期刊
MOLECULAR BIOLOGY OF THE CELL
卷 24, 期 6, 页码 704-714出版社
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E12-06-0471
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资金
- National Institutes of Health [T32EY007092, F30HL110447, R01HL77870, R01GM065918, R01AR050501]
- National Science Foundation [BES0827719]
- National Science Foundation Graduate Research Fellowship Award
Vascular endothelial (VE)-cadherin, the major adherens junction adhesion molecule in endothelial cells, interacts with p120-catenin and beta-catenin through its cytoplasmic tail. However, the specific functional contributions of the catenins to the establishment of strong adhesion are not fully understood. Here we use bioengineering approaches to identify the roles of cadherin-catenin interactions in promoting strong cellular adhesion and the ability of the cells to spread on an adhesive surface. Our results demonstrate that the domain of VE-cadherin that binds to beta-catenin is required for the establishment of strong steady-state adhesion strength. Surprisingly, p120 binding to the cadherin tail had no effect on the strength of adhesion when the available adhesive area was limited. Instead, the binding of VE-cadherin to p120 regulates adhesive contact area in a Rac1-dependent manner. These findings reveal that p120 and beta-catenin have distinct but complementary roles in strengthening cadherin-mediated adhesion.
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