Ontology type: schema:ScholarlyArticle
2002-02-18
AUTHORSPeter Koulen, Yiqiang Cai, Lin Geng, Yoshiko Maeda, Sayoko Nishimura, Ralph Witzgall, Barbara E. Ehrlich, Stefan Somlo
ABSTRACTPolycystin-2, the product of the gene mutated in type 2 autosomal dominant polycystic kidney disease (ADPKD), is the prototypical member of a subfamily of the transient receptor potential (TRP) channel superfamily, which is expressed abundantly in the endoplasmic reticulum (ER) membrane. Here, we show by single channel studies that polycystin-2 behaves as a calcium-activated, high conductance ER channel that is permeable to divalent cations. Epithelial cells overexpressing polycystin-2 show markedly augmented intracellular calcium release signals that are lost after carboxy-terminal truncation or by the introduction of a disease-causing missense mutation. These data suggest that polycystin-2 functions as a calcium-activated intracellular calcium release channel in vivo and that polycystic kidney disease results from the loss of a regulated intracellular calcium release signalling mechanism. More... »
PAGES191-197
http://scigraph.springernature.com/pub.10.1038/ncb754
DOIhttp://dx.doi.org/10.1038/ncb754
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