期刊
JOURNAL OF CELL BIOLOGY
卷 177, 期 3, 页码 527-538出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200610076
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- Wellcome Trust [045225, 061149, 074941, 077100] Funding Source: Medline
Cell migration in wound healing and disease is critically dependent on integration with the extra-cellular 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 C alpha (PKC alpha)-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 PKC alpha regulation fall to localize active Rac1 to points of matrix engagement and consequently fail to recognize and respond to topographical changes in the matrix.
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