Journal
CELL CALCIUM
Volume 69, Issue -, Pages 37-45Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.ceca.2017.05.011
Keywords
Polycystins; TRPP2; Apoptosis; Autophagy; ADPKD; Calcium signaling
Categories
Funding
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico - Brazil
- NIH [5P01DK057751, P30DK090744]
- NATIONAL CENTER FOR ADVANCING TRANSLATIONAL SCIENCES [UL1TR001863] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P01DK057751, P30DK090744] Funding Source: NIH RePORTER
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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. (c) 2017 Elsevier Ltd. All rights reserved.
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