Статті в журналах: "Durotaxie"

1

Sunyer, Raimon, and Xavier Trepat. "Durotaxis." Current Biology 30, no. 9 (May 2020): R383—R387. http://dx.doi.org/10.1016/j.cub.2020.03.051.

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2

Huang, Yuxing, Jing Su, Jiayong Liu, Xin Yi, Fang Zhou, Jiaran Zhang, Jiaxiang Wang, Xuan Meng, Lu Si, and Congying Wu. "YAP Activation in Promoting Negative Durotaxis and Acral Melanoma Progression." Cells 11, no. 22 (November 9, 2022): 3543. http://dx.doi.org/10.3390/cells11223543.

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Directed cell migration towards a softer environment is called negative durotaxis. The mechanism and pathological relevance of negative durotaxis in tumor progression still requires in-depth investigation. Here, we report that YAP promotes the negative durotaxis of melanoma. We uncovered that the RhoA-myosin II pathway may underlie the YAP enhanced negative durotaxis of melanoma cells. Acral melanoma is the most common subtype of melanoma in non-Caucasians and tends to develop in a stress-bearing area. We report that acral melanoma patients exhibit YAP amplification and increased YAP activity. We detected a decreasing stiffness gradient from the tumor to the surrounding area in the acral melanoma microenvironment. We further identified that this stiffness gradient could facilitate the negative durotaxis of melanoma cells. Our study advanced the understanding of mechanical force and YAP in acral melanoma and we proposed negative durotaxis as a new mechanism for melanoma dissemination.

3

Puleo, Julieann I., Sara S. Parker, Mackenzie R. Roman, Adam W. Watson, Kiarash Rahmani Eliato, Leilei Peng, Kathylynn Saboda, et al. "Mechanosensing during directed cell migration requires dynamic actin polymerization at focal adhesions." Journal of Cell Biology 218, no. 12 (October 8, 2019): 4215–35. http://dx.doi.org/10.1083/jcb.201902101.

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The mechanical properties of a cell’s microenvironment influence many aspects of cellular behavior, including cell migration. Durotaxis, the migration toward increasing matrix stiffness, has been implicated in processes ranging from development to cancer. During durotaxis, mechanical stimulation by matrix rigidity leads to directed migration. Studies suggest that cells sense mechanical stimuli, or mechanosense, through the acto-myosin cytoskeleton at focal adhesions (FAs); however, FA actin cytoskeletal remodeling and its role in mechanosensing are not fully understood. Here, we show that the Ena/VASP family member, Ena/VASP-like (EVL), polymerizes actin at FAs, which promotes cell-matrix adhesion and mechanosensing. Importantly, we show that EVL regulates mechanically directed motility, and that suppression of EVL expression impedes 3D durotactic invasion. We propose a model in which EVL-mediated actin polymerization at FAs promotes mechanosensing and durotaxis by maturing, and thus reinforcing, FAs. These findings establish dynamic FA actin polymerization as a central aspect of mechanosensing and identify EVL as a crucial regulator of this process.

4

Style, R. W., Y. Che, S. J. Park, B. M. Weon, J. H. Je, C. Hyland, G. K. German, et al. "Patterning droplets with durotaxis." Proceedings of the National Academy of Sciences 110, no. 31 (June 24, 2013): 12541–44. http://dx.doi.org/10.1073/pnas.1307122110.

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5

Hartman, Christopher D., Brett C. Isenberg, Samantha G. Chua, and Joyce Y. Wong. "Vascular smooth muscle cell durotaxis depends on extracellular matrix composition." Proceedings of the National Academy of Sciences 113, no. 40 (September 19, 2016): 11190–95. http://dx.doi.org/10.1073/pnas.1611324113.

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Mechanical compliance has been demonstrated to be a key determinant of cell behavior, directing processes such as spreading, migration, and differentiation. Durotaxis, directional migration from softer to more stiff regions of a substrate, has been observed for a variety of cell types. Recent stiffness mapping experiments have shown that local changes in tissue stiffness in disease are often accompanied by an altered ECM composition in vivo. However, the importance of ECM composition in durotaxis has not yet been explored. To address this question, we have developed and characterized a polyacrylamide hydrogel culture platform featuring highly tunable gradients in mechanical stiffness. This feature, together with the ability to control ECM composition, allows us to isolate the effects of mechanical and biological signals on cell migratory behavior. Using this system, we have tracked vascular smooth muscle cell migration in vitro and quantitatively analyzed differences in cell migration as a function of ECM composition. Our results show that vascular smooth muscle cells undergo durotaxis on mechanical gradients coated with fibronectin but not on those coated with laminin. These findings indicate that the composition of the adhesion ligand is a critical determinant of a cell’s migratory response to mechanical gradients.

6

Yuehua, YANG, and JIANG Hongyuan. "Research Advances in Cell Durotaxis." 应用数学和力学 42, no. 10 (2021): 999–1007. http://dx.doi.org/10.21656/1000-0887.420265.

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7

Bueno, Jesus, Yuri Bazilevs, Ruben Juanes, and Hector Gomez. "Wettability control of droplet durotaxis." Soft Matter 14, no. 8 (2018): 1417–26. http://dx.doi.org/10.1039/c7sm01917c.

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8

Doering, Charles R., Xiaoming Mao, and Leonard M. Sander. "Random walker models for durotaxis." Physical Biology 15, no. 6 (September 11, 2018): 066009. http://dx.doi.org/10.1088/1478-3975/aadc37.

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9

Stefanoni, Filippo, Maurizio Ventre, Francesco Mollica, and Paolo A. Netti. "A numerical model for durotaxis." Journal of Theoretical Biology 280, no. 1 (July 2011): 150–58. http://dx.doi.org/10.1016/j.jtbi.2011.04.001.

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10

Parida, Lipika, and Venkat Padmanabhan. "Durotaxis in Nematode Caenorhabditis elegans." Biophysical Journal 111, no. 3 (August 2016): 666–74. http://dx.doi.org/10.1016/j.bpj.2016.06.030.

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11

DuChez, Brian J., Andrew D. Doyle, Emilios K. Dimitriadis, and Kenneth M. Yamada. "Durotaxis by Human Cancer Cells." Biophysical Journal 116, no. 4 (February 2019): 670–83. http://dx.doi.org/10.1016/j.bpj.2019.01.009.

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12

Moriyama, Kousuke, and Satoru Kidoaki. "Cellular Durotaxis Revisited: Initial-Position-Dependent Determination of the Threshold Stiffness Gradient to Induce Durotaxis." Langmuir 35, no. 23 (September 19, 2018): 7478–86. http://dx.doi.org/10.1021/acs.langmuir.8b02529.

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13

Feng, Jingchen, Herbert Levine, Xiaoming Mao, and Leonard M. Sander. "Cell motility, contact guidance, and durotaxis." Soft Matter 15, no. 24 (2019): 4856–64. http://dx.doi.org/10.1039/c8sm02564a.

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14

Novikova, Elizaveta A., Matthew Raab, Dennis E. Discher, and Cornelis Storm. "Cellular Durotaxis from Differentially Persistent Motility." Biophysical Journal 112, no. 3 (February 2017): 436a. http://dx.doi.org/10.1016/j.bpj.2016.11.2327.

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15

Lazopoulos, Konstantinos A., and Dimitrije Stamenović. "Durotaxis as an elastic stability phenomenon." Journal of Biomechanics 41, no. 6 (2008): 1289–94. http://dx.doi.org/10.1016/j.jbiomech.2008.01.008.

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16

Gomez, Hector, and Mirian Velay-Lizancos. "Thin-film model of droplet durotaxis." European Physical Journal Special Topics 229, no. 2-3 (February 2020): 265–73. http://dx.doi.org/10.1140/epjst/e2019-900127-x.

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17

Wei, Jie, Xiaofeng Chen, and Bin Chen. "Harnessing structural instability for cell durotaxis." Acta Mechanica Sinica 35, no. 2 (March 21, 2019): 355–64. http://dx.doi.org/10.1007/s10409-019-00853-2.

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18

Raab, Matthew, Joe Swift, P. C. Dave P. Dingal, Palak Shah, Jae-Won Shin, and Dennis E. Discher. "Crawling from soft to stiff matrix polarizes the cytoskeleton and phosphoregulates myosin-II heavy chain." Journal of Cell Biology 199, no. 4 (November 5, 2012): 669–83. http://dx.doi.org/10.1083/jcb.201205056.

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On rigid surfaces, the cytoskeleton of migrating cells is polarized, but tissue matrix is normally soft. We show that nonmuscle MIIB (myosin-IIB) is unpolarized in cells on soft matrix in 2D and also within soft 3D collagen, with rearward polarization of MIIB emerging only as cells migrate from soft to stiff matrix. Durotaxis is the tendency of cells to crawl from soft to stiff matrix, and durotaxis of primary mesenchymal stem cells (MSCs) proved more sensitive to MIIB than to the more abundant and persistently unpolarized nonmuscle MIIA (myosin-IIA). However, MIIA has a key upstream role: in cells on soft matrix, MIIA appeared diffuse and mobile, whereas on stiff matrix, MIIA was strongly assembled in oriented stress fibers that MIIB then polarized. The difference was caused in part by elevated phospho-S1943–MIIA in MSCs on soft matrix, with site-specific mutants revealing the importance of phosphomoderated assembly of MIIA. Polarization is thus shown to be a highly regulated compass for mechanosensitive migration.

19

Liu, Yang, Jiwen Cheng, Hui Yang, and Guang-Kui Xu. "Rotational constraint contributes to collective cell durotaxis." Applied Physics Letters 117, no. 21 (November 23, 2020): 213702. http://dx.doi.org/10.1063/5.0031846.

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20

Harland, Ben, Sam Walcott, and Sean X. Sun. "Adhesion dynamics and durotaxis in migrating cells." Physical Biology 8, no. 1 (February 1, 2011): 015011. http://dx.doi.org/10.1088/1478-3975/8/1/015011.

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21

Harland, Ben, Sam Walcott, and Sean X. Sun. "Adhesion Dynamics and Durotaxis in Migrating Cells." Biophysical Journal 100, no. 3 (February 2011): 303a. http://dx.doi.org/10.1016/j.bpj.2010.12.1855.

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22

Jain, Gaurav, Andrew J. Ford, and Padmavathy Rajagopalan. "Opposing Rigidity-Protein Gradients Reverse Fibroblast Durotaxis." ACS Biomaterials Science & Engineering 1, no. 8 (July 30, 2015): 621–31. http://dx.doi.org/10.1021/acsbiomaterials.5b00229.

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23

McKenzie, Andrew J., Kathryn V. Svec, Tamara F. Williams, and Alan K. Howe. "Protein kinase A activity is regulated by actomyosin contractility during cell migration and is required for durotaxis." Molecular Biology of the Cell 31, no. 1 (January 1, 2020): 45–58. http://dx.doi.org/10.1091/mbc.e19-03-0131.

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Here, we show that localized PKA activity in migrating cells is regulated by cell–matrix tension, correlates with cellular traction forces, is enhanced by acute mechanical stimulation, and is required for durotaxis. This establishes PKA as an effector of cellular mechanotransduction and as a regulator of mechanically guided cell migration.

24

Riaz, Maryam, Marie Versaevel, and Sylvain Gabriele. "On the Mechanism of Durotaxis in Motile Cells." Biophysical Journal 106, no. 2 (January 2014): 571a. http://dx.doi.org/10.1016/j.bpj.2013.11.3167.

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25

Escribano, Jorge, Raimon Sunyer, María Teresa Sánchez, Xavier Trepat, Pere Roca-Cusachs, and José Manuel García-Aznar. "A hybrid computational model for collective cell durotaxis." Biomechanics and Modeling in Mechanobiology 17, no. 4 (March 2, 2018): 1037–52. http://dx.doi.org/10.1007/s10237-018-1010-2.

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26

Wieland, Annalena, Pamela L. Strissel, Hannah Schorle, Ezgi Bakirci, Dieter Janzen, Matthias W. Beckmann, Markus Eckstein, Paul D. Dalton, and Reiner Strick. "Brain and Breast Cancer Cells with PTEN Loss of Function Reveal Enhanced Durotaxis and RHOB Dependent Amoeboid Migration Utilizing 3D Scaffolds and Aligned Microfiber Tracts." Cancers 13, no. 20 (October 14, 2021): 5144. http://dx.doi.org/10.3390/cancers13205144.

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Background: Glioblastoma multiforme (GBM) and metastatic triple-negative breast cancer (TNBC) with PTEN mutations often lead to brain dissemination with poor patient outcome, thus new therapeutic targets are needed. To understand signaling, controlling the dynamics and mechanics of brain tumor cell migration, we implemented GBM and TNBC cell lines and designed 3D aligned microfibers and scaffolds mimicking brain structures. Methods: 3D microfibers and scaffolds were printed using melt electrowriting. GBM and TNBC cell lines with opposing PTEN genotypes were analyzed with RHO-ROCK-PTEN inhibitors and PTEN rescue using live-cell imaging. RNA-sequencing and qPCR of tumor cells in 3D with microfibers were performed, while scanning electron microscopy and confocal microscopy addressed cell morphology. Results: In contrast to the PTEN wildtype, GBM and TNBC cells with PTEN loss of function yielded enhanced durotaxis, topotaxis, adhesion, amoeboid migration on 3D microfibers and significant high RHOB expression. Functional studies concerning RHOB-ROCK-PTEN signaling confirmed the essential role for the above cellular processes. Conclusions: This study demonstrates a significant role of the PTEN genotype and RHOB expression for durotaxis, adhesion and migration dependent on 3D. GBM and TNBC cells with PTEN loss of function have an affinity for stiff brain structures promoting metastasis. 3D microfibers represent an important tool to model brain metastasizing tumor cells, where RHO-inhibitors could play an essential role for improved therapy.

27

Wieland, Annalena, Pamela L. Strissel, Hannah Schorle, Ezgi Bakirci, Dieter Janzen, Matthias W. Beckmann, Markus Eckstein, Paul D. Dalton, and Reiner Strick. "Brain and Breast Cancer Cells with PTEN Loss of Function Reveal Enhanced Durotaxis and RHOB Dependent Amoeboid Migration Utilizing 3D Scaffolds and Aligned Microfiber Tracts." Cancers 13, no. 20 (October 14, 2021): 5144. http://dx.doi.org/10.3390/cancers13205144.

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Background: Glioblastoma multiforme (GBM) and metastatic triple-negative breast cancer (TNBC) with PTEN mutations often lead to brain dissemination with poor patient outcome, thus new therapeutic targets are needed. To understand signaling, controlling the dynamics and mechanics of brain tumor cell migration, we implemented GBM and TNBC cell lines and designed 3D aligned microfibers and scaffolds mimicking brain structures. Methods: 3D microfibers and scaffolds were printed using melt electrowriting. GBM and TNBC cell lines with opposing PTEN genotypes were analyzed with RHO-ROCK-PTEN inhibitors and PTEN rescue using live-cell imaging. RNA-sequencing and qPCR of tumor cells in 3D with microfibers were performed, while scanning electron microscopy and confocal microscopy addressed cell morphology. Results: In contrast to the PTEN wildtype, GBM and TNBC cells with PTEN loss of function yielded enhanced durotaxis, topotaxis, adhesion, amoeboid migration on 3D microfibers and significant high RHOB expression. Functional studies concerning RHOB-ROCK-PTEN signaling confirmed the essential role for the above cellular processes. Conclusions: This study demonstrates a significant role of the PTEN genotype and RHOB expression for durotaxis, adhesion and migration dependent on 3D. GBM and TNBC cells with PTEN loss of function have an affinity for stiff brain structures promoting metastasis. 3D microfibers represent an important tool to model brain metastasizing tumor cells, where RHO-inhibitors could play an essential role for improved therapy.

28

Vicente-Manzanares, Miguel. "Cell Migration: Cooperation between Myosin II Isoforms in Durotaxis." Current Biology 23, no. 1 (January 2013): R28—R29. http://dx.doi.org/10.1016/j.cub.2012.11.024.

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29

Vicente-Manzanares, Miguel. "Cell Migration: Cooperation between Myosin II Isoforms in Durotaxis." Current Biology 23, no. 5 (March 2013): 441. http://dx.doi.org/10.1016/j.cub.2013.02.014.

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30

Shellard, Adam, and Roberto Mayor. "Collective durotaxis along a self-generated stiffness gradient in vivo." Nature 600, no. 7890 (December 8, 2021): 690–94. http://dx.doi.org/10.1038/s41586-021-04210-x.

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31

Sunyer, R., V. Conte, J. Escribano, A. Elosegui-Artola, A. Labernadie, L. Valon, D. Navajas, et al. "Collective cell durotaxis emerges from long-range intercellular force transmission." Science 353, no. 6304 (September 8, 2016): 1157–61. http://dx.doi.org/10.1126/science.aaf7119.

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32

Martinez, Jessica S., Ali M. Lehaf, Joseph B. Schlenoff, and Thomas C. S. Keller. "Cell Durotaxis on Polyelectrolyte Multilayers with Photogenerated Gradients of Modulus." Biomacromolecules 14, no. 5 (April 2, 2013): 1311–20. http://dx.doi.org/10.1021/bm301863a.

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33

Vincent, Ludovic G., Yu Suk Choi, Baldomero Alonso-Latorre, Juan C. del Álamo, and Adam J. Engler. "Mesenchymal stem cell durotaxis depends on substrate stiffness gradient strength." Biotechnology Journal 8, no. 4 (February 28, 2013): 472–84. http://dx.doi.org/10.1002/biot.201200205.

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34

Pamonag, Michael, Abigail Hinson, Elisha J. Burton, Nojan Jafari, Dominic Sales, Sarah Babcock, Rozlan Basha, Xiaofeng Hu, and Kristopher E. Kubow. "Individual cells generate their own self-reinforcing contact guidance cues through local matrix fiber remodeling." PLOS ONE 17, no. 3 (March 25, 2022): e0265403. http://dx.doi.org/10.1371/journal.pone.0265403.

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Directed cell migration arises from cells following a microenvironmental gradient (e.g. of a chemokine) or polarizing feature (e.g. a linear structure). However cells not only follow, but in many cases, also generate directionality cues by modifying their microenvironment. This bi-directional relationship is seen in the alignment of extracellular matrix (ECM) fibers ahead of invading cell masses. The forces generated by many migrating cells cause fiber alignment, which in turn promotes further migration in the direction of fiber alignment via contact guidance and durotaxis. While this positive-feedback relationship has been widely described for cells invading en masse, single cells are also able to align ECM fibers, as well as respond to contact guidance and durotaxis cues, and should therefore exhibit the same relationship. In this study, we directly tested this hypothesis by studying the migration persistence of individual HT-1080 fibrosarcoma cells migrating in photocrosslinked collagen matrices with limited remodeling potential. Our results demonstrate that this positive-feedback relationship is indeed a fundamental aspect of cell migration in fibrillar environments. We observed that the cells’ inability to align and condense fibers resulted in a decrease in persistence relative to cells in native collagen matrices and even relative to isotropic (glass) substrates. Further experiments involving 2D collagen and electrospun polymer scaffolds suggest that substrates composed of rigid, randomly oriented fibers reduce cells’ ability to follow another directionality cue by forcing them to meander to follow the available adhesive area (i.e. fibers). Finally, our results demonstrate that the bi-directional relationship between cell remodeling and migration is not a “dimensionality” effect, but a fundamental effect of fibrous substrate structure.

35

Aubry, D., M. Gupta, B. Ladoux, and R. Allena. "Mechanical link between durotaxis, cell polarity and anisotropy during cell migration." Physical Biology 12, no. 2 (April 17, 2015): 026008. http://dx.doi.org/10.1088/1478-3975/12/2/026008.

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36

Isenberg, Brett C., Paul A. DiMilla, Matthew Walker, Sooyoung Kim, and Joyce Y. Wong. "Vascular Smooth Muscle Cell Durotaxis Depends on Substrate Stiffness Gradient Strength." Biophysical Journal 97, no. 5 (September 2009): 1313–22. http://dx.doi.org/10.1016/j.bpj.2009.06.021.

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37

Kuntanawat, P., C. Wilkinson, and M. Riehle. "Observation of durotaxis on a well-defined continuous gradient of stiffness." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 146, no. 4 (April 2007): S192. http://dx.doi.org/10.1016/j.cbpa.2007.01.421.

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38

Wormer, Duncan B., Kevin A. Davis, James H. Henderson, and Christopher E. Turner. "The Focal Adhesion-Localized CdGAP Regulates Matrix Rigidity Sensing and Durotaxis." PLoS ONE 9, no. 3 (March 14, 2014): e91815. http://dx.doi.org/10.1371/journal.pone.0091815.

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39

Ebata, Hiroyuki, Kousuke Moriyama, Thasaneeya Kuboki, and Satoru Kidoaki. "General cellular durotaxis induced with cell-scale heterogeneity of matrix-elasticity." Biomaterials 230 (February 2020): 119647. http://dx.doi.org/10.1016/j.biomaterials.2019.119647.

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40

Shellard, Adam, and Roberto Mayor. "Publisher Correction: Collective durotaxis along a self-generated stiffness gradient in vivo." Nature 601, no. 7894 (January 12, 2022): E33. http://dx.doi.org/10.1038/s41586-021-04367-5.

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41

Budde, Ilka, David Ing, Albrecht Schwab, and Zoltan Denes Petho. "Mechanosensitive ion channels are essential for the durotaxis of pancreatic stellate cells." Biophysical Journal 121, no. 3 (February 2022): 314a. http://dx.doi.org/10.1016/j.bpj.2021.11.1181.

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42

Alert, Ricard, and Jaume Casademunt. "Role of Substrate Stiffness in Tissue Spreading: Wetting Transition and Tissue Durotaxis." Langmuir 35, no. 23 (October 3, 2018): 7571–77. http://dx.doi.org/10.1021/acs.langmuir.8b02037.

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43

Allena, R., M. Scianna, and L. Preziosi. "A Cellular Potts Model of single cell migration in presence of durotaxis." Mathematical Biosciences 275 (May 2016): 57–70. http://dx.doi.org/10.1016/j.mbs.2016.02.011.

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44

Malik, Adam A., and Philip Gerlee. "Mathematical modelling of cell migration: stiffness dependent jump rates result in durotaxis." Journal of Mathematical Biology 78, no. 7 (April 10, 2019): 2289–315. http://dx.doi.org/10.1007/s00285-019-01344-5.

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45

Whang, Minji, and Jungwook Kim. "Synthetic hydrogels with stiffness gradients for durotaxis study and tissue engineering scaffolds." Tissue Engineering and Regenerative Medicine 13, no. 2 (April 2016): 126–39. http://dx.doi.org/10.1007/s13770-016-0026-x.

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46

Marzban, Bahador, Xin Yi, and Hongyan Yuan. "A minimal mechanics model for mechanosensing of substrate rigidity gradient in durotaxis." Biomechanics and Modeling in Mechanobiology 17, no. 3 (January 22, 2018): 915–22. http://dx.doi.org/10.1007/s10237-018-1001-3.

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47

Zhang, Zhiwen, Phoebus Rosakis, Thomas Y. Hou, and Guruswami Ravichandran. "A minimal mechanosensing model predicts keratocyte evolution on flexible substrates." Journal of The Royal Society Interface 17, no. 166 (May 2020): 20200175. http://dx.doi.org/10.1098/rsif.2020.0175.

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A mathematical model is proposed for shape evolution and locomotion of fish epidermal keratocytes on elastic substrates. The model is based on mechanosensing concepts: cells apply contractile forces onto the elastic substrate, while cell shape evolution depends locally on the substrate stress generated by themselves or external mechanical stimuli acting on the substrate. We use the level set method to study the behaviour of the model numerically, and predict a number of distinct phenomena observed in experiments, such as (i) symmetry breaking from the stationary centrosymmetric to the well-known steadily propagating crescent shape, (ii) asymmetric bipedal oscillations and travelling waves in the lamellipodium leading edge, (iii) response to remote mechanical stress externally applied to the substrate (tensotaxis) and (iv) changing direction of motion towards an interface with a rigid substrate (durotaxis).

48

Lachowski, Dariusz, Ernesto Cortes, Benjamin Robinson, Alistair Rice, Krista Rombouts, and Armando E. Del Río Hernández. "FAK controls the mechanical activation of YAP, a transcriptional regulator required for durotaxis." FASEB Journal 32, no. 2 (January 3, 2018): 1099–107. http://dx.doi.org/10.1096/fj.201700721r.

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49

Walker, Matthew L., David House, Margrit Betke, and Joyce Y. Wong. "Using Automated Cell Tracking Software to Quantifying Durokinesis and Durotaxis in Real Time." Biophysical Journal 96, no. 3 (February 2009): 633a. http://dx.doi.org/10.1016/j.bpj.2008.12.3347.

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Sunyer, Raimon, Albert J. Jin, Ralph Nossal, and Dan L. Sackett. "Fabrication of Hydrogels with Gradient of Compliance: Application to Cell Mechanotaxis and Durotaxis." Biophysical Journal 102, no. 3 (January 2012): 565a. http://dx.doi.org/10.1016/j.bpj.2011.11.3077.

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