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Cell Calcium. 2018 Jan;69:37-45. doi: 10.1016/j.ceca.2017.05.011. Epub 2017 May 24.

Polycystin and calcium signaling in cell death and survival.

Author information

1
Department of Pharmacology, Yale University, 333 Cedar St, New Haven, CT, 06520, USA.
2
Department of Pharmacology, Yale University, 333 Cedar St, New Haven, CT, 06520, USA; Department of Cellular and Molecular Physiology, Yale University, 333 Cedar St, New Haven, CT, 06520, USA. Electronic address: barbara.ehrlich@yale.edu.

Abstract

Mutations in polycystin-1 (PC1) and polycystin-2 (PC2) result in a commonly occurring genetic disorder, called Autosomal Dominant Polycystic Kidney Disease (ADPKD), that is characterized by the formation and development of kidney cysts. Epithelial cells with loss-of-function of PC1 or PC2 show higher rates of proliferation and apoptosis and reduced autophagy. PC1 is a large multifunctional transmembrane protein that serves as a sensor that is usually found in complex with PC2, a calcium (Ca2+)-permeable cation channel. In addition to decreased Ca2+ signaling, several other cell fate-related pathways are de-regulated in ADPKD, including cAMP, MAPK, Wnt, JAK-STAT, Hippo, Src, and mTOR. In this review we discuss how polycystins regulate cell death and survival, highlighting the complexity of molecular cascades that are involved in ADPKD.

KEYWORDS:

ADPKD; Apoptosis; Autophagy; Calcium signaling; Polycystins; TRPP2

PMID:
28601384
PMCID:
PMC5701862
DOI:
10.1016/j.ceca.2017.05.011
[Indexed for MEDLINE]
Free PMC Article

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