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Cancer related gene p53 not regulated as indicated by previous tissue culture research

in with an altered C-terminus instead of the normal version. Previous tissue culture studies by several labs around the world indicated that tinkering with the tail end prevented the protein from being flagged for degradation or activation. Instead of accumulating in mouse cells and halting cell division in the genetically engineered mice, the altered p53 protein performed flawlessly: it was unstable when no DNA damage was present and was stable and fully functional when needed to halt the cycle cell to repair DNA damage or to induce apoptosis.

"It came as a complete surprise. We even used a system that would have allowed us to switch on the modified p53 protein at will because we feared that the mice might not be viable and would die during early embryonic development," says Krummel.

More detailed investigations revealed that the altered p53 protein still binds to Mdm2, one of the negative regulators of p53 that facilitate its degradation.

When p53 is activated by DNA damage the same sites that are modified when the protein is slated for degradation, a different kind of chemical modification, so-called acetylation, takes place. But without acetylation, p53 functions just as well in mice, found the researchers.


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Source:Salk Institute


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