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Artykuły w czasopismach na temat „Cell migration”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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1

Trepat, Xavier, Zaozao Chen, and Ken Jacobson. "Cell Migration." Comprehensive Physiology 2, no. 4 (2012): 2369–92. https://doi.org/10.1002/j.2040-4603.2012.tb00467.x.

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AbstractCell migration is fundamental to establishing and maintaining the proper organization of multicellular organisms. Morphogenesis can be viewed as a consequence, in part, of cell locomotion, from large‐scale migrations of epithelial sheets during gastrulation, to the movement of individual cells during development of the nervous system. In an adult organism, cell migration is essential for proper immune response, wound repair, and tissue homeostasis, while aberrant cell migration is found in various pathologies. Indeed, as our knowledge of migration increases, we can look forward to, for

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Thomas, L. A., and K. M. Yamada. "Contact stimulation of cell migration." Journal of Cell Science 103, no. 4 (1992): 1211–14. http://dx.doi.org/10.1242/jcs.103.4.1211.

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Mass migrations of dense cell populations occur periodically during embryonic development. It is known that extracellular matrices, through which the cells migrate, facilitate locomotion. However, this does not explain how cells, such as neural crest, can migrate as a dense cohort of cells in essentially continuous contact with one another. We report here that unique behavioral characteristics of the migrating cells may contribute to cohesive migration. We used time-lapse video microscopy to analyze the migration of quail neural crest cells and of two crest derivatives, human melanoma cells an

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Deniz, Özdemir. "KAN0438757: A NOVEL PFKFB3 INHIBITOR THAT INDUCES PROGRAMMED CELL DEATH AND SUPPRESSES CELL MIGRATION IN NON-SMALL CELL LUNG CARCINOMA CELLS." Biotechnologia Acta 16, no. 5 (2023): 34–44. http://dx.doi.org/10.15407/biotech16.05.034.

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Aim. PFKFB3 is glycolytic activators that is overexpressed in human lung cancer and plays a crucial role in multiple cellular functions including programmed cell death. Despite the many small molecules described as PFKFB3 inhibitors, some of them have shown disappointing results in vitro and in vivo. On the other hand KAN0438757, selective and potent, small molecule inhibitor has been developed. However, the effects of KAN0438757, in non-small cell lung carcinoma cells remain unknown. Herein, we sought to decipher the effect of KAN0438757 on proliferation, migration, DNA damage, and programmed

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Ffrench-Constant, C., and R. O. Hynes. "Patterns of fibronectin gene expression and splicing during cell migration in chicken embryos." Development 104, no. 3 (1988): 369–82. http://dx.doi.org/10.1242/dev.104.3.369.

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A variety of evidence suggests that fibronectin (FN) promotes cell migration during embryogenesis, and it has been suggested that the deposition of FN along migratory pathways may also play a role in cell guidance. In order to investigate such a role for FN, it is important to determine the relative contribution of migrating and pathway-forming cells to the FN in the migratory track, as any synthesis of FN by the migrating cells might be expected to mask guidance cues provided by the exogenous FN from pathway-forming cells. We have therefore used in situ hybridization to determine in developin

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Deryugina, E. I., and M. A. Bourdon. "Tenascin mediates human glioma cell migration and modulates cell migration on fibronectin." Journal of Cell Science 109, no. 3 (1996): 643–52. http://dx.doi.org/10.1242/jcs.109.3.643.

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The role of tenascin in mediating tumor cell migration was studied using two cell migration models. In migration/invasion Transwell assays U251.3 glioma cells rapidly migrated through the 8 mu m pore size membranes onto tenascin- and fibronectin-coated surfaces. In this assay the number of cells migrating onto tenascin was 52.2 +/- 9.6% greater than on fibronectin within 4 hours. To assess cell migration rates and cell morphology, U251.3 migration was examined in a two-dimension spheroid outgrowth assay. The radial distance migrated by U251.3 cells from tumor spheroids was found to be 53.8 +/-

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6

Torrence, S. A. "Positional cues governing cell migration in leech neurogenesis." Development 111, no. 4 (1991): 993–1005. http://dx.doi.org/10.1242/dev.111.4.993.

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The stereotyped distribution of identified neurons and glial cells in the leech nervous system is the product of stereotyped cell migrations and rearrangements during embryogenesis. To examine the dependence of long-distance cell migrations on positional cues provided by other tissues, embryos of Theromyzon rude were examined for the effects of selective ablation of various embryonic cell lines on the migration and final distribution of neural and glial precursor cells descended from the bilaterally paired ectodermal cell lines designated q bandlets. The results suggest that neither the commit

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7

Li, David, and Yu-li Wang. "Coordination of cell migration mediated by site-dependent cell–cell contact." Proceedings of the National Academy of Sciences 115, no. 42 (2018): 10678–83. http://dx.doi.org/10.1073/pnas.1807543115.

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Contact inhibition of locomotion (CIL), the repulsive response of cells upon cell–cell contact, has been the predominant paradigm for contact-mediated responses. However, it is difficult for CIL alone to account for the complex behavior of cells within a multicellular environment, where cells often migrate in cohorts such as sheets, clusters, and streams. Although cell–cell adhesion and mechanical interactions play a role, how individual cells coordinate their migration within a multicellular environment remains unclear. Using micropatterned substrates to guide cell migration and manipulate ce

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8

Bradley, David. "Cell migration." Materials Today 14, no. 1-2 (2011): 10. http://dx.doi.org/10.1016/s1369-7021(11)70010-4.

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Horwitz, Rick, and Donna Webb. "Cell migration." Current Biology 13, no. 19 (2003): R756—R759. http://dx.doi.org/10.1016/j.cub.2003.09.014.

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10

Wang, Heng, and Jiong Chen. "Cell migration: Collective cell migration is intrinsically stressful." Current Biology 34, no. 7 (2024): R275—R278. http://dx.doi.org/10.1016/j.cub.2024.02.061.

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Harris, J., L. Honigberg, N. Robinson, and C. Kenyon. "Neuronal cell migration in C. elegans: regulation of Hox gene expression and cell position." Development 122, no. 10 (1996): 3117–31. http://dx.doi.org/10.1242/dev.122.10.3117.

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In C. elegans, the Hox gene mab-5, which specifies the fates of cells in the posterior body region, has been shown to direct the migrations of certain cells within its domain of function. mab-5 expression switches on in the neuroblast QL as it migrates into the posterior body region. mab-5 activity is then required for the descendants of QL to migrate to posterior rather than anterior positions. What information activates Hox gene expression during this cell migration? How are these cells subsequently guided to their final positions? We address these questions by describing four genes, egl-20,

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12

Ridley, Anne J. "Rho GTPases and cell migration." Journal of Cell Science 114, no. 15 (2001): 2713–22. http://dx.doi.org/10.1242/jcs.114.15.2713.

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Cell migration involves dynamic and spatially regulated changes to the cytoskeleton and cell adhesion. The Rho GTPases play key roles in coordinating the cellular responses required for cell migration. Recent research has revealed new molecular links between Rho family proteins and the actin cytoskeleton, showing that they act to regulate actin polymerization, depolymerization and the activity of actin-associated myosins. In addition, studies on integrin signalling suggest that the substratum continuously feeds signals to Rho proteins in migrating cells to influence migration rate. There is al

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13

Legrand, Claire, Christine Gilles, Jean-Marie Zahm, et al. "Airway Epithelial Cell Migration Dynamics: MMP-9 Role in Cell–Extracellular Matrix Remodeling." Journal of Cell Biology 146, no. 2 (1999): 517–29. http://dx.doi.org/10.1083/jcb.146.2.517.

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Cell spreading and migration associated with the expression of the 92-kD gelatinase (matrix metalloproteinase 9 or MMP-9) are important mechanisms involved in the repair of the respiratory epithelium. We investigated the location of MMP-9 and its potential role in migrating human bronchial epithelial cells (HBEC). In vivo and in vitro, MMP-9 accumulated in migrating HBEC located at the leading edge of a wound and MMP-9 expression paralleled cell migration speed. MMP-9 accumulated through an actin-dependent pathway in the advancing lamellipodia of migrating cells and was subsequently found acti

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14

Garcin, Clare, and Anne Straube. "Microtubules in cell migration." Essays in Biochemistry 63, no. 5 (2019): 509–20. http://dx.doi.org/10.1042/ebc20190016.

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Abstract Directed cell migration is critical for embryogenesis and organ development, wound healing and the immune response. Microtubules are dynamic polymers that control directional migration through a number of coordinated processes: microtubules are the tracks for long-distance intracellular transport, crucial for delivery of new membrane components and signalling molecules to the leading edge of a migrating cell and the recycling of adhesion receptors. Microtubules act as force generators and compressive elements to support sustained cell protrusions. The assembly and disassembly of micro

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15

Zhao, Jieling, Youfang Cao, Luisa A. DiPietro, and Jie Liang. "Dynamic cellular finite-element method for modelling large-scale cell migration and proliferation under the control of mechanical and biochemical cues: a study of re-epithelialization." Journal of The Royal Society Interface 14, no. 129 (2017): 20160959. http://dx.doi.org/10.1098/rsif.2016.0959.

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Computational modelling of cells can reveal insight into the mechanisms of the important processes of tissue development. However, current cell models have limitations and are challenged to model detailed changes in cellular shapes and physical mechanics when thousands of migrating and interacting cells need to be modelled. Here we describe a novel dynamic cellular finite-element model (DyCelFEM), which accounts for changes in cellular shapes and mechanics. It also models the full range of cell motion, from movements of individual cells to collective cell migrations. The transmission of mechan

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16

Shellard, Adam, and Roberto Mayor. "Supracellular migration – beyond collective cell migration." Journal of Cell Science 132, no. 8 (2019): jcs226142. http://dx.doi.org/10.1242/jcs.226142.

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17

Murakami, Shinya, Yo Otsuka, Manabu Sugimoto, and Toshiyuki Mitsui. "3H1010 Controlled cell migration with ultrasound(Cell Biology III:Cytoskeleton & Motility,Oral Presentation)." Seibutsu Butsuri 52, supplement (2012): S70. http://dx.doi.org/10.2142/biophys.52.s70_4.

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Boehm, Manfred, and Elizabeth G. Nabel. "Cell Cycle and Cell Migration." Circulation 103, no. 24 (2001): 2879–81. http://dx.doi.org/10.1161/01.cir.103.24.2879.

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McLane, Louis T., Anthony Kramer, Carrie Harris, Edward Park, Hang Lu, and Jennifer E. Curtis. "Cell Coat Mediated Cell Migration." Biophysical Journal 96, no. 3 (2009): 629a. http://dx.doi.org/10.1016/j.bpj.2008.12.3325.

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20

Chen, Zaozao, Qiwei Li, Shihui Xu, Jun Ouyang, and Hongmei Wei. "Nanotopography-Modulated Epithelial Cell Collective Migration." Journal of Biomedical Nanotechnology 17, no. 6 (2021): 1079–87. http://dx.doi.org/10.1166/jbn.2021.3086.

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Matrix nanotopography plays an essential role in regulating cell behaviors including cell proliferation, differentiation, and migration. While studies on isolated single cell migration along the nanostructural orientation have been reported for various cell types, there remains a lack of understanding of how nanotopography regulates the behavior of collectively migrating cells during processes such as epithelial wound healing. We demonstrated that collective migration of epithelial cells was promoted on nanogratings perpendicular to, but not on those parallel to, the wound-healing axis. We fur

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21

Augustin-Voss, H. G., and B. U. Pauli. "Migrating endothelial cells are distinctly hyperglycosylated and express specific migration-associated cell surface glycoproteins." Journal of Cell Biology 119, no. 2 (1992): 483–91. http://dx.doi.org/10.1083/jcb.119.2.483.

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Migration of endothelial cells is one of the first cellular responses in the cascade of events that leads to re-endothelialization of an injured vessel and neovascularization of growing tissues and tumors. To examine the hypothesis that endothelial cells express a specific migration-associated phenotype, we analyzed the cell surface glycoprotein expression of migrating bovine aortic endothelial cell (BAECs). Light microscopic analysis revealed an upregulation of binding sites for the lectins Concanavalin A (Con A), wheat germ agglutinin (WGA), and peanut agglutinin after neuraminidase treatmen

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Kim, Jin Man, Minji Lee, Nury Kim, and Won Do Heo. "Optogenetic toolkit reveals the role of Ca2+sparklets in coordinated cell migration." Proceedings of the National Academy of Sciences 113, no. 21 (2016): 5952–57. http://dx.doi.org/10.1073/pnas.1518412113.

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Cell migration is controlled by various Ca2+signals. Local Ca2+signals, in particular, have been identified as versatile modulators of cell migration because of their spatiotemporal diversity. However, little is known about how local Ca2+signals coordinate between the front and rear regions in directionally migrating cells. Here, we elucidate the spatial role of local Ca2+signals in directed cell migration through combinatorial application of an optogenetic toolkit. An optically guided cell migration approach revealed the existence of Ca2+sparklets mediated by L-type voltage-dependent Ca2+chan

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23

Rørth, Pernille. "Collective Cell Migration." Annual Review of Cell and Developmental Biology 25, no. 1 (2009): 407–29. http://dx.doi.org/10.1146/annurev.cellbio.042308.113231.

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Cumberbatch, M., R. J. Dearman, C. E. M. Griffiths, and I. Kimber. "Langerhans cell migration." Clinical and Experimental Dermatology 25, no. 5 (2000): 413–18. http://dx.doi.org/10.1046/j.1365-2230.2000.00678.x.

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Spector, Mario, Leandro Peretti, Favio Vincitorio, and Luciano Iglesias. "Bacterial Migration Cell." Procedia Materials Science 8 (2015): 346–50. http://dx.doi.org/10.1016/j.mspro.2015.04.083.

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Sutherland, Stephani. "Targeting cell migration." Drug Discovery Today 8, no. 1 (2003): 6–7. http://dx.doi.org/10.1016/s1359-6446(02)02549-7.

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Golden, J. A., J. C. Zitz, K. McFadden, and C. L. Cepko. "Cell migration in the developing chick diencephalon." Development 124, no. 18 (1997): 3525–33. http://dx.doi.org/10.1242/dev.124.18.3525.

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We previously reported that retrovirally marked clones in the mature chick diencephalon were widely dispersed in the mediolateral, dorsoventral and rostrocaudal planes. The current study was undertaken to define the migration routes that led to the dispersion. Embryos were infected between stages 10 and 14 with a retroviral stock encoding alkaline phosphatase and a library of molecular tags. Embryos were harvested 2.5-5.5 days later and the brains were fixed and serially sectioned. Sibling relationships were determined following PCR amplification and sequencing of the molecular tag. On embryon

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Nishita, Michiru, Chinatsu Tomizawa, Masahiro Yamamoto, Yuji Horita, Kazumasa Ohashi, and Kensaku Mizuno. "Spatial and temporal regulation of cofilin activity by LIM kinase and Slingshot is critical for directional cell migration." Journal of Cell Biology 171, no. 2 (2005): 349–59. http://dx.doi.org/10.1083/jcb.200504029.

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Cofilin mediates lamellipodium extension and polarized cell migration by accelerating actin filament dynamics at the leading edge of migrating cells. Cofilin is inactivated by LIM kinase (LIMK)–1-mediated phosphorylation and is reactivated by cofilin phosphatase Slingshot (SSH)-1L. In this study, we show that cofilin activity is temporally and spatially regulated by LIMK1 and SSH1L in chemokine-stimulated Jurkat T cells. The knockdown of LIMK1 suppressed chemokine-induced lamellipodium formation and cell migration, whereas SSH1L knockdown produced and retained multiple lamellipodial protrusion

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Petrie, Ryan J., Núria Gavara, Richard S. Chadwick, and Kenneth M. Yamada. "Nonpolarized signaling reveals two distinct modes of 3D cell migration." Journal of Cell Biology 197, no. 3 (2012): 439–55. http://dx.doi.org/10.1083/jcb.201201124.

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We search in this paper for context-specific modes of three-dimensional (3D) cell migration using imaging for phosphatidylinositol (3,4,5)-trisphosphate (PIP3) and active Rac1 and Cdc42 in primary fibroblasts migrating within different 3D environments. In 3D collagen, PIP3 and active Rac1 and Cdc42 were targeted to the leading edge, consistent with lamellipodia-based migration. In contrast, elongated cells migrating inside dermal explants and the cell-derived matrix (CDM) formed blunt, cylindrical protrusions, termed lobopodia, and Rac1, Cdc42, and PIP3 signaling was nonpolarized. Reducing Rho

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Bachmann, Alice, and Anne Straube. "Kinesins in cell migration." Biochemical Society Transactions 43, no. 1 (2015): 79–83. http://dx.doi.org/10.1042/bst20140280.

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Human cells express 45 kinesins, microtubule motors that transport a variety of molecules and organelles within the cell. Many kinesins also modulate the tracks they move on by either bundling or sliding or regulating the dynamic assembly and disassembly of the microtubule polymer. In migrating cells, microtubules control the asymmetry between the front and rear of the cell by differentially regulating force generation processes and substrate adhesion. Many of these functions are mediated by kinesins, transporters as well as track modulators. In this review, we summarize the current knowledge

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Hammad, Ayat S., and Khaled Machaca. "Store Operated Calcium Entry in Cell Migration and Cancer Metastasis." Cells 10, no. 5 (2021): 1246. http://dx.doi.org/10.3390/cells10051246.

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Ca2+ signaling is ubiquitous in eukaryotic cells and modulates many cellular events including cell migration. Directional cell migration requires the polarization of both signaling and structural elements. This polarization is reflected in various Ca2+ signaling pathways that impinge on cell movement. In particular, store-operated Ca2+ entry (SOCE) plays important roles in regulating cell movement at both the front and rear of migrating cells. SOCE represents a predominant Ca2+ influx pathway in non-excitable cells, which are the primary migrating cells in multicellular organisms. In this revi

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Schwab, Albrecht. "Function and spatial distribution of ion channels and transporters in cell migration." American Journal of Physiology-Renal Physiology 280, no. 5 (2001): F739—F747. http://dx.doi.org/10.1152/ajprenal.2001.280.5.f739.

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Cell migration plays a central role in many physiological and pathophysiological processes, such as embryogenesis, immune defense, wound healing, or the formation of tumor metastases. Detailed models have been developed that describe cytoskeletal mechanisms of cell migration. However, evidence is emerging that ion channels and transporters also play an important role in cell migration. The purpose of this review is to examine the function and subcellular distribution of ion channels and transporters in cell migration. Topics covered will be a brief overview of cytoskeletal mechanisms of migrat

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Maeda, Nobuaki, та Masaharu Noda. "Involvement of Receptor-like Protein Tyrosine Phosphatase ζ/RPTPβ and Its Ligand Pleiotrophin/Heparin-binding Growth-associated Molecule (HB-GAM) in Neuronal Migration". Journal of Cell Biology 142, № 1 (1998): 203–16. http://dx.doi.org/10.1083/jcb.142.1.203.

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Pleiotrophin/heparin-binding growth-associated molecule (HB-GAM) is a specific ligand of protein tyrosine phosphatase ζ (PTPζ)/receptor-like protein tyrosine phosphatase β (RPTPβ) expressed in the brain as a chondroitin sulfate proteoglycan. Pleiotrophin and PTPζ isoforms are localized along the radial glial fibers, a scaffold for neuronal migration, suggesting that these molecules are involved in migratory processes of neurons during brain development. In this study, we examined the roles of pleiotrophin-PTPζ interaction in the neuronal migration using cell migration assay systems with glass

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Canver, Adam C., and Alisa Morss Clyne. "Quantification of Multicellular Organization, Junction Integrity, and Substrate Features in Collective Cell Migration." Microscopy and Microanalysis 23, no. 1 (2017): 22–33. http://dx.doi.org/10.1017/s1431927617000071.

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AbstractQuantitative analysis of multicellular organization, cell–cell junction integrity, and substrate properties is essential to understand the mechanisms underlying collective cell migration. However, spatially and temporally defining these properties is difficult within collectively migrating cell groups due to challenges in accurate cell segmentation within the monolayer. In this paper, we present Matlab®-based algorithms to spatially quantify multicellular organization (migration distance, interface roughness, and cell alignment, area, and morphology), cell–cell junction integrity, and

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Bradley, Pamela L., and Deborah J. Andrew. "ribbon encodes a novel BTB/POZ protein required for directed cell migration in Drosophila melanogaster." Development 128, no. 15 (2001): 3001–15. http://dx.doi.org/10.1242/dev.128.15.3001.

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During development, directed cell migration is crucial for achieving proper shape and function of organs. One well-studied example is the embryonic development of the larval tracheal system of Drosophila, in which at least four signaling pathways coordinate cell migration to form an elaborate branched network essential for oxygen delivery throughout the larva. FGF signaling is required for guided migration of all tracheal branches, whereas the DPP, EGF receptor, and Wingless/WNT signaling pathways each mediate the formation of specific subsets of branches. Here, we characterize ribbon, which e

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Zhu, Zhiwen, Yongping Chai, Huifang Hu, et al. "Spatial confinement of receptor activity by tyrosine phosphatase during directional cell migration." Proceedings of the National Academy of Sciences 117, no. 25 (2020): 14270–79. http://dx.doi.org/10.1073/pnas.2003019117.

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Directional cell migration involves signaling cascades that stimulate actin assembly at the leading edge, and additional pathways must inhibit actin polymerization at the rear. During neuroblast migration inCaenorhabditis elegans, the transmembrane protein MIG-13/Lrp12 acts through the Arp2/3 nucleation-promoting factors WAVE and WASP to guide the anterior migration. Here we show that a tyrosine kinase, SRC-1, directly phosphorylates MIG-13 and promotes its activity on actin assembly at the leading edge. In GFP knockin animals, SRC-1 and MIG-13 distribute along the entire plasma membrane of mi

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Ozcelikkale, Altug, J. Craig Dutton, Frederick Grinnell, and Bumsoo Han. "Effects of dynamic matrix remodelling on en masse migration of fibroblasts on collagen matrices." Journal of The Royal Society Interface 14, no. 135 (2017): 20170287. http://dx.doi.org/10.1098/rsif.2017.0287.

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Fibroblast migration plays a key role during various physiological and pathological processes. Although migration of individual fibroblasts has been well studied, migration in vivo often involves simultaneous locomotion of fibroblasts sited in close proximity, so-called ‘ en masse migration’, during which intensive cell–cell interactions occur. This study aims to understand the effects of matrix mechanical environments on the cell–matrix and cell–cell interactions during en masse migration of fibroblasts on collagen matrices. Specifically, we hypothesized that a group of migrating cells can si

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Andalur Nandagopal, Saravanan, Deepak Upreti, Susy Santos, et al. "Dual roles of GM-CSF in modulating NK-cell migratory properties (CAM4P.147)." Journal of Immunology 194, no. 1_Supplement (2015): 185.5. http://dx.doi.org/10.4049/jimmunol.194.supp.185.5.

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Abstract Background: Natural Killer (NK) cells play a key role in innate immunity against viral, microbial infections and transformed cells and their migration for effector function to peripheral tissues or inflamed lymph nodes are tightly regulated. Of interest, production of Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) by cancer cells is correlated to host immune suppression and tumor metastasis, suggesting an immune evasion property of GM-CSF. Here we examined role(s) of recombinant GM-CSF in the regulation of NK-cell migratory properties in vitro. Methods: Previously published

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Brückner, David B., Alexandra Fink, Joachim O. Rädler, and Chase P. Broedersz. "Disentangling the behavioural variability of confined cell migration." Journal of The Royal Society Interface 17, no. 163 (2020): 20190689. http://dx.doi.org/10.1098/rsif.2019.0689.

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Cell-to-cell variability is inherent to numerous biological processes, including cell migration. Quantifying and characterizing the variability of migrating cells is challenging, as it requires monitoring many cells for long time windows under identical conditions. Here, we observe the migration of single human breast cancer cells (MDA-MB-231) in confining two-state micropatterns. To describe the stochastic dynamics of this confined migration, we employ a dynamical systems approach. We identify statistics to measure the behavioural variance of the migration, which significantly exceeds that pr

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Venkatachalam, Thejasvi, Sushma Mannimala, Yeshaswi Pulijala, and Martha C. Soto. "CED-5/CED-12 (DOCK/ELMO) can promote and inhibit F-actin formation via distinct motifs that may target different GTPases." PLOS Genetics 20, no. 7 (2024): e1011330. http://dx.doi.org/10.1371/journal.pgen.1011330.

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Coordinated activation and inhibition of F-actin supports the movements of morphogenesis. Understanding the proteins that regulate F-actin is important, since these proteins are mis-regulated in diseases like cancer. Our studies of C. elegans embryonic epidermal morphogenesis identified the GTPase CED-10/Rac1 as an essential activator of F-actin. However, we need to identify the GEF, or Guanine-nucleotide Exchange Factor, that activates CED-10/Rac1 during embryonic cell migrations. The two-component GEF, CED-5/CED-12, is known to activate CED-10/Rac1 to promote cell movements that result in th

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Hathaway, HJ, and BD Shur. "Cell surface beta 1,4-galactosyltransferase functions during neural crest cell migration and neurulation in vivo." Journal of Cell Biology 117, no. 2 (1992): 369–82. http://dx.doi.org/10.1083/jcb.117.2.369.

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Mesenchymal cell migration and neurite outgrowth are mediated in part by binding of cell surface beta 1,4-galactosyltransferase (GalTase) to N-linked oligosaccharides within the E8 domain of laminin. In this study, we determined whether cell surface GalTase functions during neural crest cell migration and neural development in vivo using antibodies raised against affinity-purified chicken serum GalTase. The antibodies specifically recognized two embryonic proteins of 77 and 67 kD, both of which express GalTase activity. The antibodies also immunoprecipitated and inhibited chick embryo GalTase

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Goldfinger, Lawrence E., Jaewon Han, William B. Kiosses, Alan K. Howe та Mark H. Ginsberg. "Spatial restriction of α4 integrin phosphorylation regulates lamellipodial stability and α4β1-dependent cell migration". Journal of Cell Biology 162, № 4 (2003): 731–41. http://dx.doi.org/10.1083/jcb.200304031.

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Întegrins coordinate spatial signaling events essential for cell polarity and directed migration. Such signals from α4 integrins regulate cell migration in development and in leukocyte trafficking. Here, we report that efficient α4-mediated migration requires spatial control of α4 phosphorylation by protein kinase A, and hence localized inhibition of binding of the signaling adaptor, paxillin, to the integrin. In migrating cells, phosphorylated α4 accumulated along the leading edge. Blocking α4 phosphorylation by mutagenesis or by inhibition of protein kinase A drastically reduced α4-dependen

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Runyan, R. B., G. D. Maxwell, and B. D. Shur. "Evidence for a novel enzymatic mechanism of neural crest cell migration on extracellular glycoconjugate matrices." Journal of Cell Biology 102, no. 2 (1986): 432–41. http://dx.doi.org/10.1083/jcb.102.2.432.

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Migrating embryonic cells have high levels of cell surface galactosyltransferase (GalTase) activity. It has been proposed that GalTase participates during migration by recognizing and binding to terminal N-acetylglucosamine (GlcNAc) residues on glycoconjugates within the extracellular matrix (Shur, B. D., 1982, Dev. Biol. 91:149-162). We tested this hypothesis using migrating neural crest cells as an in vitro model system. Cell surface GalTase activity was perturbed using three independent sets of reagents, and the effects on cell migration were analyzed by time-lapse microphotography. The Gal

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Montell, D. J. "The genetics of cell migration in Drosophila melanogaster and Caenorhabditis elegans development." Development 126, no. 14 (1999): 3035–46. http://dx.doi.org/10.1242/dev.126.14.3035.

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Cell migrations are found throughout the animal kingdom and are among the most dramatic and complex of cellular behaviors. Historically, the mechanics of cell migration have been studied primarily in vitro, where cells can be readily viewed and manipulated. However, genetic approaches in relatively simple model organisms are yielding additional insights into the molecular mechanisms underlying cell movements and their regulation during development. This review will focus on these simple model systems where we understand some of the signaling and receptor molecules that stimulate and guide cell

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Isozaki, Yusuke, Kouki Sakai, Kenta Kohiro, et al. "The Rho-guanine nucleotide exchange factor Solo decelerates collective cell migration by modulating the Rho-ROCK pathway and keratin networks." Molecular Biology of the Cell 31, no. 8 (2020): 741–52. http://dx.doi.org/10.1091/mbc.e19-07-0357.

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Collective cell migration is crucial for tissue remodeling and cancer invasion. A RhoA-targeting guanine nucleotide exchange factor, Solo, localizes to the cell–cell contact sites in collectively migrating cells and acts as a brake for collective cell migration via promoting the RhoA-ROCK pathway and regulating the keratin-8/keratin-18 networks.

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Law, Ah-Lai, Anne Vehlow, Maria Kotini, et al. "Lamellipodin and the Scar/WAVE complex cooperate to promote cell migration in vivo." Journal of Cell Biology 203, no. 4 (2013): 673–89. http://dx.doi.org/10.1083/jcb.201304051.

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Cell migration is essential for development, but its deregulation causes metastasis. The Scar/WAVE complex is absolutely required for lamellipodia and is a key effector in cell migration, but its regulation in vivo is enigmatic. Lamellipodin (Lpd) controls lamellipodium formation through an unknown mechanism. Here, we report that Lpd directly binds active Rac, which regulates a direct interaction between Lpd and the Scar/WAVE complex via Abi. Consequently, Lpd controls lamellipodium size, cell migration speed, and persistence via Scar/WAVE in vitro. Moreover, Lpd knockout mice display defectiv

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Rappel, Wouter-Jan. "Cell–cell communication during collective migration." Proceedings of the National Academy of Sciences 113, no. 6 (2016): 1471–73. http://dx.doi.org/10.1073/pnas.1524893113.

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Mishra, Abhinava K., Joseph P. Campanale, James A. Mondo, and Denise J. Montell. "Cell interactions in collective cell migration." Development 146, no. 23 (2019): dev172056. http://dx.doi.org/10.1242/dev.172056.

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Conway, James R. W., and Guillaume Jacquemet. "Cell matrix adhesion in cell migration." Essays in Biochemistry 63, no. 5 (2019): 535–51. http://dx.doi.org/10.1042/ebc20190012.

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Abstract The ability of cells to migrate is a fundamental physiological process involved in embryonic development, tissue homeostasis, immune surveillance and wound healing. In order for cells to migrate, they must interact with their environment using adhesion receptors, such as integrins, and form specialized adhesion complexes that mediate responses to different extracellular cues. In this review, we discuss the role of integrin adhesion complexes (IACs) in cell migration, highlighting the layers of regulation that are involved, including intracellular signalling cascades, mechanosensing an

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Kino-oka, Masahiro, Yasunori Takezawa, Ngo Xuan Trung, and Masahito Taya. "Cell migration in multilayer cell sheet." Journal of Bioscience and Bioengineering 108 (November 2009): S36. http://dx.doi.org/10.1016/j.jbiosc.2009.08.085.

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