Click here to close Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly. We suggest using a current version of Chrome, FireFox, or Safari.
J Am Soc Nephrol October 1, 2004; 15 (10): 2528-36.

Intraflagellar transport and cilia-dependent renal disease: the ciliary hypothesis of polycystic kidney disease.

Pazour GJ .

Epithelial cells that line mammalian kidney nephrons have solitary nonmotile primary cilium projecting from their surface into the lumens of the ducts and tubules. Mutations that block the assembly of these cilia cause cystic kidney disease. The products of human autosomal dominant and recessive polycystic kidney disease genes and products of the nephronophthisis disease genes are at least partially localized to primary cilia. This suggests that the cilium serves as an organizing center for the early steps of the signal transduction pathway that is responsible for monitoring the integrity of the kidney nephron and controlling cell proliferation and differentiation.

PubMed ID: 15466257
Article link: J Am Soc Nephrol

Xenbase: The Xenopus laevis and X. tropicalis resource.
Version: 4.11.3

Major funding for Xenbase is provided by grant P41 HD064556