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Scripps Research study reveals new function of protein kinase pathway in tumor suppression

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"After these findings, we wanted to look downstream of p38 to see exactly how this MAP kinase mediates senescence," Sun explained. "We knew the effect of p38 is achieved through its ability to regulate its downstream substrates, so we started to investigate various substrate candidates to see which ones were involved."

Fortunately, Sun added, his research team could easily link up with a leading expert in the p38 field, Professor Jiahuai Han. The p38 gene was cloned by Han in 1994. Since then, the Han lab has identified some p38 downstream protein kinases, including PRAK, and has shown that PRAK can be activated by various stresses. The Han research group also engineered PRAK knockout mice, animals that lack the PRAK gene, expecting that these mice would be defective in stress response. To the researchers' surprise, the mice responded normally to stresses, an indication that this gene may not be required for the stress pathway.

Joining forces, Sun and Han collaborated to investigate the role of PRAK in senescence response and tumor suppression. They also enlisted the expertise of Scripps Research investigators John Yates and Peter Wright and their laboratory groups.

What the researchers found was that PRAK is required for ras to induce senescence in vitro in normal cells derived from a mouse. They also did an experiment to see if the lack of PRAK would make a difference in senescence induction in human cells. The team introduced double-strand RNA into normal human fibroblast cells to inhibit the expression of PRAK and then activated the ras oncogene in these cells. The results were identical to those in mouse cells. When PRAK was inactivated in normal human cells, these cells did not undergo premature senescence.

"These experiments tell us that PRAK in both human cells and in mouse cells is an essential component that mediates ras-induced senescence," said Sun.

The researchers wanted, next, to f
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Contact: Keith McKeown
kmckeown@scripps.edu
858-784-8134
Scripps Research Institute
25-Jan-2007


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