ARF-p19, a novel regulator of the mammalian cell cycle (SJ-95-0006)
- *Abstract
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This invention provides nucleic acids, polypeptides, peptide fragments, antibodies and methods of using an alternative reading frame of the Ink4a locus (ARF). Also provided are domains involved in the interaction between ARF and Hdm2. ARF encodes a potent tumor suppressor protein that interacts with the regulator protein Hdm2 to induce p53 mediated cell cycle arrest. ARF is a potential prodrug for cancer therapy as well as a useful screening target for anti-cancer drug design and discovery.
Key words: Tumor suppressor, cancer therapy, cancer drug, screening target, ARF, Hdm2, p53
Granted patents or published applications: US Patent Nos. 5,723,313; 5,876,965;6,172,194; 6,407,062; 6482,929; 6,586,203; 7,704,703
Related scientific references: Sherr C. J., Weber J. D. "The ARF/p53 pathway" Curr. Opin. Genet. Dev. 10: 94-99 (2000).
Weber J. D., et. al. "p53-independent functions of the p19ARF tumor suppressor" Genes Dev. 14: 2358-2365 (2000);Quelle D.E. et. al. "Alternative reading frames of the INK4a tumor suppressor gene encode unrelated proteins capable of inducing cell cycle arrest" Cell 83(6):993-1000 (1995);
Bothner, B. et al., "Peptides derived from two dynamically disordered proteins self-assemble into amyloid-like fibrils", J. Am. Chem. Soc. 125(11): 3200-3201 (March 2003)
Williams RT et al., "Arf gene loss enhances oncogenicity and limits imatinib response in mouse models of Bcr-Abl-induced acute lymphoblastic leukemia" Proc Natl Acad Sci USA.;103(17):6688-93; Apr 25 2006
- Country/Region
- USA
