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Tumor suppressor pulls double shift as reprogramming watchdog
Date:8/9/2009

l cells, demonstrating that p53 clearly played an important role in reigning in cells trying to revert back into a stem-like state.

Because iPSCs generated with the full complement of reprogramming factors run the risk to turn malignant, Belmonte and his team wanted to know whether mouse cells lacking p53 could be reprogrammed using only two factors, Oct4 and Sox2. The cells readily converted into iPSCs and gave rise to healthy, full term mice that were able to reproduce passing the ultimate test for pluripotent embryonic stem cells.

"This very successful collaboration is a prime example of what makes the Salk such a special place," says Wahl. "Juan Carlos and I talk every day and we approach the same question from very different perspectives. He comes from a developmental biology perspective, while I come from the cancer side but when put together they can make for a great story."


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Contact: Gina Kirchweger
kirchweger@salk.edu
858-453-4100 x1340
Salk Institute
Source:Eurekalert  

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Tumor suppressor pulls double shift as reprogramming watchdog
Tumor suppressor pulls double shift as reprogramming watchdog
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