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Books on the topic 'Cell adhesion and migration'

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Author: Grafiati

Published: 10 March 2023

Last updated: 11 March 2023

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1

McGrath, John. CELL ADHESION AND MIGRATION IN SKIN DISEASE. Edited by Jonathan Barker. Abingdon, UK: Taylor & Francis, 2001. http://dx.doi.org/10.4324/9780203304594.

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2

Chen, Ning. Role of cell adhesion molecules in melanoma transendothelial migration. Ottawa: National Library of Canada, 2001.

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3

Hennigan, Shauna M. The effects of transendothelial migration on neutrophil function and programmed cell death. Dublin: University College Dublin, 1996.

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4

Behrens, Jürgen, and W. James Nelson, eds. Cell Adhesion. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-68170-0.

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5

C, Beckerle Mary, ed. Cell adhesion. New York: Oxford University Press, 2001.

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6

Bongrand, Pierre, Per M. Claesson, and Adam S. G. Curtis, eds. Studying Cell Adhesion. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-662-03008-0.

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7

Berezin, Vladimir, and Peter S. Walmod, eds. Cell Adhesion Molecules. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8090-7.

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8

Hemler, Martin E., and Enrico Mihich, eds. Cell Adhesion Molecules. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2830-2.

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9

Pierre, Bongrand, Claesson P. M, and Curtis A. S. G, eds. Studying cell adhesion. Berlin: Springer-Verlag, 1994.

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10

G, Curtis A. S., Lackie J. M, and Council of Europe, eds. Measuring cell adhesion. Chichester, West Sussex, England: Wiley, 1991.

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11

R, Preedy Victor, ed. Adhesion molecules. Enfield, N.H: Science Publishers, 2010.

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12

Preedy, Victor R. Adhesion molecules. Enfield, N.H: Science Publishers, 2010.

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13

Pierre, Bongrand, ed. Physical basis of cell-cell adhesion. Boca Raton, Fla: CRC Press, 1988.

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14

R, Hart I., Hogg Nancy, and Imperial Cancer Research Fund (Great Britain), eds. Cell adhesion and cancer. Plainview, NY: Cold Spring Harbor Laboratory Press, 1995.

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15

Patrick, Nott, and Temple Matthew, eds. New cell adhesion research. Hauppauge, NY: Nova Science Publishers, 2009.

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16

D, Richardson Peter, and Steiner Manfred, eds. Principles of cell adhesion. Boca Raton: CRC Press, 1995.

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17

D, Shimizu Yoji Ph, ed. Lymphocyte adhesion molecules. Austin: R.G. Landes Co., 1993.

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18

Media, Springer Science+Business, ed. Adhesion protein protocols. New York: Humana Press, 2013.

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19

International, Conference on Structure Function and Regulation of Molecules Involved in Leukocyte Adhesion (1st 1988 Titisee Germany). Leukocyte adhesion molecules. New York: Springer-Verlag, 1990.

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20

Elisabetta, Dejana, and Corada Monica, eds. Adhesion protein protocols. Totowa, N.J: Humana Press, 1999.

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21

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

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22

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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23

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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24

Pigott, Rod. The adhesion molecules. London: Academic Press London, 1993.

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25

A, Roberts J., and Gonzalez-Carranza Zinnia, eds. Plant cell separation and adhesion. Oxford: Blackwell, 2007.

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26

Buttenschön, Andreas, and Thomas Hillen. Non-Local Cell Adhesion Models. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-67111-2.

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27

Shimaoka, Motomu, ed. Integrin and Cell Adhesion Molecules. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-166-6.

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28

Roberts, Jeremy A., and Zinnia Gonzalez-Carranza, eds. Plant Cell Separation and Adhesion. Oxford, UK: Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470988824.

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29

E, Jones Gareth, Wigley C. B, Warn Richard, and Society for Experimental Biology (Great Britain), eds. Cell behaviour: Adhesion and motility. Cambridge, UK: Published for the Society for Experimental Biology by the Company of Biologists Limited, Department of Zoology, University of Cambridge, 1993.

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30

C, Adams Josephine, and American Society for Cell Biology., eds. Methods in cell-matrix adhesion. San Diego: Academic Press, 2002.

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31

Jun-Lin, Guan, ed. Signaling through cell adhesion molecules. Boca Raton, Fla: CRC Press, 1999.

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32

Joan, Marsh, Goode Jamie, and Ciba Foundation, eds. Cell adhesion and human disease. Chichester: Wiley, 1995.

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33

A, Horton Michael, ed. Molecular biology of cell adhesion molecules. Chichester: Wiley, 1996.

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34

A, Horton Michael, ed. Adhesion receptors as therapeutic targets. Boca Raton, Fla: CRC Press, 1996.

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35

Russell, Stevenson Bruce, Gallin Warren J, and Paul David Louis, eds. Cell-cell interactions: A practical approach. Oxford: IRL Press at Oxford University Press, 1992.

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36

David, Garrod, ed. Structure and function in cell adhesion. London: Portland Press, 2008.

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37

G, Gahmberg C., ed. Leukocyte adhesion: Basic and clinical aspects : proceedings of the 6th Novo Nordisk Foundation Symposium 'Leukocyte Adhesion', Copenhagen, Denmark, 29 June-1 July 1992. Amsterdam: Excerpta Medica, 1992.

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38

McGrath, John, and Jonathan Barker. Cell Adhesion and Migration in Skin Disease (Cell Adhesion and Communication). CRC, 2001.

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39

McGrath, John, and Jonathan Barker. Cell Adhesion and Migration in Skin Disease. Taylor & Francis Group, 2001.

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40

McGrath, John, and Jonathan Barker. Cell Adhesion and Migration in Skin Disease. Taylor & Francis Group, 2001.

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41

McGrath, John, and Jonathan Barker. Cell Adhesion and Migration in Skin Disease. Taylor & Francis Group, 2001.

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42

Mierke, Claudia Tanja, and Akihiko Ito, eds. Editor’s Pick 2021: Highlights in Cell Adhesion and Migration. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-782-5.

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43

Matsui, Takaaki, Mitsugu Fujita, and Akihiko Ito, eds. Cell Adhesion and Migration in the Development of Multicellular Organisms. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88945-694-9.

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44

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.

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45

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.

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46

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.

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Abstract:

Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.

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47

Cell Adhesion. Elsevier, 1996. http://dx.doi.org/10.1016/s1569-2558(08)x6005-9.

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48

Colman, D. R. Cell Adhesion. Elsevier Science & Technology Books, 1997.

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49

W. James Nelson,J. Rgen Behrens. Cell Adhesion. Springer, 2008.

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50

Behrens, Jürgen, and Warren James Nelson. Cell Adhesion. Springer, 2011.

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