It has recently been recognized that cellular stresses activate certain members of the
mitogen-activated protein kinase (MAPK) superfamily. One role of these “stress-activated” …

" Stress-regulated" mitogen-activated protein kinases (SR-MAPKs) comprise the stress-
activated protein kinases (SAPKs)/c-Jun N-terminal kinases (JNKs) and the p38-MAPKs. In …

In this report we investigate the molecular mechanisms that contribute to tissue damage
following ischemia and ischemia coupled with reperfusion (ischemia/reperfusion) in the rat …

The best-characterized subfamilies of the mitogen-activated protein kinase (MAPK)
superfamily are the extracellularly responsive kinases (ERKs) and the two “stress …

Activation of stress-activated protein kinases, including the p38 and the c-Jun NH 2-terminal
kinases (JNK), have been associated with the onset of cardiac hypertrophy and cell death in …

We investigated the ability of phenylephrine (PE), an α-adrenergic agonist and promoter of
hypertrophic growth in the ventricular myocyte, to activate the three best-characterized …

Three well-characterized mitogen-activated protein kinase (MAPK) subfamilies are
expressed in rodent and rabbit hearts, and are activated by pathophysiological stimuli. We …

Ischemia and reperfusion lead to the rapid induction of proto-oncogenes in the heart and
subsequent induction of genes with cardioprotective functions. The activity of the …

Activation of stress-activated mitogen-activated protein kinases (SAPKs), mainly c-Jun N-
terminal kinase (JNK) and p38, have long been associated with different forms of cardiac …

Mitogen-activated protein kinases (MAPKs) have been shown to be activated in both in vitro
and in vivo models of cardiac tissue in response to ischemia/reperfusion injury. We …