Готові списки джерел за темами / Cell migration

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Добірка наукової літератури з теми "Cell migration"

Автор: Grafiati
Опубліковано: 4 червня 2021
Оновлено: 6 липня 2024

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Статті в журналах з теми "Cell migration"

1

Thomas, L. A., and K. M. Yamada. "Contact stimulation of cell migration." Journal of Cell Science 103, no. 4 (December 1, 1992): 1211–14. http://dx.doi.org/10.1242/jcs.103.4.1211.

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Анотація:
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 and melanocytes. These cells migrated poorly, if at all, when isolated, but could be stimulated up to 200-fold to travel following contact with migrating cells. This phenomenon, which we have termed “contact-stimulated migration,” appeared to activate and sustain migration of the mass of cells. Cells that became dissociated from the others ceased directional migration, thereby limiting aberrant cell dispersion. Fibroblasts were minimally responsive to this novel phenomenon, which may be crucial for major, mass cell migrations.
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2

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 (October 31, 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 cell death in non-small cell lung carcinoma cells. Methods. The effects of KAN0438757 on cell viability, proliferation, DNA damage, migration, apoptosis, and autophagy in in non-small cell lung carcinoma cells was tested by WST-1, real-time cell analysis, comet assay, wound-healing migration test, and MMP/JC-1 and AO/ER dual staining assays as well as western blot analysis. Results. Our results revealed that KAN0438757 significantly suppressed the viability and proliferation of A549 and H1299 cells and inhibited migration of A549 cells. More importantly, KAN0438757 caused DNA damage and triggered apoptosis and this was accompanied by the up-regulation of cleaved PARP in A549 cells. Furthermore, treatment with KAN0438757 resulted in increased LC3 II and Beclin1, which indicated that KAN0438757 stimulated autophagy. Conclusions. Overall, targeting PFKFB3 with KAN0438757 may be a promising effective treatment approach, requiring further in vitro and in vivo evaluation of KAN0438757 as a therapy in non-small cell lung carcinoma cells.
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3

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 (March 1, 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 +/- 4.9% greater on tenascin than on fibronectin. Cells migrating on tenascin display a very motile appearance, while cells migrating on fibronectin spread and maintain close intercellular contacts. Cell migration in the presence of integrin blocking antibodies demonstrated that migration on tenascin and fibronectin is mediated by distinct integrins, alpha2beta1 and alphavbeta5/alphavbeta3, respectively. Since tenascin is coexpressed in malignant tumor matrices with fibronectin, we assessed the effects of tenascin on U251.3 cell migration mediated by fibronectin. Tenascin was found to provide a positive effect on fibronectin-mediated migration by altering cell morphology and enhancing cell motility. These effects of tenascin on fibronectin-mediated cell migration were inhibited by blocking beta1 and alpha2beta1 integrins. The results suggest that tenascin may play a significant role in promoting tumor cell migration and invasiveness by modulating cell responses to normal matrix components.
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4

Torrence, S. A. "Positional cues governing cell migration in leech neurogenesis." Development 111, no. 4 (April 1, 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 commitment of q-bandlet cells to migrate nor the general lateral-to-medial direction of their migration depend on interactions with any other cell line. However, the ability of the migrating cells to follow their normal pathways and to find their normal destinations does depend on interactions with cells of the mesodermal cell line, which appears to provide positional cues that specify the migration pathways.
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5

Ffrench-Constant, C., and R. O. Hynes. "Patterns of fibronectin gene expression and splicing during cell migration in chicken embryos." Development 104, no. 3 (November 1, 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 developing chicken embryos the distribution and alternative splicing of FN mRNA during three different cell migrations known to occur through FN-rich environments; neural crest cell migration, mesenchymal cell migration in the area vasculosa and endocardial cushion cell migration in the heart. Our results show that trunk neural crest cells do not contain significant FN mRNA during their initial migration. In contrast, migrating mesenchymal cells of the area vasculosa and endocardial cushion cells both contain abundant FN mRNA. Furthermore, the FN mRNA in these migrating mesenchymal and endocardial cells appears to be spliced in a manner identical with that present in the cells adjacent to their pathways. This in vivo evidence for FN synthesis by migrating and pathway cells argues against a generalized role for exogenously produced FN as a guidance mechanism for cell migration.
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6

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 (October 1, 2018): 10678–83. http://dx.doi.org/10.1073/pnas.1807543115.

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Анотація:
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 cell–cell contact, we show that contacts between different regions of cells elicit different responses. Repulsive responses were limited to interaction with the head of a migrating cell, while contact with the tail of a neighboring cell promoted migration toward the tail. The latter behavior, termed contact following of locomotion (CFL), required the Wnt signaling pathway. Inhibition of the Wnt pathway disrupted not only CFL but also collective migration of epithelial cells, without affecting the migration of individual cells. In contrast, inhibition of myosin II with blebbistatin disrupted the migration of both individual epithelial cells and collectives. We propose that CFL, in conjunction with CIL, plays a major role in guiding and coordinating cell migration within a multicellular environment.
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7

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

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8

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

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

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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 (October 15, 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 treatment (N-PNA) on migrating endothelial cells relative to contact-inhibited cells. These findings were confirmed and quantitated with an enzyme-linked lectin assay (ELLA) of circularly scraped BAEC monolayers. The expression of migration-associated cell surface glycoproteins was also analyzed by SDS-PAGE. The overall expression of cell surface glycoproteins was upregulated on migrating BAECs. Migrating BAECs expressed Con A- and WGA-binding glycoproteins with apparent molecular masses of 25 and 48 kD that were not expressed by contact-inhibited BAEC monolayers and, accordingly, disappeared as circularly scraped monolayers reached confluence. Subconfluent BAEC monolayers expressed the same cell surface glycoconjugate pattern as migrating endothelial cells. FACS analysis of circularly scraped BAEC monolayers showed that the phenotypic changes of cell surface glycoprotein expression after release from growth arrest occurred before the recruitment of the cells into the cell cycle (3 vs. 12 h). Suramin, which inhibits endothelial cell migration, abrogated the expression of the migration-associated phenotype and induced the expression of a prominent 28-kD Con A- and WGA-binding cell surface glycoprotein. These results indicate that endothelial cells express a specific migration-associated phenotype, which is characterized by the upregulation of distinct cellular glycoconjugates and the expression of specific migration-associated cell surface glycoproteins.
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Дисертації з теми "Cell migration"

1

Falk, Anna. "Stem cells : proliferation, differentiation, migration /." Stockholm, 2005. http://diss.kib.ki.se/2006/91-7140-497-X/.

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2

Sundström, Magnus. "Signal transduction in mast cell migration /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-5130-6/.

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3

SUN, Xue-Zhi, Sentaro TAKAHASHI, Chun GUI, Rui ZHANG, Kazuo KOGA, Minoru NOUYE, and Yoshiharu MURATA. "Neuronal Migration and Neuronal Migration Disorder in Cerebral Cortex." Research Institute of Environmental Medicine, Nagoya University, 2002. http://hdl.handle.net/2237/2773.

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4

Chometon-Luthe, Gretel. "Epithelial cell migration on laminins." [S.l. : s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=975579185.

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5

Burthem, John. "Hairy cell adhesion and migration." Thesis, University of Liverpool, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240394.

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Dawson, M. "Mast cell migration in allergy." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1357935/.

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Анотація:
The symptomology associated with allergic diseases are a direct consequence of the release of pro-inflammatory mediators from mast cells following bi- or multivalent antigen cross-linking with the high affinity immunoglobulin (Ig) E receptor, FcεR1. Chemokines, small 8-15 kDa polypeptides, control the activation and recruitment of immune cells during the allergic response. Previous studies have demonstrated that co-stimulation by the chemokine, macrophage inflammatory protein-1α (Mip-1α) and cross-linking by IgE with antigen result in four phenomenon 1) enhanced degranulation in ex vivo conjunctival mast cells and rat basophilic leukemia (RBL-2H3) cell line via its chemokine receptor (CCR) 1, cell line also referred to as RBL-CCR1; 2) arrested Mip-1α-induced chemotaxis of RBL-CCR1 cells; 3) enhanced production of proinflammatory mediators from RBL-CCR1 cells and 4) enhanced gene expression in RBL-CCR1 cells of regulatory molecules downstream of CCR1 and FcεR1 signaling pathways, Regulator of G-protein Signaling (RGS)-1 and Tribbles (TRB)- 3. It has therefore been proposed that co-engagement of CCR1 and FcεR1 affects other mast cell processes such as chemotaxis, and moreover these data indicate cross-talk between CCR1 and and FcεR1 signaling pathways. Chemotaxis of mast cells to sites of inflammation and the subsequent release of pro-inflammatory mediators are key to eliciting allergic response. Although there is a vast amount of information pertaining to the molecular mechanisms of chemotaxis in several cell types, there is very little evidence to understand mast cell chemotaxis at this level. Based on current knowledge, the main objective of this thesis was to investigate 1) the effect of CCR1 and FcεR1 co-engagement on mast cell motility and 2) the role of RGS1 and TRB3 on mast degranulation, mediator release and chemotaxis. The data obtained from this thesis is the first to demonstrate the role of WASP, CCR1 and actin polymerisation as mechanisms underlying Mip-1α induced RBLCCR1 chemotaxis, using real time microscopy. Moreover, CCR1 and FcεR1 engagement inhibits RBL-CCR1 actin cytoskeletal re-organisation and significantly increases other cell motility parameters such as directionality and Euclidean distances which are required for efficient Mip-1α-induced chemotaxis. Also, by using a murine model of allergic conjunctivitis, conjunctival mast cells accumulate in the forniceal area of an inflamed conjunctiva in comparison to non-diseased vi mice. In addition, by using siRNA the present study is also the first to show that RGS1 and TRB3 serve as negative regulators of RBL-CCR1 degranulation, mediator release and chemotaxis upon CCR1 and FcεR1 engagement. In conclusion, the data presented in this thesis could advance our understanding of the mechanisms responsible for mast cell migration and arrest during an allergic response, and hence provide new targets for anti-allergic drugs.
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Erlandsson, Anna. "Neural Stem Cell Differentiation and Migration." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl.[distributör], 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3546.

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8

Belotti, Yuri. "Microfluidic methods for investigating cell migration and cell mechanics." Thesis, University of Dundee, 2016. https://discovery.dundee.ac.uk/en/studentTheses/fb5ac03d-a752-45a1-8b95-37c8180dc7d9.

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In this thesis I explore how migratory properties of the model organism Dictyostelium discoideum are influenced by dimensionality and topology of the environment that surrounds the cell. Additionally, I sought to develop a microfluidic device able to measure mechanical properties of single cells with a sufficient throughput to account for the inherent heterogeneity of biological samples. Throughout this thesis I made use of microfabrication methods such as photo-lithography and soft-lithography, to develop ad hoc microstructured substrates. These tools enabled me to tackle different biological and biomedical questions related to cell migration and cell mechanics. Confining cells into channels with low dimensionality appeared to regulate the velocity of cellular locomotion, as well as the migration strategy adopted by the cell. Spatial confinement induced an altered arrangement of the acto-myosin cytoskeleton and microtubules. Moreover, the spatial constraint resulted in a simplified, mono-dimensional migration, characterised by constant average speed. Additionally, some cellular processes tended to occur in a periodic fashion, upon confinement. Interestingly, if Dictyostelium cells migrated through asymmetric bifurcating micro- channels, they appeared to be able to undergo a ’decision-making’ process leading to a directional bias. Although the biophysical mechanism underlying this response is yet to be understood, the data shown in this thesis suggest that Dictyostelium cells respond to differences in local concentrations of chemoattractants. The speed of a cell that crawls in a channel also depends on the cell’s stiffness, that in turn represents a measure of the density and structure of its cytoskeleton. To date, only a few methods have been developed to investigate cell mechanics with sufficient throughput. This motivated my interest in developing a microfluidic-based device that, exploiting the recording capabilities of a modern high speed camera, enabled me to assess the cellular mechanical properties at a rate greater than 10,000 cells per second, without the need for cell labelling. In this thesis I presented an example of how this method can be employed to detect differences between healthy and cancerous prostate cells, as well as to differentiate between prostate and bladder cancer cells based on their mechanical response. In conclusion, the work presented in this thesis highlights the interdisciplinarity required to investigate complex biological and biomedical problems. Specifically, the use of quantitative approaches that span from microtechnology, live imaging, computer vision and computational modelling enabled me to investigate novel biological processes as well as to explore new diagnostic technologies that aim to promote the improvement of the future healthcare.
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9

RUNYAN, CHRISTOPHER MICHAEL. "The Role of Cell Death in Germ Cell Migration." University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1210732680.

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10

Shuib, Anis Suhaila. "Investigation of blood cells migration in large stenosed artery." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6265.

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Atherosclerosis is one of the main diseases responsible for the high global mortality rate involving heart and blood vessel disorders. The build-up of fatty materials in the inner wall of the human artery prevents sufficient oxygen and nutrients reaching the organs of the body. Atherosclerosis is a chronic, long term condition, which develops and progresses over time; however, the disease does not present any symptoms until an advanced stage is reached, which results in potential permanent debility and sometimes sudden death. This thesis is concerned with the progression of atherosclerosis in an artery with mild stenosis that has resulted in a 30% reduction in its diameter. To this end, data on the low wall shear stress has been correlated with the atherosclerotic prone region. In a stenosed artery, this region corresponds to the separation zone that is formed distal to the lumen reduction. Atherosclerosis is a complex phenomenon, and not only involves wall shear stress, but also cellular interactions. Previous research has shown that even in the absence of wall biological effects, the blood cell distribution is strongly influenced by the hydrodynamics of the fluid. The mechanisms of blood cell distribution and the dynamic behaviour of the blood flow were investigated by developing a physical model of the stenosed artery, and by using particles to represent the presence of the blood cells. Particle Image Velocimetry system was employed and the size of particles were the 10μm and 20μm. The flow field was characterised and the particle distribution was measured. The characteristics of steady flow in the stenosed artery at Reynolds numbers of 250 and 320 revealed the importance of fluid inertia and the shear gradient distal to stenosis. Unequal distribution of the particles modelling the blood cells was observed, as more particles occupied the recirculation zones than the high shear region and central jet. The particle migration was found to depend on the particle size, particle concentration and fluid flow rates. The results suggested that the presence of similar effects in the real human arterial system may be significant to the progression of atherosclerotic plaques. At lower Reynolds number of 130, a particle depleted layer was observed at the wall region. In physiological flow the cell free layer will prevent the transport of oxygen and nitrogen oxide (NO) to the muscle tissues. A numerical method was used to simulate the flow characteristics measured in the experiment. The numerical results revealed the importance of the hydrodynamic mechanism of particle migration. Drag and lift forces were found to affect the residence time of particles in the recirculation region. The findings of this work have suggested that for a complex geometry like a large stenosed artery at physiological flow rates, hydrodynamic forces are important in cell migration in the flow separation zone. Even without biological forces, the cells migrate to the low wall shear stress region. For computational dynamics studies, this study has demonstrated the need for higher-order modelling at the cellular level in order to establish the particle migration mechanisms.
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Книги з теми "Cell migration"

1

Guan, Jun-Lin. Cell Migration. New Jersey: Humana Press, 2004. http://dx.doi.org/10.1385/1592598609.

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2

Wells, Claire M., and Maddy Parsons, eds. Cell Migration. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-207-6.

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3

Gautreau, Alexis, ed. Cell Migration. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7701-7.

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4

Filippi, Marie-Dominique, and Hartmut Geiger, eds. Stem Cell Migration. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-145-1.

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5

Stem cell migration: Methods and protocols. New York: Humana Press, 2011.

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6

Frank, Entschladen, and Zänker Kurt S, eds. Cell migration: Signalling and mechanisms. Basel: Karger, 2010.

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7

Margadant, Coert, ed. Cell Migration in Three Dimensions. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2887-4.

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8

Cell migration: Developmental methods and protocols. 2nd ed. New York: Humana Press, 2011.

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9

D'Ambrosio, Daniele, and Francesco Sinigaglia. Cell Migration in Inflammation and Immunity. New Jersey: Humana Press, 2003. http://dx.doi.org/10.1385/1592594352.

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10

Doris, Wedlich, ed. Cell migration in development and disease. Weinheim: Wiley-VCH, 2005.

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Частини книг з теми "Cell migration"

1

Rovensky, Yury A. "Cell Migration." In Adhesive Interactions in Normal and Transformed Cells, 121–44. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-304-2_6.

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2

Seynhaeve, Ann L. B., and Timo L. M. ten Hagen. "An In Vivo Model to Study Cell Migration in XYZ-T Dimension Followed by Whole-Mount Re-evaluation." In Cell Migration in Three Dimensions, 325–41. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2887-4_19.

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AbstractCell migration is a very dynamic process involving several chemical as well as biological interactions with other cells and the environment. Several models exist to study cell migration ranging from simple 2D in vitro cultures to more demanding 3D multicellular assays, to complex evaluation in animals. High-resolution 4D (XYZ, spatial + T, time dimension) intravital imaging using transgenic animals with a fluorescent label in cells of interest is a powerful tool to study cell migration in the correct environment. Here we describe an advanced dorsal skinfold chamber model to study endothelial cell and pericyte migration and association.
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Preziosi, Luigi. "Cell Migration, Biomechanics." In Encyclopedia of Applied and Computational Mathematics, 189–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-540-70529-1_69.

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4

Twyman, R. M. "Germ-cell migration." In BIOS Instant Notes in Developmental Biology, 130–34. London: Taylor & Francis, 2023. http://dx.doi.org/10.1201/9781003416371-26.

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Moissoglu, Konstadinos, Stephen J. Lockett, and Stavroula Mili. "Visualizing and Quantifying mRNA Localization at the Invasive Front of 3D Cancer Spheroids." In Cell Migration in Three Dimensions, 263–80. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2887-4_16.

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AbstractLocalization of mRNAs at the front of migrating cells is a widely used mechanism that functionally supports efficient cell movement. It is observed in single cells on two-dimensional surfaces, as well as in multicellular three-dimensional (3D) structures and in tissue in vivo. 3D multicellular cultures can reveal how the topology of the extracellular matrix and cell-cell contacts influence subcellular mRNA distributions. Here we describe a method for mRNA imaging in an inducible system of collective cancer cell invasion. MDA-MB-231 cancer cell spheroids are embedded in Matrigel, induced to invade, and processed to image mRNAs with single-molecule sensitivity. An analysis algorithm is used to quantify and compare mRNA distributions at the front of invasive leader cells. The approach can be easily adapted and applied to analyze RNA distributions in additional settings where cells polarize along a linear axis.
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Bradbury, Joshua J., Holly E. Lovegrove, Marta Giralt-Pujol, and Shane P. Herbert. "Analysis of mRNA Subcellular Distribution in Collective Cell Migration." In Cell Migration in Three Dimensions, 389–407. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2887-4_22.

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AbstractThe movement of groups of cells by collective cell migration requires division of labor between group members. Therefore, distinct cell identities, unique cell behaviors, and specific cellular roles are acquired by cells undergoing collective movement. A key driving force behind the acquisition of discrete cell states is the precise control of where, when, and how genes are expressed, both at the subcellular and supracellular level. Unraveling the mechanisms underpinning the spatiotemporal control of gene expression in collective cell migration requires not only suitable experimental models but also high-resolution imaging of messenger RNA and protein localization during this process. In recent times, the highly stereotyped growth of new blood vessels by sprouting angiogenesis has become a paradigm for understanding collective cell migration, and consequently this has led to the development of numerous user-friendly in vitro models of angiogenesis. In parallel, single-molecule fluorescent in situ hybridization (smFISH) has come to the fore as a powerful technique that allows quantification of both RNA number and RNA spatial distribution in cells and tissues. Moreover, smFISH can be combined with immunofluorescence to understand the precise interrelationship between RNA and protein distribution. Here, we describe methods for use of smFISH and immunofluorescence microscopy in in vitro angiogenesis models to enable the investigation of RNA and protein expression and localization during endothelial collective cell migration.
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Svoren, Martin, Elena Camerini, Merijn van Erp, Feng Wei Yang, Gert-Jan Bakker, and Katarina Wolf. "Approaches to Determine Nuclear Shape in Cells During Migration Through Collagen Matrices." In Cell Migration in Three Dimensions, 97–114. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2887-4_7.

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AbstractFibrillar collagen is an abundant extracellular matrix (ECM) component of interstitial tissues which supports the structure of many organs, including the skin and breast. Many different physiological processes, but also pathological processes such as metastatic cancer invasion, involve interstitial cell migration. Often, cell movement takes place through small ECM gaps and pores and depends upon the ability of the cell and its stiff nucleus to deform. Such nuclear deformation during cell migration may impact nuclear integrity, such as of chromatin or the nuclear envelope, and therefore the morphometric analysis of nuclear shapes can provide valuable insight into a broad variety of biological processes. Here, we describe a protocol on how to generate a cell-collagen model in vitro and how to use confocal microscopy for the static and dynamic visualization of labeled nuclei in single migratory cells. We developed, and here provide, two scripts that (Fidler, Nat Rev Cancer 3(6):453–458, 2003) enable the semi-automated and fast quantification of static single nuclear shape descriptors, such as aspect ratio or circularity, and the nuclear irregularity index that forms a combination of four distinct shape descriptors, as well as (Frantz et al., J Cell Sci 123 (Pt 24):4195–4200, 2010) a quantification of their changes over time. Finally, we provide quantitative measurements on nuclear shapes from cells that migrated through collagen either in the presence or the absence of an inhibitor of collagen degradation, showing the distinctive power of this approach. This pipeline can also be applied to cell migration studied in different assays, ranging from 3D microfluidics to migration in the living organism.
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Jacobs, Kathryn A., and Julie Gavard. "3D Endothelial Cell Migration." In Methods in Molecular Biology, 51–58. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7701-7_6.

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Prahl, Louis S., and David J. Odde. "Modeling Cell Migration Mechanics." In Advances in Experimental Medicine and Biology, 159–87. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95294-9_9.

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Gomperts, Miranda, Chris Wylie, and Janet Heasman. "Primordial Germ Cell Migration." In Ciba Foundation Symposium 182 - Germline Development, 121–39. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514573.ch7.

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Тези доповідей конференцій з теми "Cell migration"

1

Maini, Philip K. "Modelling collective cell migration." In INTERNATIONAL CONFERENCE OF NUMERICAL ANALYSIS AND APPLIED MATHEMATICS ICNAAM 2019. AIP Publishing, 2020. http://dx.doi.org/10.1063/5.0026549.

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Na, Sungsoo. "Engineering Tools for Studying Coordination Between Biochemical and Biomechanical Activities in Cell Migration." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53709.

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Cell migration is achieved by the dynamic feedback interactions between traction forces generated by the cell and exerted onto the underlying extracellular matrix (ECM), and intracellular mechano-chemical signaling pathways, e.g., Rho GTPase (RhoA, Rac1, and Cdc42) activities [1,2,3]. These components are differentially distributed within a cell, and thus the coordination between tractions and mechanotransduction (i.e, RhoA and Rac1 activities) must be implemented at a precise spatial and temporal order to achieve optimized, directed cell migration [4,5]. Recent studies have shown that focal adhesions at the leading edge exert strong tractions [6], and these traction sites are co-localized with focal adhesion sites [7]. Further, by using the fluorescence resonance energy transfer (FRET) technology coupled with genetically encoded biosensors, researchers reported that Rho GTPases, such as RhoA [8], Rac1 [9], and Cdc42 [10] are maximally activated at the leading edge, suggesting the leading edge of the cell as its common functional site for Rho GTPase activities. All these works, however, were done separately, and the relationship between tractions and mechanotransduction during cell migration has not been demonstrated directly because of the difficulty in simultaneously recording tractions and mechanotransduction in migrating cells, precluding direct comparison between these results. Furthermore, these studies have been conducted by monitoring cells on glass coverslips, the stiffness of which is ∼ 65 giga pascal (GPa), at least three to six order higher than the physiological range of ECM stiffness. Although it is increasingly accepted that ECM stiffness influences cell migration, it is not known exactly how physiologically relevant ECM stiffness (order of kPa range) affects the dynamics of RhoA and Rac1 activities. For a complete understanding of the mechanism of mechano-chemical signaling in the context of cell migration, the dynamics and interplay between biomechanical (e.g., tractions) and biochemical (e.g., Rho GTPase) activities should be visualized within the physiologically relevant range of ECM stiffness.
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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 array of posts. The migration cycle includes extension of the leading edge, formation of new adhesions at the front, contraction of the cytoskeleton, and the release of adhesions at the rear. In the model, an activation signal triggers the assembly of actin and myosin into a stress fiber, which generates a cytoskeletal tension in a manner similar to Hill’s muscle model. In addition, the role that adhesion dynamics has in regulating cytoskeletal tension has been added to the model. The multiphysics model was simulated in Matlab for 1-D simulations, and in Comsol for 2-D simulations. The model was able to predict the spatial distribution of traction forces observed with previous experiments in which large forces were seen at the leading and trailing edges. The large traction force at the trailing edge during the extension phase likely contributes to detachment of the focal adhesion by overcoming its adhesion strength with the post. Moreover, the model found that the mechanical work of a migrating cell underwent a cyclic relationship that rose with the formation of a new adhesion and fell with the release of an adhesion at its rear. We applied a third activation signal at the time of release and found it helped to maintain a more consistent level of work during migration. Therefore, the results from both our 1-D and 2-D migration simulations strongly suggest that cells use biochemical activation to supplement the loss in cytoskeletal tension upon adhesion release.
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Krishnamoorthy, Srikumar, and Changxue Xu. "Fabrication of a Graded Micropillar Surface for Guided Cell Migration." In ASME 2020 15th International Manufacturing Science and Engineering Conference. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/msec2020-8332.

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Abstract The migration of cells is caused by the interaction of cells and the local microenvironment around them, such as changes in stiffness, chemical gradients etc. The local topography of substrates in contact with cells is a key factor that regulates the migration of cells. The interaction between the topography of the substrate and cells is crucial for the understanding of tissue development and regeneration. In this paper, the fabrication of a graded micropillar substrate for studying topography-based cell migration is described in detail. The fabrication protocol comprises of the utilization of dynamic maskless lithography system, capillary molding, and corona arc surface treatment. The fabricated micropillar substrate has been shown and the cells have been successfully seeded on the substrate. Guided cell migration on the substrate with graded microtopography has been demonstrated to occur from the sparser zone to the denser zone. Moreover, some examples of potential applications are provided.
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Monteiro, Gary A., Harini G. Sundararaghavan, Anthony V. Fernandes, and David I. Shreiber. "Enhancing Cell Migration in Collagen Gels by Modulating Collagen Adhesivity." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192945.

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The organized movement of cells is critical during tissue morphogenesis and wound healing. While different tissue cells use distinct mechanisms for migration, the underlying biophysical balance of adhesive and tractional forces for effective migration is similar. The extracellular matrix provides the structural framework through which a cell can migrate. In particular, collagen is an abundant and ubiquitous ECM protein that supports cell migration. The excellent biocompatibility and physiological relevance of collagen have made it a primary material for tissue engineered regenerative therapies and in vitro studies with tissue equivalents.
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Zielinski, Rachel, Cosmin Mihai, and Samir Ghadiali. "Multi-Scale Modeling of Cancer Cell Migration and Adhesion During Epithelial-to-Mesenchymal Transition." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53511.

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Cancer is a leading cause of death in the US, and tumor cell metastasis and secondary tumor formation are key factors in the malignancy and prognosis of the disease. The regulation of cell motility plays an important role in the migration and invasion of cancer cells into surrounding tissues. The primary modes of increased motility in cancerous tissues may include collective migration of a group of epithelial cells during tumor growth and single cell migration of mesenchymal cells after detachment from the primary tumor site [1]. In epithelial cancers, metastasizing cells lose their cell-cell adhesions, detach from the tumor mass, begin expressing mesenchymal markers, and become highly motile and invasive, a process known as epithelial-to-mesenchymal transition (EMT) (Fig. 1) [2]. Although the cellular and biochemical signaling mechanisms underlying EMT have been studied extensively, there is limited information about the biomechanical mechanisms of EMT. In particular, it is not known how changes in cell mechanics (cell stiffness, cell-cell adhesion strength, traction forces) influence the detachment, migration and invasion processes that occur during metastasis.
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Kraning-Rush, Casey M., Shawn P. Carey, and Cynthia A. Reinhart-King. "Molded Collagen Microchannels for the Study of Cancer Cell Invasion." In ASME 2012 10th International Conference on Nanochannels, Microchannels, and Minichannels collocated with the ASME 2012 Heat Transfer Summer Conference and the ASME 2012 Fluids Engineering Division Summer Meeting. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/icnmm2012-73093.

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Metastasis is the cause of 90% of cancer-related deaths and yet the precise mechanism of metastasis is poorly understood[1]. To metastasize, cells break free from the primary tumor, migrate through the surrounding tissue, and enter the vascular system to move to a secondary site. To migrate through the stroma, cell can both degrade the tissue and use physical force to move the tissue from its path. However, the relative roles of matrix degradation and cellular force are not well-understood. Previous work has shown that as cell move through the matrix, they create channels that other cells can then use to more easily escape from the primary tumor [2, 3]. To investigate the mechanisms by which metastatic cells move through 3D matrices, we fabricated microchannels from collagen that simulate the paths that are made and used by cells during metastasis. Here, we will present our method for molding channels in compliant collagen gels to investigate cell migration. The channels dimensions approximate the size of a cell and permit cell migration without the need for matrix degradation. We demonstrate that the channels cause persistent, unidirectional cell migration that is significantly faster than the migration observed in 3D matrices without channels. These channels provide a unique platform to probe 3D cellular migration and permit the dissection of the relative roles of matrix degradation and force generation in facilitating cell invasion.
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Ohashi, Toshiro, and Akito Sugawara. "Traction Force Measurement During Collective Cell Migration Measured by Multichannel Micropillar Device." In ASME 2013 11th International Conference on Nanochannels, Microchannels, and Minichannels. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/icnmm2013-73163.

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Cell migration is essential for a variety of biological and pathological processes such as wound healing, inflammation and tumor metastasis. However, the mechanical environment within a group of cells during collective migration has not been well characterized. In this study, a polydimethylsiloxane (PDMS) multichannel device was fabricated using standard photolithography and soft lithography techniques and was used to monitor cellular traction forces during migration. A migration rate of 5.7 μm/h was measured in microchannels and leading cells in the moving front of the migration generated traction forces with a maximum magnitude of 14 nN at their front side. Traction forces generated by cells behind the leading cells directed forces backward at both the front and rear sides. However, traction forces generated by cells behind the second row had forces in random directions and with smaller magnitudes compared to those on the front and the second row. It is assumed that cells on the front line generated large traction forces and migrated actively as single cells, pulling adjacent cells forward, whereas the cell movement after the third row was restricted by mechanical linkages between their neighboring cells.
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Mauck, Robert L., Pen-hsiu G. Chao, Beth Gilbert, Wilmot B. Valhmu, and Clark T. Hung. "Chondrocyte Translocation and Orientation to Applied DC Electric Fields." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0405.

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Abstract Chemical and mechanical stimuli are known to cause directed movement in a number of different cell types. Less prominently studied, direct current (DC) electric fields are known to induce a similar response. In this study, we report on DC electric field-induced chondrocyte migration and re-orientation. Galvanotaxis and galvanotropism, migration and shape change in response to applied DC electric fields, respectively, have been demonstrated in many cells. For instance, field strengths of 1–10 V/cm have been reported to induce migration in keratinocytes. corneal epithelial cells, bone cells, fibroblasts and neural cells [1,7,8,11]. Recently, we have demonstrated for the first time that chondrocytes exhibit a galvanotactic response, realigning and migrating in response to applied DC electric fields (6 V/cm) [6]. In cartilage, chondrocytes may see electric fields associated with streaming potentials estimated to be up to 15 V/cm with current densities of up to 0.1A/cm2 [2]. The aim of this study was to explore basic science aspects of directed cell migration under applied DC electric fields and to investigate the potential application of this phenomena for tissue engineering, healing and repair of cartilage. The ability to direct cell growth and function will have significant implications on the bioengineering of replacement tissues.
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Peng, Ching-An. "Effects of Fluid Dynamics and Mass Transfer on Cell Migration and Growth in Confined Geometry." In ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-0801.

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Abstract We consider a mathematical model of the physical and biological processes involved in the bioreactors for cultivating tissues. In a laminar flow duct bioreactor, the Navier-Stokes and convective-diffusion equations are solved to obtain the concentration distribution of chemoattractant secreted from the stromal cells. Then, it is concoitmently used to solve the proposed chemotactic model and stem cell growth kinetics. The simulation results elucidate the spatio-temporal distribution of cells is governed by the interaction of cell chemotactic migration and cell mitosis. A dimensionless number that balances these two effects predicts the extent of non-uniformity in duct chambers. That is, if the directed cell migration rate is much larger than the cell growth rate, the cells will have enough time to move toward the side walls and proliferate rapidly causing prominent non-uniform growth. On the contrary, if the directed cell migration rate is much smaller than the cell growth rate, the cell growth on the cell bed is in comparison more uniform.
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Звіти організацій з теми "Cell migration"

1

Gonzalez-Nieves, Reyda. Regulation of Cell Migration in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2011. http://dx.doi.org/10.21236/ada553111.

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2

Cutler, Mary L. Targeting Epithelial Cell Migration to Accelerate Wound Healing. Fort Belvoir, VA: Defense Technical Information Center, June 2010. http://dx.doi.org/10.21236/ada552380.

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Cutler, Mary. Targeting Epithelial Cell Migration to Accelerate Wound Healing. Fort Belvoir, VA: Defense Technical Information Center, February 2012. http://dx.doi.org/10.21236/ada627078.

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4

Paul, Satashree. Flavivirus and its Threat. Science Repository, March 2021. http://dx.doi.org/10.31487/sr.blog.30.

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A number of studies found that the virus can activate the endothelial cells and affect the structure and function of the blood?brain barrier, promoting immune cell migration to benefit the virus nervous system target cells infected by flaviviruses.
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Flopper, George E., and Jr. Cell Migration as a Therapeutic Target in Malignant Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada396961.

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Plopper, George E., and Jr. Cell Migration as a Therapeutic Target in Malignant Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada409486.

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Plopper, George E. Cell Migration as a Therapeutic Target in Malignant Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada390932.

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Plopper, George E., and Jr. Cell Migration as a Therapeutic Target in Malignant Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada392816.

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9

Haugh, Jason M. Integration of Soluble and Adhesive Gradient Signals in Directed Cell Migration. Fort Belvoir, VA: Defense Technical Information Center, November 2006. http://dx.doi.org/10.21236/ada467054.

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10

Modzelewska, Katarzyna. Ack-1 Tyrosine Kinase Regulates Integrin Signaling Leading to Breast Cell Migration. Fort Belvoir, VA: Defense Technical Information Center, March 2004. http://dx.doi.org/10.21236/ada426124.

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