Kidney-specific inactivation of the KIF3A subunit of kinesin-II inhibits renal ciliogenesis and produces polycystic kidney disease.

@article{Lin2003KidneyspecificIO,
  title={Kidney-specific inactivation of the KIF3A subunit of kinesin-II inhibits renal ciliogenesis and produces polycystic kidney disease.},
  author={Fangming Lin and Thomas Hiesberger and Kimberly R. Cordes and Angus M. Sinclair and Lawrence S. B. Goldstein and Stefan Somlo and Peter Igarashi},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2003},
  volume={100 9},
  pages={5286-91}
}
Polycystic kidney disease (PKD) is the most common genetic cause of renal failure in humans. Several proteins that are encoded by genes associated with PKD have recently been identified in primary cilia in renal tubular epithelia. These findings have suggested that abnormalities in cilia formation and function may play a role in the pathogenesis of PKD. To directly determine whether cilia are essential to maintain tubular integrity, we conditionally inactivated KIF3A, a subunit of kinesin-II… CONTINUE READING
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