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The team found depleting TRAF6 in prostate cancer cells reduced Akt activation. And mice with TRAF6 knocked down developed smaller prostate cancer tumors than those with active TRAF6. “We believe that TRAF6 is a previously unrecognized oncogene and is a new potential target for treating human cancers,” Lin said.

Having discovered this Akt activation pathway, Lin and colleagues are now trying to identify the enzyme that normally turns it off.

This is a short but fascinating news release from MD Anderson Cancer Center that is absolutely worth reading.

The researchers analysed a mutant form of Akt implicated in human breast cancer, finding that increased Akt ubiquitination contributes to the hyperactivation of Akt in the mutant cells. “We discovered this oncogenic Akt mutant is hyperubiquitinated,” Lin said. “If you disrupt its ubiquitination, you deactivate the mutant.”

Wow. So now all they have to do is identify the enzyme that turns it off… stuff like this reminds me why I’ve loved science since junior school – there’s something awesome and fascinating about science and biology.

Posted via web from sally church’s posterous

One Response to “Researchers from MD Anderson Cancer Center Identify New, Cancer-Causing Role for Protein”

  1. Pharma Ed

    Very promising news, and yes it is exciting! All I can say is good luck in identifying the enzyme that turns it off, its going to take a lot of persistance!

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