Dissociation of p44 and p42 Mitogen-activated Protein Kinase Activation from Receptor-induced Hypertrophy in Neonatal Rat Ventricular Myocytes (*)
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Summary
MAPK activation is not sufficient for G protein receptor-mediated induction of cardiac cell growth and gene expression and is apparently not required for transcriptional activation of the ANF gene.
- Type
- article
- Published
- 1996-04-05
- Cited by
- 187
- References
- 42
- Access
- Open access
- OpenAlex
- https://openalex.org/W1968672667
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:6642361
Keywords
MAPK/ERK pathway, Internal medicine, Endocrinology, Protein kinase A, Phenylephrine
References
- MAP kinases: charting the regulatory pathways.
- Requirement for integration of signals from two distinct phosphorylation pathways for activation of MAP kinase
- Cell signalling and the control of gene transcription.
- Endothelin‐1, phorbol esters and phenylephrine stimulate MAP kinase activities in ventricular cardiomyocytes
- Mechanical stretch rapidly activates multiple signal transduction pathways in cardiac myocytes: potential involvement of an autocrine/paracrine mechanism.
- Gq- and ras-dependent pathways mediate hypertrophy of neonatal rat ventricular myocytes following alpha 1-adrenergic stimulation.
- Co-regulation of the atrial natriuretic factor and cardiac myosin light chain-2 genes during alpha-adrenergic stimulation of neonatal rat ventricular cells. Identification of cis sequences within an embryonic and a constitutive contractile protein gene which mediate inducible expression.
- Structure, organization, and expression of the rat cardiac myosin light chain-2 gene. Identification of a 250-base pair fragment which confers cardiac-specific expression.
- Regulation of cardiac gene expression during myocardial growth and hypertrophy: molecular studies of an adaptive physiologic response
- Alpha- and beta-adrenergic stimulation induces distinct patterns of immediate early gene expression in neonatal rat myocardial cells. fos/jun expression is associated with sarcomere assembly; Egr-1 induction is primarily an alpha 1-mediated response.
- Endothelin-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.
- Alpha 1-adrenergic stimulation of cardiac gene transcription in neonatal rat myocardial cells. Effects on myosin light chain-2 gene expression.
- The mitogen-activated protein kinase signal transduction pathway.
- The alpha 1A-adrenergic receptor subtype mediates biochemical, molecular, and morphologic features of cultured myocardial cell hypertrophy.
- Endothelin induction of inositol phospholipid hydrolysis, sarcomere assembly, and cardiac gene expression in ventricular myocytes. A paracrine mechanism for myocardial cell hypertrophy.
- Differential activation of protein kinase C isoforms by endothelin-1 and phenylephrine and subsequent stimulation of p42 and p44 mitogen-activated protein kinases in ventricular myocytes cultured from neonatal rat hearts.
- HRas-dependent pathways can activate morphological and genetic markers of cardiac muscle cell hypertrophy.
- Nuclear localization and regulation of erk- and rsk-encoded protein kinases
- Extracellular signal-regulated kinases: ERKs in progress.
- A synthetic inhibitor of the mitogen-activated protein kinase cascade.
Cited by
- A Role for the p38 Mitogen-activated Protein Kinase Pathway in Myocardial Cell Growth, Sarcomeric Organization, and Cardiac-specific Gene Expression
- Acute pressure overload could induce hypertrophic responses in the heart of angiotensin II type 1a knockout mice.
- Opposing Effects of Jun Kinase and p38 Mitogen-Activated Protein Kinases on Cardiomyocyte Hypertrophy
- Roles of heterotrimeric GTP-binding proteins in the progression of heart failure.
- Significance of ERK cascade compared with JAK/STAT and PI3-K pathway in gp130-mediated cardiac hypertrophy.
- Characterization of MAP kinase and PKC isoform and effect of ACE inhibition in hypertrophy in vivo.
- The role of Extracellular-Regulated Protein Kinase 2 (ERK2) in cardiac hypertrophic remodelling
- Changes in Cardiac Phenotype in Hypertrophy and Failure: From Receptor to Gene
- Cytokines and their receptors in cardiovascular diseases — role of gp130 signalling pathway in cardiac myocyte growth and maintenance
- Regulation of MAPK pathways in response to purinergic stimulation of adult rat cardiac myocytes
- G protein‐coupled receptors and signaling pathways regulating growth responses 1
- Analysis of the expression regulation of the human atrial myosin light chain 1 upon hypertrophic stimulation
- Mechanism of ATP-induced [Ca(2+)](i) mobilization in rat basilar smooth muscle cells.
- Adrenergic and muscarinic receptors in the human heart.
- Lactosylceramide promotes hypertrophy through ROS generation and activation of ERK1/2 in cardiomyocytes
- Multiple Signal Transduction Pathways Link Na+/K+-ATPase to Growth-related Genes in Cardiac Myocytes
- Phosphorylation of elk-1 by MEK/ERK pathway is necessary for c-fos gene activation during cardiac myocyte hypertrophy.
- Mechanical Strain Increases Expression of the Brain Natriuretic Peptide Gene in Rat Cardiac Myocytes*
- Cardiotrophin 1 (CT-1) Inhibition of Cardiac Myocyte Apoptosis via a Mitogen-activated Protein Kinase-dependent Pathway
- Cyclic Adenosine Monophosphate Inhibits Nitric Oxide‐Induced Apoptosis of Cardiac Muscle Cells in a c‐Jun N‐Terminal Kinase‐Dependent Manner
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