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The Journal of Clinical Investigation|July 18, 2002
The MEKK1-JNK pathway plays a protective role in pressure overload but does not mediate cardiac hypertrophyJunichi Sadoshima, Olivier Montagne, Qian Wang, et al.
Circulation Research|July 19, 2003
Type 5 adenylyl cyclase disruption alters not only sympathetic but also parasympathetic and calcium-mediated cardiac regulationSatoshi Okumura, Jun-ichi Kawabe, Atsuko Yatani, et al.
Circulation Research|October 18, 2008
Lats2 is a negative regulator of myocyte size in the heartYutaka Matsui, Noritsugu Nakano, Dan Shao, et al.
American Journal of Physiology. Heart and Circulatory Physiology|June 22, 2010
Effects of cardiac overexpression of type 6 adenylyl cyclase affects on the response to chronic pressure overloadAziz Guellich, Shumin Gao, Chull Hong, et al.
Circulation Research|December 24, 2005
H11 kinase prevents myocardial infarction by preemptive preconditioning of the heartChristophe Depre, Li Wang, Xiangzhen Sui, et al.
Circulation|October 18, 2006
Activation of the cardiac proteasome during pressure overload promotes ventricular hypertrophyChristophe Depre, Qian Wang, Lin Yan, et al.
Cardiovascular Research|September 23, 2003
Neurally-mediated increase in calcineurin activity regulates cardiac contractile function in absence of hypertrophyJoan Li, Atsuko Yatani, Song-Jung Kim, et al.
The Journal of Clinical Investigation|May 17, 2003
Activation of Mst1 causes dilated cardiomyopathy by stimulating apoptosis without compensatory ventricular myocyte hypertrophyShimako Yamamoto, Guiping Yang, Daniela Zablocki, et al.
Circulation|July 13, 2011
H11 kinase/heat shock protein 22 deletion impairs both nuclear and mitochondrial functions of STAT3 and accelerates the transition into heart failure on cardiac overloadHongyu Qiu, Paulo Lizano, Lydie Laure, et al.
American Journal of Physiology. Heart and Circulatory Physiology|September 1, 2009
Genetic inhibition of calcineurin induces diastolic dysfunction in mice with chronic pressure overloadRicardo J Gelpi, Shumin Gao, Peiyong Zhai, et al.
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