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This model carries a deletion of all five established Slco1a and 1b and two predicted Slco1a-like mouse genes.
Contains a cre-mediated deletion of the following established genes in the Slco1a/1b cluster: Slco1a1, Slco1a4, Slco1a5, Slco1a6 and Slco1b2.
OATPs facilitate sodium-independent uptake transport of a wide variety of organic endo and exogenous compounds, such as bile acids, steroid and thyroid hormones and their conjugates, and numerous drugs and toxins.
Useful in dissecting the contribution of the Slco1a/1b family in these processes.
Taconic cannot accept orders by weight for this model. Please note that shipments may contain animals with a larger weight variation.
Genetic Background: FVB/N Background
Origin: The Oatp1a/1b Cluster Knockout Mouse was developed in the laboratory of Alfred Schinkel of the Netherlands Cancer Institute in 2010. The model was generated by insertion of loxP sites into the Slco1a5 and Slco1b2 genes at both ends of the Slco1a/1b gene cluster in E14 embryonic stem cells derived from 129P2/OlaHsd mice, followed by Cre-mediated deletion and injecting the targeted cells into C57BL/6J blastocysts. Resultant chimeras were backcrossed to FVB/N mice for at least 7 generations (N7). Taconic received stock in 2010. The mice were derived by embryo transfer and are maintained by incrossing of homozygous mice.
Genetics: Wild type for Nnt mutation; carries Pde6brd1 mutation
van de Steeg E, Wagenaar E, van der Kruijssen CM, Burggraaff JE, de Waart DR, Elferink RP, Kenworthy KE, Schinkel AH (2010). Organic anion transporting polypeptide 1a/1b-knockout mice provide insights into hepatic handling of bilirubin, bile acids, and drugs. J. Clin. Invest. 120(8): 2942-52