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(St. Jude Reference #)
|p53 Inhibitory Oligonucloeotides (SJ-09-0015)|
Researchers led by former Cancer Center Director Michael Kastan, MD, PhD, have discovered a small DNA oligonucleotide that can be used to inhibit the induction of p53 protein following exposure to DNA damaging agents and other types of cellular stress by a unique mechanism. This oligonucleotide, which can be as small as 8-15 bases in length, has potential to protect normal tissues from toxicity during treatment with chemotherapy or radiation therapy, to protect individuals from tissue toxicity associated with unplanned radiation exposures, and perhaps to reduce tissue injury during a heart attack or stroke.
|Keywords||p53 inhibition, oligonucleotide|
|Granted Patents or Published Applications||Pending provisional application|
|Related Scientific References||
Chen, J. et al., “Interactions of nucleolin and ribosomal protein L26 (RPL26) in the translational control of human p53”, J. Biol. Chem. (Epub. Mar. 20, 2012)
Chen, J. and Kastan, M., “5’–3’-UTR interactions regulate p53 mRNA translation and provide a target for modulating p53 induction after DNA damage”, Genes & Development 24(19): 2146-56 (Oct. 1, 2010).
|Licensing Opportunities||We are currently seeking licensing opportunities in all fields for the development of this technology.|
Contact the Office of Technology Licensing (Phone: 901-595-2342, Fax: 901-595-3148) for more information.
Last update: April 2012