Stress-responsive mitogen-activated protein kinases (c-Jun N-terminal kinases and p38 mitogen-activated protein kinases) in the myocardium

被引：437

作者：

Sugden, PH

Clerk, A

机构：

[1] Univ London Imperial Coll Sci Technol & Med, Sch Med, NHLI Div Cardiac Med, London SW3 6LY, England

[2] Univ London Imperial Coll Sci Technol & Med, Sch Med, Div Biomed Sci, London SW3 6LY, England

来源：

CIRCULATION RESEARCH | 1998年 / 83卷 / 04期

关键词：

D O I：

10.1161/01.RES.83.4.345

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

引用

页码：345 / 352

页数：8

共 79 条

[11] Cell stress-induced phosphorylation of ATF2 and c-Jun transcription factors in rat ventricular myocytes
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[13] Stimulation of the p38 mitogen-activated protein kinase pathway in neonatal rat ventricular myocytes by the G protein-coupled receptor agonists, endothelin-1 and phenylephrine: A role in cardiac myocyte hypertrophy?
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[14] 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
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[15] The p38-MAPK inhibitor, SB203580, inhibits cardiac stress-activated protein kinases/c-Jun N-terminal kinases (SAPKs/JNKs)
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[20] SB-203580 IS A SPECIFIC INHIBITOR OF A MAP KINASE HOMOLOG WHICH IS STIMULATED BY CELLULAR STRESSES AND INTERLEUKIN-1
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