<figcaption> Credit: Courtesy of Kevan Shokat</figcaption>
Credit: Courtesy of Kevan Shokat

Applying chemical genetics to mice, Roger Davis at University of Massachusetts Medical School and the Howard Hughes Medical Institute, and colleagues found that JNK2 promotes phosphorylation and activation of cJun.1 "It is an elegant and solid paper that illustrates the power of chemical genetics and it settles a controversy in the field," says Faculty of 1000 member Filippo Giancotti of Memorial Sloan-Kettering Cancer Center in New York.

"Based on the knockout approach, it had been concluded that JNK2 is a negative regulator of cJun and cell proliferation whereas JNK1 promotes this process. [This contradicts] observations that both kinases phosphorylate the same sites in cJun. By introducing in mice a mutant form of JNK2 [that is] exquisitely sensitive to an otherwise inactive kinase inhibitor, the authors demonstrated that JNK2 promotes phosphorylation of cJun and cell proliferation.

This is a particularly vivid illustration that the interpretation...

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