Key result
Supervillin interacts with TRIP6 at focal adhesions to promote the loss of focal adhesion structure and function, and RNAi-mediated decreases in either protein increase cell adhesion to fibronectin.
Population
In vitro cell model (rapidly moving cells)
Design
Preclinical
Authors
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SV negatively regulates FAs via TRIP6/LPP; leaves open its role in cardiovascular cell motility.
Supervillin interacts with TRIP6 at focal adhesions to promote the loss of focal adhesion structure and function, thereby regulating cell-substrate adhesion.
Takizawa et al. (2006) studied this question. Supervillin and TRIP6 modulation (RNAi) was evaluated on Focal adhesion structure and function. Supervillin interacts with TRIP6 at focal adhesions to promote the loss of focal adhesion structure and function, and RNAi-mediated decreases in either protein increase cell adhesion to fibronectin.