The tumor suppressor, p53, is mutated in over 50% of human tumors, disabling its ability to bind DNA and induce transcription of its target genes. The aim is to stabilize mutant p53 into wild type conformation and restore its tumor suppressive activity. We found that mutant p53 conformation is stabilized towards a wild-type conformation in mouse embryonic stem cells. We proceeded and performed mass spectrometry and found several candidate proteins for the stabilization of the mutant form into a wild type form. It might be possible to use the knowledge we obtained to produce peptides or increase protein expression of such proteins (by chemical inducers etc.) in malignant cells harboring mutant p53 and thus convert mutant p53 into wild type conformation, thus restoring its tumor suppressive activity leading to apoptosis of the malignant cells. We hope that by knocking down these factors in ESCs we can show that their presence is leading to the conversion of mutant p53 into wild type conformation and that in their absence mutant remains in its mutant conformation.
Project ID : 10-2013-696
The invention provides methods for stabilization of mutant p53 in embryonic stem cells by interacting proteins, compositions comprising the same and uses thereof for treatment of various conditions associated with mut-p53, such as, cancer.
Additional information can be provided upon request.
Project manager
Adi Elkeles
BD Manager
Project researchers
Tamar Geiger
T.A.U Tel Aviv University, Medicine-Sackler Faculty
Human Molecular Genetics
Varda Rotter
Weizmann Institute of Science (WIS),
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