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 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.

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.

An anchored phosphatase-deacetylase complex participates in primary cilia development.

Structural dynamic insights revealed the mechanisms of PC1 activation by stalk-derived peptide agonists which can form a foundation for development of PC1 as a therapeutic target for ADPKD treatment.

Genetic and chemical genetic analysis pinpoint defective epithelial cells as the driver for NPHP like phenotypes in Invs mutants, demonstrate genetic interaction between Invs and Ift88 and identify the HDAC inhibitor valproic acid as a suppressor for Invs mutant phenotypes.

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.

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