Familial focal segmental glomerulosclerosis (FSGS)-linked α-actinin 4 (ACTN4) protein mutants lose ability to activate transcription by nuclear hormone receptors.

@article{Khurana2012FamilialFS,
  title={Familial focal segmental glomerulosclerosis (FSGS)-linked α-actinin 4 (ACTN4) protein mutants lose ability to activate transcription by nuclear hormone receptors.},
  author={Simran Khurana and Sharmistha Chakraborty and M. P. Lam and Yu Liu and Yu-Ting Su and Xuan Jen Zhao and Moin Saleem and Peter William Mathieson and Leslie A. Bruggeman and Hung-Ying Kao},
  journal={The Journal of biological chemistry},
  year={2012},
  volume={287 15},
  pages={12027-35}
}
Mutations in α-actinin 4 (ACTN4) are linked to familial forms of focal segmental glomerulosclerosis (FSGS), a kidney disease characterized by proteinuria due to podocyte injury. The mechanisms underlying ACTN4 mutant-associated FSGS are not completely understood. Although α-actinins are better known to cross-link actin filaments and modulate cytoskeletal organization, we have previously shown that ACTN4 interacts with transcription factors including estrogen receptor and MEF2s and potentiates… CONTINUE READING