The action of nitric oxide to enhance cell survival in chick cardiomyocytes is mediated through a cGMP and ERK1/2 pathway while p38 mitogen-activated protein kinase-dependent pathways do not alter cell death-Reference-Cited by-同舟云学术

The action of nitric oxide to enhance cell survival in chick cardiomyocytes is mediated through a cGMP and ERK1/2 pathway while p38 mitogen-activated protein kinase-dependent pathways do not alter cell death

Published:2008-06-28 Issue:7 Volume:93 Page:834-842
ISSN:0958-0670
Container-title:Experimental Physiology
language:en
Short-container-title:

Author:

Rabkin Simon W.,Tsang Michael Y. C.

Publisher

Wiley

Subject

Physiology,Physiology (medical),Nutrition and Dietetics

Link

http://onlinelibrary.wiley.com/wol1/doi/10.1113/expphysiol.2008.042176/fullpdf

Reference72 articles.

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3. Mitochondrial PKCɛ and MAPK form signaling modules in the murine heart: enhanced mitochondrial PKCɛ-MAPK interactions and differential MAPK activation in PKCɛ-induced cardioprotection;Baines;Circ Res,2002

4. Inhibition of the cardiac p38-MAPK pathway by SB203580 delays ischemic cell death;Barancik;J Cardiovasc Pharmacol,2000

5. Hypertensive end-organ damage and premature mortality are p38 mitogen-activated protein kinase-dependent in a rat model of cardiac hypertrophy and dysfunction;Behr;Circulation,2001

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