Article
Alpha-actinin-4 and CLP36 protein deficiencies contribute to podocyte defects in multiple human glomerulopathies.
The Journal of biological chemistry - 2 Sept 2011
Liu Zhongmin, Blattner Simone Monika, Tu Yizeng, Tisherman Robert, Wang James H, Rastaldi Maria Pia, Kretzler Matthias, Wu Chuanyue
Abstract excerpt
Genetic alterations of α-actinin-4 can cause podocyte injury through multiple mechanisms. Although a mechanism involving gain-of-α-actinin-4 function was well described and is responsible for a dominantly inherited form of human focal segmental glomerulosclerosis (FSGS), evidence supporting mechanisms involving loss-of-α-actinin-4 function in human glomerular diseases remains elusive. Here we show that...
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