Engineered open reading frame for p53

Details Engineered open reading frame for p53 Engineered open reading frame for p53

2005-06-28

2005-06-28

Switzer, Juliet C. (Department: 1634)

Organic compounds -- part of the class 532-570 series

Organic compounds

Carbohydrates or derivatives

C536S024300

Reexamination Certificate

active

06911538

ABSTRACT:
The transcription factor and tumor suppressor protein p53 is inactivated in many human cancers. Approximately forty percent of cancers carry large amounts of mutated full-length p53 protein with one of over 900 reported single amino acid changes in the p53 core domain that recognizes p53 DNA binding sites. The ability to restore function to these inactive p53 proteins would dramatically improve cancer therapy. Alternative open reading frames that are more easily engineered encode a wild-type p53. The alternative open reading frames are optimized for codon usage and expression of p53 proteins inE. coli, yeast and mammalian cells. The alternative open reading frames may additionally contain mutations that are naturally found in human cancers, substitutions that correspond to polymorphic p53 alleles, or mutations in residues that can be post-translationally modified.

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GenBank Accession (X60012, Jun. 23, 1994).
“Preferred Codons for Selected Species” obtained from http://www.uky.edu/pharmacy/ps/porter/codonusage/preferred_codons.htm, accessed Oct. 14, 2004; copyright 1999, last modified Sep. 28, 2001.
R. K. Brachmann et al., “Genetic selection of intragenic suppressor mutations that reverse the effect of common p53 cancer mutations”, The EMBO Journal, 1998, pp. 1847-1859, vol. 17, no. 7.

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