Outward calcium ion currents desensitize the human PKD2-L1 ion channel via a mechanism that is independent of cytosolic motifs.

Kidney-specific TFEB overexpression in transgenic mice closely recapitulates features observed in both TFEB- and TFE3-mediated human kidney tumors.

The primary cilia polycystin proteins, polycystin-1 and polycystin-2, affect cilia length in the kidney collecting duct epithelia, but only polycystin-2 is required for the functional ion channel in this organelle.

The selectivity characteristics of PC-2L1, which make it a principal source of calcium in primary cilia function, is presented and advances understanding of the similarity and differences of TRPP ion channels.

Arterial myocyte PKD2 channels are activated by vasoconstrictor stimuli, which increases blood pressure, are upregulated during hypertension and cell-specific knockout in vivo reduces both physiological blood pressure and hypertension.

Three-dimensional imaging was used to identify structural and quantitative features of developing lymphatics in the kidneys of mice, humans and in a genetic mouse model of polycystic kidney disease.

The RAB-28 GTPase regulates ciliary extracellular vesicle shedding, which may be important for neuron-glia communication.

PKD2 (polycystin-2) channels are a major component of a flow-sensing signaling mechanism in endothelial cells that stimulates vasodilation and reduces blood pressure.

Soluble fragments cleaved from the N-terminus of PC-1 activate the PC-1/PC-2 heteromeric polycystin channel, describing for the first time that the N-terminus itself is an endogenous ligand.

A transient receptor channel in Toxoplasma gondii that conducts calcium represents the first molecular element that initiates upstream calcium signals that activate parasite pathogenic pathways.