ArticleMolecular and cellular biology2001
Regulation of mitogen-activated protein kinases in cardiac myocytes through the small G protein Rac1.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 151 citations in OpenAlex.
- KCNA2 variants cause dilated cardiomyopathy, obesity and sleep apnea through RAC-ERK pathway.EMBO molecular medicine · 2026Article
- Cardiomyocyte Rac1 signaling in hypertrophy, arrhythmia, and cardiac stress adaptation.Journal of molecular and cellular cardiology plus · 2025Review
- Cell division cycle protein 42-driven activation of the MKK3/6-p38 signaling pathway participates in cardiac remodeling in mice.Cellular and molecular life sciences : CMLS · 2025Article
- Roles of small GTPases in cardiac hypertrophy (Review).Molecular medicine reports · 2024Review
- DEF6(differentially exprehomolog) exacerbates pathological cardiac hypertrophy via RAC1.Cell death & disease · 2023Article
- Natriuretic Peptides: It Is Time for Guided Therapeutic Strategies Based on Their Molecular Mechanisms.International journal of molecular sciences · 2023Review
- Nexinhib20 Inhibits Neutrophil Adhesion and βJournal of immunology (Baltimore, Md. : 1950) · 2022Article
- Cardiomyocyte BRAF and type 1 RAF inhibitors promote cardiomyocyte and cardiac hypertrophy in mice in vivo.The Biochemical journal · 2022Article
- The glomerular filtration barrier: a structural target for novel kidney therapies.Nature reviews. Drug discovery · 2021Review
- Review
- Scoparone alleviates Ang II-induced pathological myocardial hypertrophy in mice by inhibiting oxidative stress.Journal of cellular and molecular medicine · 2021Article
- Long non-coding RNAs in the failing heart and vasculature.Non-coding RNA research · 2018Review
- Receptor-stimulated transamidation induces activation of Rac1 and Cdc42 and the regulation of dendritic spines.Neuropharmacology · 2017Article
- Phenanthrene exposure induces cardiac hypertrophy via reducing miR-133a expression by DNA methylation.Scientific reports · 2016Article
- Enriched environment reduces glioma growth through immune and non-immune mechanisms in mice.Nature communications · 2015Article
- Article
- A purine nucleotide biosynthesis enzyme guanosine monophosphate reductase is a suppressor of melanoma invasion.Cell reports · 2013Article
- p90 ribosomal S6 kinases play a significant role in early gene regulation in the cardiomyocyte response to G(q)-protein-coupled receptor stimuli, endothelin-1 and α(1)-adrenergic receptor agonists.The Biochemical journal · 2013Article
- Role of Rac1-mineralocorticoid-receptor signalling in renal and cardiac disease.Nature reviews. Nephrology · 2013Review
- Rac1 and RhoA differentially regulate angiotensinogen gene expression in stretched cardiac fibroblasts.Cardiovascular research · 2011Article
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Small guanine nucleotide-binding proteins of the Ras and Rho (Rac, Cdc42, and Rho) families have been implicated in cardiac myocyte hypertrophy, and this may involve the extracellular signal-related kinase (ERK), c-Jun N-terminal kinase (JNK), and/or p38 mitogen-activated protein kinase (MAPK) cascades. In other systems, Rac and Cdc42 have been particularly implicated in the activation of JNKs and p38-MAPKs. We examined the activation of Rho family small G proteins and the regulation of MAPKs through Rac1 in cardiac myocytes. Endothelin 1 and phenylephrine (both hypertrophic agonists) induced rapid activation of endogenous Rac1, and endothelin 1 also promoted significant activation of RhoA. Toxin B (which inactivates Rho family proteins) attenuated the activation of JNKs by hyperosmotic shock or endothelin 1 but had no effect on p38-MAPK activation. Toxin B also inhibited the activation of the ERK cascade by these stimuli. In transfection experiments, dominant-negative N17Rac1 inhibited activation of ERK by endothelin 1, whereas activated V12Rac1 cooperated with c-Raf to activate ERK. Rac1 may stimulate the ERK cascade either by promoting the phosphorylation of c-Raf or by increasing MEK1 and/or -2 association with c-Raf to facilitate MEK1 and/or -2 activation. In cardiac myocytes, toxin B attenuated c-Raf(Ser-338) phosphorylation (50 to 70% inhibition), but this had no effect on c-Raf activity. However, toxin B decreased both the association of MEK1 and/or -2 with c-Raf and c-Raf-associated ERK-activating activity. V12Rac1 cooperated with c-Raf to increase expression of atrial natriuretic factor (ANF), whereas N17Rac1 inhibited endothelin 1-stimulated ANF expression, indicating that the synergy between Rac1 and c-Raf is potentially physiologically important. We conclude that activation of Rac1 by hypertrophic stimuli contributes to the hypertrophic response by modulating the ERK and/or possibly the JNK (but not the p38-MAPK) cascades.
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