Klaus B. Piontek

A functional floxed allele of Pkd1 that can be conditionally inactivated in vivo.

Loss of polycystin-1 or polycystin-2 results in dysregulated apolipoprotein expression in murine tissues via alterations in nuclear hormone receptors.

The mTOR pathway is regulated by polycystin-1, and its inhibition reverses renal cystogenesis in polycystic kidney disease.

Genetic interaction studies link autosomal dominant and recessive polycystic kidney disease in a common pathway.

Inactivation of Pkd1 in principal cells causes a more severe cystic kidney disease than in intercalated cells.

Polycystin-1 regulates extracellular signal-regulated kinase-dependent phosphorylation of tuberin to control cell size through mTOR and its downstream effectors S6K and 4EBP1.

Rapamycin ameliorates PKD resulting from conditional inactivation of Pkd1.

Pkd1 and Pkd2 are required for normal placental development.

Ectopic expression of Cux1 is associated with reduced p27 expression and increased apoptosis during late stage cyst progression upon inactivation of Pkd1 in collecting ducts.

Polycystin-1 regulates the stability and ubiquitination of transcription factor Jade-1.

Network analysis of a Pkd1-mouse model of autosomal dominant polycystic kidney disease identifies HNF4α as a disease modifier.

Impaired glomerulogenesis and endothelial cell migration in Pkd1-deficient renal organ cultures.

Small-molecule screening of PC3 prostate cancer cells identifies tilorone dihydrochloride to selectively inhibit cell growth based on cyclin-dependent kinase 5 expression.

MicroRNA-224 Induces G1/S Checkpoint Release in Liver Cancer.