Syndecan-4-dependent Rac1 regulation determines directional migration in response to the extracellular matrix. Export

@article{citeulike:2948476, abstract = {Cell migration in wound healing and disease is critically dependent on integration with the extracellular matrix, but the receptors that couple matrix topography to migratory behavior remain obscure. Using nano-engineered fibronectin surfaces and cell-derived matrices, we identify syndecan-4 as a key signaling receptor determining directional migration. In wild-type fibroblasts, syndecan-4 mediates the matrix-induced protein kinase Calpha (PKCalpha)-dependent activation of Rac1 and localizes Rac1 activity and membrane protrusion to the leading edge of the cell, resulting in persistent migration. In contrast, syndecan-4-null fibroblasts migrate randomly as a result of high delocalized Rac1 activity, whereas cells expressing a syndecan-4 cytodomain mutant deficient in PKCalpha regulation fail to localize active Rac1 to points of matrix engagement and consequently fail to recognize and respond to topographical changes in the matrix.}, address = {Wellcome Trust Centre for Cell-Matrix Research, Faculty of Life Sciences, University of Manchester, Manchester, England, UK.}, author = {Bass, M. D. and Roach, K. A. and Morgan, M. R. and Mostafavi-Pour, Z. and Schoen, T. and Muramatsu, T. and Mayer, U. and Ballestrem, C. and Spatz, J. P. and Humphries, M. J.}, citeulike-article-id = {2948476}, citeulike-linkout-0 = {http://dx.doi.org/10.1083/jcb.200610076}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/17485492}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=17485492}, day = {7}, doi = {10.1083/jcb.200610076}, issn = {0021-9525}, journal = {The Journal of cell biology}, keywords = {adhesion\_complex, directional\_migration, rac1, rhoa, syndecan, vincullin}, month = {May}, number = {3}, pages = {527--538}, posted-at = {2008-07-01 15:36:04}, priority = {2}, title = {Syndecan-4-dependent Rac1 regulation determines directional migration in response to the extracellular matrix.}, url = {http://dx.doi.org/10.1083/jcb.200610076}, volume = {177}, year = {2007} }

TY - JOUR ID - citeulike:2948476 L3 - citeulike-article-id:2948476 N2 - Cell migration in wound healing and disease is critically dependent on integration with the extracellular matrix, but the receptors that couple matrix topography to migratory behavior remain obscure. Using nano-engineered fibronectin surfaces and cell-derived matrices, we identify syndecan-4 as a key signaling receptor determining directional migration. In wild-type fibroblasts, syndecan-4 mediates the matrix-induced protein kinase Calpha (PKCalpha)-dependent activation of Rac1 and localizes Rac1 activity and membrane protrusion to the leading edge of the cell, resulting in persistent migration. In contrast, syndecan-4-null fibroblasts migrate randomly as a result of high delocalized Rac1 activity, whereas cells expressing a syndecan-4 cytodomain mutant deficient in PKCalpha regulation fail to localize active Rac1 to points of matrix engagement and consequently fail to recognize and respond to topographical changes in the matrix. IS - 3 JF - The Journal of cell biology SN - 0021-9525 AD - Wellcome Trust Centre for Cell-Matrix Research, Faculty of Life Sciences, University of Manchester, Manchester, England, UK. EP - 538 TI - Syndecan-4-dependent Rac1 regulation determines directional migration in response to the extracellular matrix. VL - 177 SP - 527 KW - adhesion_complex KW - directional_migration KW - rac1 KW - rhoa KW - syndecan KW - vincullin AU - Bass, MD AU - Roach, KA AU - Morgan, MR AU - Mostafavi-Pour, Z AU - Schoen, T AU - Muramatsu, T AU - Mayer, U AU - Ballestrem, C AU - Spatz, JP AU - Humphries, MJ PY - 2007/05/07/ UR - http://dx.doi.org/10.1083/jcb.200610076 ER -