ArticleThe EMBO journal1997
MAP kinase- and Rho-dependent signals interact to regulate gene expression but not actin morphology in cardiac muscle cells.
Article in The EMBO journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 155 citations in OpenAlex.
- Advances in the mechanisms of the NLRP3 inflammasome in sepsis‑induced cardiomyopathy and targeted therapeutic studies (Review).Molecular medicine reports · 2026Review
- Review
- C3 exoenzyme impairs cell proliferation and apoptosis by altering the activity of transcription factors.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
- Reactive Oxygen Species: A Key Hallmark of Cardiovascular Disease.Advances in medicine · 2016Review
- Rho-associated kinase activity is an independent predictor of cardiovascular events in acute coronary syndrome.Hypertension (Dallas, Tex. : 1979) · 2015Article
- Substance P receptor antagonism: a potential novel treatment option for viral-myocarditis.BioMed research international · 2015Article
- Compartmentalization role of A-kinase anchoring proteins (AKAPs) in mediating protein kinase A (PKA) signaling and cardiomyocyte hypertrophy.International journal of molecular sciences · 2014Review
- Rho-associated kinase activity is a predictor of cardiovascular outcomes.Hypertension (Dallas, Tex. : 1979) · 2014Article
- RhoA regulation of cardiomyocyte differentiation.TheScientificWorldJournal · 2013Article
- Increased Rho kinase activity in congestive heart failure.European journal of heart failure · 2012Article
- Myocardin-related transcription factor A is a common mediator of mechanical stress- and neurohumoral stimulation-induced cardiac hypertrophic signaling leading to activation of brain natriuretic peptide gene expression.Molecular and cellular biology · 2010Article
- Revisited and revised: is RhoA always a villain in cardiac pathophysiology?Journal of cardiovascular translational research · 2010Review
- Differential effects of Pyk2 and FAK on the hypertrophic response of cardiac myocytes.Cell and tissue research · 2009Article
- RhoA-ROCK signaling is involved in contraction-mediated inhibition of SERCA2a expression in cardiomyocytes.Pflugers Archiv : European journal of physiology · 2009Article
- Focal adhesion kinase as a RhoA-activable signaling scaffold mediating Akt activation and cardiomyocyte protection.The Journal of biological chemistry · 2008Article
- RhoA GTPase and F-actin dynamically regulate the permeability of Cx43-made channels in rat cardiac myocytes.The Journal of biological chemistry · 2008Article
- The A-kinase anchoring protein (AKAP)-Lbc-signaling complex mediates alpha1 adrenergic receptor-induced cardiomyocyte hypertrophy.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- In Vivo beta-adrenergic activation of atrial natriuretic factor (ANF) reporter expression.Molecular and cellular biochemistry · 2006Article
- Phosphorylation-dependent degradation of p300 by doxorubicin-activated p38 mitogen-activated protein kinase in cardiac cells.Molecular and cellular biology · 2005Article
- Pleiotropic effects of statins.Annual review of pharmacology and toxicology · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Post-natal growth of cardiac muscle cells occurs by hypertrophy rather than division and is associated with changes in gene expression and muscle fiber morphology. We show here that the protein kinase MEKK1 can induce reporter gene expression from the atrial natriuretic factor (ANF) promoter, a genetic marker that is activated during in vivo hypertrophy. MEKK1 induced both stress-activated protein kinase (SAPK) and extracellular signal-regulated protein kinase (ERK) activity; however, while the SAPK cascade stimulated ANF expression, activation of the ERK cascade inhibited expression. C3 transferase, a specific inhibitor of the small GTPase Rho, also inhibited both MEKK- and phenylephrine-induced ANF expression, indicating an additional requirement for Rho-dependent signals. Microinjection or transfection of C3 transferase into the same cells did not disrupt actin muscle fiber morphology, indicating that Rho-dependent pathways do not regulate actin morphology in cardiac muscle cells. While active MEKK1 was a potent activator of hypertrophic gene expression, this kinase did not induce actin organization and prevented phenylephrine-induced organization. These data suggest that multiple signals control hypertrophic phenotypes. Positive and negative signals mediated by parallel MAP kinase cascades interact with Rho-dependent pathways to regulate hypertrophic gene expression while other signals induce muscle fiber morphology in cardiac muscle cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.