The objective of this core is to facilitate the use of mouse models to study Polycystic Kidney Disease.
- Pkd1 and Pkd2 Knock out alleles in a BL/6 background1,3.
- Pkd1v/v (knock in GPS cleavage mutant) in a BL/6 background4.
- Pkhd1del3-4 in a BL/6 background5.
- Pkd1 and Pkd2 conditional alleles in a BL/6 background1-3
- Pkd1 and Pkd2 conditional alleles with a reporter and tamoxifen Cre recombinase1-3.
- Pkd1 and Pkd2 conditional alleles with Pax8-rtTA and TetO-Cre which allows renal tubular inactivation6.
- Conditional alleles with other Cre recombinase lines available on request.
- Tissue specimens from Pkd1 null and Pkd2 null animals at E10.5, E12.5, E14.5
- Tissue specimens, blood and urine from Pkd1cond/cond; tamoxifen Cre, Rosa (and controls) induced at P212
- Specimens collected monthly post induction, correlated with ultrasound.
- Samples available from additional models upon request
- Model development and characterization
- Assistance with design of efficient breeding strategies
- Preclinical therapeutic trial assistance for research base members on a limited basis
- Piontek KB et al. A functional floxed allele of Pkd1 that can be conditionally inactivated in vivo. J Am Soc Nephrol. 2004; 15: 3035-43.
- Piontek KB et al. A critical developmental switch defines the kinetics of kidney cyst formation after loss of Pkd1. Nature Medicine. 2007; 13: 1490-5.
- Garcia-Gonzalez MA et al. Pkd1 and Pkd2 are required for normal placental development. PLoS One. 2010; 5, issue 9.
- Yu S, Hackmann K, Gao J et al. Essential role of cleavage of Polycystin-1 at G protein-coupled receptor proteolytic site for kidney tubular structure. Proc Natl Acad Sci USA. 2007; 104:18688-93.
- Garcia-Gonzalez MA et al. Genetic interaction studies link autosomal dominant and recessive polycystic kidney disease in a common pathway. Hum Mol Genet. 2007; 16:1940-50.
- Traykova-Brauch M et al. An efficient and versatile system for acute and chronic modulation of renal tubular function in transgenic mice. Nat Med. 2008; 14: 979-84.