by severalfold among the strains. Each strain showed a transient, two- to sixfold increase in chemotactic responsiveness toward glutamine within a few hours after transfer to SB, ev

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27

Nieman, Marvin T., Ryan S. Prudoff, Keith R. Johnson, and Margaret J. Wheelock. "N-Cadherin Promotes Motility in Human Breast Cancer Cells Regardless of Their E-Cadherin Expression." Journal of Cell Biology 147, no. 3 (November 1, 1999): 631–44. http://dx.doi.org/10.1083/jcb.147.3.631.

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E-cadherin is a transmembrane glycoprotein that mediates calcium-dependent, homotypic cell–cell adhesion and plays a role in maintaining the normal phenotype of epithelial cells. Decreased expression of E-cadherin has been correlated with increased invasiveness of breast cancer. In other systems, inappropriate expression of a nonepithelial cadherin, such as N-cadherin, by an epithelial cell has been shown to downregulate E-cadherin expression and to contribute to a scattered phenotype. In this study, we explored the possibility that expression of nonepithelial cadherins may be correlated with

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Starruß, Jörn, Fernando Peruani, Vladimir Jakovljevic, Lotte Søgaard-Andersen, Andreas Deutsch, and Markus Bär. "Pattern-formation mechanisms in motility mutants of Myxococcus xanthus." Interface Focus 2, no. 6 (October 3, 2012): 774–85. http://dx.doi.org/10.1098/rsfs.2012.0034.

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Formation of spatial patterns of cells is a recurring theme in biology and often depends on regulated cell motility. Motility of the rod-shaped cells of the bacterium Myxococcus xanthus depends on two motility machineries, type IV pili (giving rise to S-motility) and the gliding motility apparatus (giving rise to A-motility). Cell motility is regulated by occasional reversals. Moving M. xanthus cells can organize into spreading colonies or spore-filled fruiting bodies, depending on their nutritional status. To ultimately understand these two pattern-formation processes and the contributions by

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Ashmore, Jonathan. "Cochlear Outer Hair Cell Motility." Physiological Reviews 88, no. 1 (January 2008): 173–210. http://dx.doi.org/10.1152/physrev.00044.2006.

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Normal hearing depends on sound amplification within the mammalian cochlea. The amplification, without which the auditory system is effectively deaf, can be traced to the correct functioning of a group of motile sensory hair cells, the outer hair cells of the cochlea. Acting like motor cells, outer hair cells produce forces that are driven by graded changes in membrane potential. The forces depend on the presence of a motor protein in the lateral membrane of the cells. This protein, known as prestin, is a member of a transporter superfamily SLC26. The functional and structural properties of pr

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L Zanella, Eraldo. "Melatonin Effect on Cryopreserved Sperm Cells of Crioulo Stallions." Open Access Journal of Veterinary Science & Research 5, no. 2 (2020): 1–8. http://dx.doi.org/10.23880/oajvsr-16000202.

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The freezing/thawing process of spermatozoa can cause cellular damage to the male gamete, decreasing the fertilization potential due to the increase in the production of reactive oxygen species (ROS). Melatonin is a potent endogenous antioxidant that protects the body against the damage caused by ROS. This study has evaluated different melatonin concentrations on the sperm viability of cryopreserved semen of Crioulo stallions. For that, three ejaculates were collected from five stallions diluted in a commercial extender followed by centrifugation and resuspension in a commercial freezing exten

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Ohnishi, Takanori, Norio Arita, Toru Hayakawa, Shuichi Izumoto, Takuyu Taki, and Hiroshi Yamamoto. "Motility factor produced by malignant glioma cells: role in tumor invasion." Journal of Neurosurgery 73, no. 6 (December 1990): 881–88. http://dx.doi.org/10.3171/jns.1990.73.6.0881.

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✓ To better understand the cellular mechanism of tumor invasion, the production of a cell motility-stimulating factor by malignant glioma cells was studied in vitro. Serum-free conditioned media from cultures of rat C6 and human T98G cell lines contained a factor that stimulated the locomotion of the producer cells. This factor was termed the “glioma-derived motility factor.” The glioma-derived motility factor is a heat-labile protein with a molecular weight greater than 10 kD and has relative stability to acid. The factor showed not only chemotactic activity but also chemokinetic (stimulated

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Chen, H., N. E. Paradies, M. Fedor-Chaiken, and R. Brackenbury. "E-cadherin mediates adhesion and suppresses cell motility via distinct mechanisms." Journal of Cell Science 110, no. 3 (February 1, 1997): 345–56. http://dx.doi.org/10.1242/jcs.110.3.345.

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Expression of the calcium-dependent adhesion molecule E-cadherin suppresses the invasion of cells in vitro, but the mechanism of this effect is unknown. To investigate this mechanism, we analyzed the effects of expressing E-cadherin in mouse L-cells and rat astrocyte-like WC5 cells. Increased cellular adhesion mediated by E-cadherin reduced invasion in WC5 cells and in some L-cells, but not in others. In all cases, suppression of invasion was correlated with decreased cell movement as assessed in an in vitro wound-filling assay and a transwell motility assay. To define the relationship between

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Ramonaite, Rima, Robertas Petrolis, Simge Unay, Gediminas Kiudelis, Jurgita Skieceviciene, Limas Kupcinskas, Mehmet Dincer Bilgin, and Algimantas Krisciukaitis. "Mathematical morphology-based imaging of gastrointestinal cancer cell motility and 5-aminolevulinic acid-induced fluorescence." Biomedical Engineering / Biomedizinische Technik 64, no. 6 (December 18, 2019): 711–20. http://dx.doi.org/10.1515/bmt-2018-0197.

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Abstract The aim of this study was the quantitative evaluation of gastrointestinal cancer cell motility and 5-aminolevulinic acid (5-ALA)-induced fluorescence in vitro using mathematical morphology and structural analysis methods. The results of our study showed that MKN28 cells derived from the lymph node have the highest motility compared with AGS or HCT116 cells derived from primary tumors. Regions of single cells were characterized as most moving, and “tightly packed” cell colonies as nearly immobile. We determined the reduction of cell motility in late passage compared to early passage. A

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Ouasti, Sihem, Alessandro Faroni, Paul J. Kingham, Matilde Ghibaudi, Adam J. Reid, and Nicola Tirelli. "Hyaluronic Acid (HA) Receptors and the Motility of Schwann Cell(-Like) Phenotypes." Cells 9, no. 6 (June 17, 2020): 1477. http://dx.doi.org/10.3390/cells9061477.

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The cluster of differentiation 44 (CD44) and the hyaluronan-mediated motility receptor (RHAMM), also known as CD168, are perhaps the most studied receptors for hyaluronic acid (HA); among their various functions, both are known to play a role in the motility of a number of cell types. In peripheral nerve regeneration, the stimulation of glial cell motility has potential to lead to better therapeutic outcomes, thus this study aimed to ascertain the presence of these receptors in Schwann cells (rat adult aSCs and neonatal nSCs) and to confirm their influence on motility. We included also a Schwa

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Braun, Timothy F., Manjeet K. Khubbar, Daad A. Saffarini, and Mark J. McBride. "Flavobacterium johnsoniae Gliding Motility Genes Identified by mariner Mutagenesis." Journal of Bacteriology 187, no. 20 (October 15, 2005): 6943–52. http://dx.doi.org/10.1128/jb.187.20.6943-6952.2005.

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ABSTRACT Cells of Flavobacterium johnsoniae glide rapidly over surfaces. The mechanism of F. johnsoniae gliding motility is not known. Eight gld genes required for gliding motility have been described. Disruption of any of these genes results in complete loss of gliding motility, deficiency in chitin utilization, and resistance to bacteriophages that infect wild-type cells. Two modified mariner transposons, HimarEm1 and HimarEm2, were constructed to allow the identification of additional motility genes. HimarEm1 and HimarEm2 each transposed in F. johnsoniae, and nonmotile mutants were identifi

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Hunnicutt, David W., and Mark J. McBride. "Cloning and Characterization of theFlavobacterium johnsoniae Gliding Motility GenesgldD and gldE." Journal of Bacteriology 183, no. 14 (July 15, 2001): 4167–75. http://dx.doi.org/10.1128/jb.183.14.4167-4175.2001.

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ABSTRACT Cells of Flavobacterium johnsoniae move over surfaces by a process known as gliding motility. The mechanism of this form of motility is not known. Cells of F. johnsoniaepropel latex spheres along their surfaces, which is thought to be a manifestation of the motility machinery. Three of the genes that are required for F. johnsoniae gliding motility,gldA, gldB, and ftsX, have recently been described. Tn4351 mutagenesis was used to identify another gene, gldD, that is needed for gliding. Tn4351-induced gldD mutants formed nonspreading colonies, and cells failed to glide. They also lacked

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Liu, Hsiao-Chuan, Eun Ji Gang, Hye Na Kim, Yongsheng Ruan, Heather Ogana, Zesheng Wan, Halvard Bönig, K. Kirk Shung, and Yong-Mi Kim. "Characterizing the Motility of Chemotherapeutics-Treated Acute Lymphoblastic Leukemia Cells by Time-Lapse Imaging." Cells 9, no. 6 (June 16, 2020): 1470. http://dx.doi.org/10.3390/cells9061470.

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Drug resistance is an obstacle in the therapy of acute lymphoblastic leukemia (ALL). Whether the physical properties such as the motility of the cells contribute to the survival of ALL cells after drug treatment has recently been of increasing interest, as they could potentially allow the metastasis of solid tumor cells and the migration of leukemia cells. We hypothesized that chemotherapeutic treatment may alter these physical cellular properties. To investigate the motility of chemotherapeutics-treated B-cell ALL (B-ALL) cells, patient-derived B-ALL cells were treated with chemotherapy for 7

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Hiraiwa, Takumi, Takahiro G. Yamada, Norihisa Miki, Akira Funahashi, and Noriko Hiroi. "Activation of cell migration via morphological changes in focal adhesions depends on shear stress in MYCN-amplified neuroblastoma cells." Journal of The Royal Society Interface 16, no. 152 (March 2019): 20180934. http://dx.doi.org/10.1098/rsif.2018.0934.

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Neuroblastoma is the most common solid tumour of childhood, and it metastasizes to distant organs. However, the mechanism of metastasis, which generally depends on the cell motility of the neuroblastoma, remains unclear. In many solid tumours, it has been reported that shear stress promotes metastasis. Here, we investigated the relationship between shear stress and cell motility in the MYCN-amplified human neuroblastoma cell line IMR32, using a microfluidic device. We confirmed that most of the cells migrated downstream, and cell motility increased dramatically when the cells were exposed to a

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Creppy, A., F. Plouraboué, O. Praud, and A. Viel. "Collective motility of sperm in confined cells." Computer Methods in Biomechanics and Biomedical Engineering 16, sup1 (July 2013): 11–12. http://dx.doi.org/10.1080/10255842.2013.815899.

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NAKAMURA, Kei-ichiro, Kiyomasa NISHII, and Yosaburo SHIBATA. "Networks of pacemaker cells for gastrointestinal motility." Folia Pharmacologica Japonica 123, no. 3 (2004): 134–40. http://dx.doi.org/10.1254/fpj.123.134.

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Small, J. V. "Microfilament-based motility in non-muscle cells." Current Opinion in Cell Biology 1, no. 1 (February 1989): 75–79. http://dx.doi.org/10.1016/s0955-0674(89)80040-7.

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42

Mandel, Savannah. "Collective motility of cancer cells in hyperthermia." Scilight 2020, no. 5 (January 31, 2020): 051106. http://dx.doi.org/10.1063/10.0000459.

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43

Rieken, S., J. Rieber, S. Brons, D. Habermehl, H. Rief, L. Orschiedt, K. Lindel, K. J. Weber, J. Debus, and S. E. Combs. "Radiation-induced motility alterations in medulloblastoma cells." Journal of Radiation Research 56, no. 3 (March 2, 2015): 430–36. http://dx.doi.org/10.1093/jrr/rru120.

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44

Chen, Xiangyu, and Susan A. Rotenberg. "PhosphoMARCKS drives motility of mouse melanoma cells." Cellular Signalling 22, no. 7 (July 2010): 1097–103. http://dx.doi.org/10.1016/j.cellsig.2010.03.003.

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45

Paksa, Azadeh, and Erez Raz. "Zebrafish germ cells: motility and guided migration." Current Opinion in Cell Biology 36 (October 2015): 80–85. http://dx.doi.org/10.1016/j.ceb.2015.07.007.

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46

Prag, Søren, Eugene A. Lepekhin, Kateryna Kolkova, Rasmus Hartmann-Petersen, Anna Kawa, Peter S. Walmod, Vadym Belman, et al. "NCAM regulates cell motility." Journal of Cell Science 115, no. 2 (January 15, 2002): 283–92. http://dx.doi.org/10.1242/jcs.115.2.283.

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Abstract (sommario):

Cell migration is required during development of the nervous system. The regulatory mechanisms for this process, however, are poorly elucidated. We show here that expression of or exposure to the neural cell adhesion molecule (NCAM) strongly affected the motile behaviour of glioma cells independently of homophilic NCAM interactions. Expression of the transmembrane 140 kDa isoform of NCAM (NCAM-140) caused a significant reduction in cellular motility, probably through interference with factors regulating cellular attachment, as NCAM-140-expressing cells exhibited a decreased attachment to a fib

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47

Spormann, Alfred M., and Dale Kaiser. "Gliding Mutants of Myxococcus xanthuswith High Reversal Frequencies and Small Displacements." Journal of Bacteriology 181, no. 8 (April 15, 1999): 2593–601. http://dx.doi.org/10.1128/jb.181.8.2593-2601.1999.

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Abstract (sommario):

ABSTRACT Myxococcus xanthus cells move on a solid surface by gliding motility. Several genes required for gliding motility have been identified, including those of the A- and S-motility systems as well as the mgl and frz genes. However, the cellular defects in gliding movement in many of these mutants were unknown. We conducted quantitative, high-resolution single-cell motility assays and found that mutants defective inmglAB or in cglB, an A-motility gene, reversed the direction of gliding at frequencies which were more than 1 order of magnitude higher than that of wild type cells (2.9 min−1fo

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48

Rezvan, Ali, Gabrielle Romain, Mohsen Fathi, Darren Heeke, Melisa Martinez-Paniagua, Xingyue An, Irfan N. Bandey, et al. "Multiomic dynamic single-cell profiling of CAR T cell populations associated with efficacy." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 54.18. http://dx.doi.org/10.4049/jimmunol.208.supp.54.18.

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Abstract (sommario):

Abstract T-cell therapy with specificity redirected through chimeric antigen receptors (CARs) has shown efficacy for the treatment of hematologic malignancies. Although treatment with CAR T cell can result in high response rates, the properties of the cells that comprise the cellular infusion product, associated with clinical benefit are incompletely understood. We utilized a suite of high-throughput single-cell assays including single-cell RNA-sequencing (scRNA-seq); confocal microscopy; and Timelapse Imaging Microscopy In Nanowell Grids (TIMING). TIMING profiling of a cohort of 16 patients s

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49

Rieppi, Monica, Veronica Vergani, Carmen Gatto, Gerardo Zanetta, Paola Allavena, Giulia Taraboletti, and Raffaella Giavazzi. "Mesothelial cells induce the motility of human ovarian carcinoma cells." International Journal of Cancer 80, no. 2 (January 18, 1999): 303–7. http://dx.doi.org/10.1002/(sici)1097-0215(19990118)80:2<303::aid-ijc21>3.0.co;2-w.

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50

Wu, Jiahao. "The activity of the Nrf2/Keap1 pathway regulates A549 Non-small-cell Lung Cancer (NSCLC) cells motility through RhoAROCK1 pathway." Theoretical and Natural Science 44, no. 1 (July 26, 2024): 227–34. http://dx.doi.org/10.54254/2753-8818/44/20240888.

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Abstract (sommario):

Purpose: It is observed that Nrf2 transcription factors initiate the production of proteins that play a role in regulating tumor growth, the study aims to discover whether Nrf2 will regulate cell motility in A549 NSCLC cells. The ROCK-RhoA pathway is a significant contributor to cell growth and migration, which can relate to cell motility. There might be a connection between Nrf2 and ROCK-RhoA pathway, the study aims to see whether Nrf2 regulates A549 NSCLC cell motility through ROCK-RhoA pathway. Method: The study will use wound healing assay to visualize cell motility, comparison is made bet

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