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December 1, 1995Journal of Biological ChemistryOpen Access

Cellular Stresses Differentially Activate c-Jun N-terminal Protein Kinases and Extracellular Signal-regulated Protein Kinases in Cultured Ventricular Myocytes

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Population

Ventricular myocytes cultured from neonatal rat hearts

Design

Preclinical

Follow-up

up to 4 hours

Authors

MBMarie A. BogoyevitchAKAlbert J. KettermanPSPeter H. Sugden

Discussion

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Overview

Should not alter clinical practice; leaves open whether JNK-ERK cross-talk modulates myocyte stress responses in vivo.

Structured PICO

P
Population
Ventricular myocytes cultured from neonatal rat hearts
I
Intervention
Cellular stresses including anisomycin, osmotic stress (sorbitol), endothelin-1, phorbol 12-myristate 13-acetate, and ATP depletion/repletion
O
Outcome
Activation of c-Jun N-terminal protein kinases (JNKs) and extracellular signal-regulated protein kinases (ERKs)surrogate

Cellular stresses differentially activate JNK and ERK pathways in cultured ventricular myocytes, suggesting cross-talk between these MAPK signaling cascades.

Cite This Study

Bogoyevitch et al. (1995) studied this question.

synapsesocial.com/papers/6a7064a68031ec7bb1dc4ea9https://doi.org/10.1074/jbc.270.50.29710
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Activation of the mitogen-activated protein kinase cascade by pertussis toxin-sensitive and -insensitive pathways in cultured ventricular cardiomyocytes1995 · 100 citations
  2. 2Endothelin-1 and fibroblast growth factors stimulate the mitogen-activated protein kinase signaling cascade in cardiac myocytes. The potential role of the cascade in the integration of two signaling pathways leading to myocyte hypertrophy.1994 · 389 citations
  3. 3Identification of an oncoprotein- and UV-responsive protein kinase that binds and potentiates the c-Jun activation domain.1993 · 1,910 citations
  4. 4Raf-1 kinase activity is necessary and sufficient for gene expression changes but not sufficient for cellular morphology changes associated with cardiac myocyte hypertrophy.1994 · 109 citations
  5. 5Endothelin inhibits adenylate cyclase and stimulates phosphoinositide hydrolysis in adult cardiac myocytes.1992 · 122 citations