共 14 条
[1]
Stimulation of "stress-regulated" mitogen-activated protein kinases (stress-activated protein kinases/c-Jun N-terminal kinases and p38-mitogen-activated protein kinases) in perfused rat hearts by oxidative and other stresses. Clerk A,Fuller SJ,Michael A,et al. Journal of Biological Chemistry . 1998
[2]
Hypoxia/reoxygenation stimulates Jun kinase activity through redox signaling in cardiac myocytes. Ladetorte KR,Webster KA. Circulation Research . 1997
[3]
Stimulation of c- Jun kinase and mitogen-activated protein kinase by ischemia and reperfusion in the perfused rat heart. Knight RJ,Baxton DB. Biochemical and Biophysical Research Communications . 1996
[4]
Stimulation of the stress-activated mitogen-activated protein kinase subfamilies in perfused heart. Bogoyevich MA,Gillespie Brown J,Ketterman AJ,et al. Circulation Research . 1996
[5]
Inhibition of p38 mitogen activated protein kinase decreases cardiomyocyte apoptosis and improves cardiac function after myocardial ischemia and reperfusion. Ma XL,Kumar S,Gao F,et al. Circulation . 1999
[6]
Tyrosine Phosphorylation and activation of mitogen-activated protein kinase in the rat brain following transient cerebral ischemia. Hu BR,Wieloch T. Journal of Neurochemistry . 1994
[7]
The stressactivated protein kinase are major c-Jun amino-terminal kinase activated by ischemia and reperfusion. Pombo CM,Bonventre JV,Arruch J,et al. Journal of Biological Chemistry . 1994
[8]
p38 MAPK inhibition decreases TNF -αproduction and enhances postischemic human myocardial function. Cain BS,Meldrum DR,Meng X,et al. Journal of Surgical Research . 1999
[9]
Oxidative stress induces DNA fragmentation and caspase activation via the c - Jun NH2 -terminal kinase pathway in H9c2 cardiac muscle cells. Turner NA,Xia F,Azhar G,et al. Journal of Molecular and Cellular Cardiology . 1998
[10]
PKC-dependent activation of p44/p42MAPKs during myocardial ischemia-reperfusion in conscious rabbits. Ping P,Zhang J,cao X,et al. American Journal of Physiology . 1999