Polycystins and cellular Ca2+ signaling.
The cystic phenotype in autosomal dominant polycystic kidney disease is characterized by a profound dysfunction of many cellular signaling patterns, ultimately leading to an increase in both cell proliferation and apoptotic cell death. Disturbance of normal cellular Ca(2+) signaling seems to be a primary event and is clearly involved in many pathways that may lead to both types of cellular responses. In this review, we summarize the current knowledge about the molecular and functional interactions between polycystins and multiple components of the cellular Ca(2+)-signaling machinery. In addition, we discuss the relevant downstream responses of the changed Ca(2+) signaling that ultimately lead to increased proliferation and increased apoptosis as observed in many cystic cell types.
Laboratory of Molecular and Cellular Signaling, Department of Cellular and Molecular Medicine, KU Leuven, Campus Gasthuisberg O/N-I, B-802, Herestraat 49, 3000, Leuven, Belgium.
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D
Mekahli
Jan B
JB
Parys
G
G
Bultynck
L
L
Missiaen
H
H
De Smedt
D017209:Apoptosis / Q000502:physiology*; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000502:physiology*; D049109:Cell Proliferation; D000242:Cyclic AMP / Q000378:metabolism; D006801:Humans; D007425:Intracellular Membranes / Q000378:metabolism; D008954:Models, Biological; D016891:Polycystic Kidney, Autosomal Dominant / Q000378:metabolism / Q000503:physiopathology*; D048493:Proto-Oncogene Proteins B-raf / Q000378:metabolism; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism; D050396:TRPP Cation Channels / Q000378:metabolism*
D050396:TRPP Cation Channels; D000242:Cyclic AMP; D048493:Proto-Oncogene Proteins B-raf; D058570:TOR Serine-Threonine Kinases; D002118:Calcium