Abstract
Cilia play diverse roles in motility and sensory reception, and defects in their formation and function underlie cilia-related human diseases [1]. One such disease is polycystic kidney disease (PKD), a heritable nephropathy associated with defects in the formation and function of sensory (also known as primary) cilia within renal tubules of the kidney [2]. Because the assembly and maintenance of these sensory cilia depends upon the intraflagellar transport (IFT) of axoneme and ciliary membrane components, such as polycystins [3], defective IFT is one of the factors that can contribute to PKD.
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