Cells That Lack p19Ink4d and p27Kip1 Activity/p19Ink4d and p27Kip1 Null Mice (SJ-98-0023)

Description

This invention describes a mouse model for neuronal proliferation, bradykinesia and seizures which lack p19ink4d and p27kip1 proteins. It is a useful model for identifying potential therapeutic agents for treatment of hearing and balance disorders.

Keywords

p19ink4d, p27Kip1

Granted Patents or Published Applications

U.S. Patent Nos. 6,245,965; 6,589,505

Related Scientific References

Chen P, et al., “Progressive hearing loss in mice lacking the cyclin-dependent kinase inhibitor Ink4d”, Nat Cell Biol. 5(5):422-6 (2003);

Cunningham J, et al., “The cyclin-dependent kinase inhibitors p19(Ink4d) and p27(Kip1) are coexpressed in select retinal cells and act cooperatively to control cell cycle exit”, Mol Cell Neurosci. 19(3):359-74 (2002);

Zindy F, et al., “Postnatal neuronal proliferation in mice lacking Ink4d and Kip1 inhibitors of cyclin-dependent kinases”, Proc Natl Acad Sci 9;96(23):13462-7 (1999);

Zindy F, et al., “Expression of INK4 inhibitors of cyclin D-dependent kinases during mouse brain development,” Cell Growth & Differ. 8(11):1139-50 (1997).

Licensing Opportunities

We are currently seeking licensing opportunities in all fields for this technology. Contact: chad.riggs@stjude.org