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Thus, Crk1/2 and CrkL are physically linked, functionally complement each other during podocyte foot process spreading, and together are required for developing typical foot process architecture.
Kim, A. H. et al. B cell-derived IL-4 acts on podocytes to induce proteinuria and foot process effacement.
In mice, podocyte-specific deletion of Crk1/2 prevents or attenuates foot process effacement in two models of podocyte injury.
Using the protamine sulfate model of acute podocyte injury, podocyte-specific deletion of Rac1 prevented foot process effacement.
These results suggest that Robo2 signaling acts as a negative regulator on nephrin to influence podocyte foot process architecture.
This suggests that cellular mechanisms governing lamellipodial protrusion in vitro are similar to those in vivo during foot process effacement.
To quantitiate these changes, the average podocyte foot process width (Wp) was measured.
This may represent a novel mechanism of podocyte foot process effacement in proteinuric disease.
Electron microscopy of glomerulus from transgenic mice showed extensive podocyte foot process effacement.
This reorganization of the actin cytoskeleton may be a situation reminiscent of foot process effacement.
Thus, the in vitro retraction of foot processes may reflect in vivo podocyte foot process effacement.
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