Previous studies report a cross-talk between the polycystic kidney disease (PKD) and
tuberous sclerosis complex (TSC) genes. mTOR signalling is upregulated in PKD and …

Elucidation of structural information can greatly facilitate the understanding of molecular
function. A recent example is the description of the G-protein-coupled receptor (GPCR) …

Primary cilia play counterregulatory roles in cystogenesis—they inhibit cyst formation in the
normal renal tubule but promote cyst growth when the function of polycystins is impaired …

Mutations at a single locus, PKHD1, are responsible for causing human autosomal
recessive polycystic kidney disease (ARPKD). Recent studies suggest that the cystic …

Autosomal-dominant polycystic kidney disease (ADPKD) is the most prevalent inherited
renal disease, characterized by multiple cysts that can eventually lead to kidney failure …

Introduction Mutations in PKD1 and PKD2 cause autosomal dominant polycystic kidney
disease (ADPKD). Experimental evidence suggests an important role of the polycystins in …

Every day, human renal tubules process 140 l of glomerular filtrate into 1 l of urine. They
accomplish this by the coordinated function of distinct cell types occupying specific positions …

Abstract Polycystin-1 (PC1) has been proposed as a chief mechanosensing molecule
implicated in skeletogenesis and bone remodeling. Mechanotransduction via PC1 involves …

At present,~ 150 different members of the adhesion‐G protein‐coupled receptor (GPCR)
family have been identified in metazoans. Surprisingly, very little is known about their …

PKD1 is the most commonly mutated gene causing autosomal dominant polycystic kidney
disease (ADPKD). It encodes Polycystin-1 (PC1), a putative membrane protein that …