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.
"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 of genetic experiments using traditional knockout ...
