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The MEKK1-JNK pathway plays a protective role in pressure overload but does not mediate cardiac hypertrophy
Junichi Sadoshima, … , Dorothy E. Vatner, Stephen F. Vatner
Junichi Sadoshima, … , Dorothy E. Vatner, Stephen F. Vatner
Published July 15, 2002
Citation Information: J Clin Invest. 2002;110(2):271-279. https://doi.org/10.1172/JCI14938.
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Article Genetics

The MEKK1-JNK pathway plays a protective role in pressure overload but does not mediate cardiac hypertrophy

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Abstract

Research Article

Authors

Junichi Sadoshima, Olivier Montagne, Qian Wang, Guiping Yang, Jill Warden, Jing Liu, Gen Takagi, Vijaya Karoor, Chull Hong, Gary L. Johnson, Dorothy E. Vatner, Stephen F. Vatner

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Figure 1

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Activation of JNK by pressure overload is abolished, while that of ERKs ...
Activation of JNK by pressure overload is abolished, while that of ERKs and p38-MAPKs is preserved, in MEKK1–/– mice. Aortic banding (B) or sham operation (S) was performed in MEKK1+/+ or MEKK1–/– mice. The animals were sacrificed at 1, 7, or 14 days. (a and b) The kinase activity of p46-JNK was determined by anti–phosphospecific JNK antibody. Duplicate samples were subjected to immunoblot analyses with anti-JNK1 antibody. In b, the mean of the phospho-p46-JNKs/total JNK1 in control mice with sham operation is expressed as 1 in each group. *P < 0.05, **P < 0.001 vs. control sham-operated in each group. (c) Animals were sacrificed at 7 days. The activity of ERKs and p38-MAPKs was evaluated by immunoblotting with anti-phosphospecific antibody. The filters were reprobed with anti–non-phosphospecific antibody after stripping. The results were representative of five samples per group.

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