Alpha-actinin-4 and CLP36 protein deficiencies contribute to podocyte defects in multiple human glomerulopathies.

@article{Liu2011Alphaactinin4AC,
  title={Alpha-actinin-4 and CLP36 protein deficiencies contribute to podocyte defects in multiple human glomerulopathies.},
  author={Zhongmin Liu and Simone Monika Blattner and Yizeng Tu and Robert Tisherman and James H-C Wang and Maria P Rastaldi and Matthias Kretzler and Chuanyue Wu},
  journal={The Journal of biological chemistry},
  year={2011},
  volume={286 35},
  pages={30795-805}
}
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 α-actinin-4 deficiency occurs in multiple human primary glomerulopathies including sporadic… CONTINUE READING
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