[PDF][PDF] JNK2 is a positive regulator of the cJun transcription factor
A Jaeschke, M Karasarides, JJ Ventura, A Ehrhardt… - Molecular cell, 2006 - cell.com
Molecular cell, 2006•cell.com
The cJun NH 2-terminal kinase (JNK) signal transduction pathway is established to be an
important mechanism of regulation of the cJun transcription factor. Studies of Jnk1−/− and
Jnk2−/− mice suggest that the JNK1 and JNK2 isoforms have opposite effects on cJun
expression and proliferation. Here, we demonstrate, using a chemical genetic approach, that
both JNK1 and JNK2 are positive regulators of these processes. We show that competition
between JNK1 and JNK2 contributes to the opposite phenotypes caused by JNK1 and JNK2 …
important mechanism of regulation of the cJun transcription factor. Studies of Jnk1−/− and
Jnk2−/− mice suggest that the JNK1 and JNK2 isoforms have opposite effects on cJun
expression and proliferation. Here, we demonstrate, using a chemical genetic approach, that
both JNK1 and JNK2 are positive regulators of these processes. We show that competition
between JNK1 and JNK2 contributes to the opposite phenotypes caused by JNK1 and JNK2 …
Summary
The cJun NH2-terminal kinase (JNK) signal transduction pathway is established to be an important mechanism of regulation of the cJun transcription factor. Studies of Jnk1−/− and Jnk2−/− mice suggest that the JNK1 and JNK2 isoforms have opposite effects on cJun expression and proliferation. Here, we demonstrate, using a chemical genetic approach, that both JNK1 and JNK2 are positive regulators of these processes. We show that competition between JNK1 and JNK2 contributes to the opposite phenotypes caused by JNK1 and JNK2 deficiency. Our analysis illustrates the power of a chemical genetics approach for the analysis of signal transduction pathways and also highlights the limitations of single gene knockout strategies for the analysis of signaling pathways that are formed by a network of interacting proteins.
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