ArticleThe Journal of biological chemistry2010
Basis for MAP4 dephosphorylation-related microtubule network densification in pressure overload cardiac hypertrophy.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- PP2Acα regulates cerebellar development via phosphorylation-dependent neuronal programs.iScience · 2026Article
- Further investigations on the influence of protein phosphatases on the signaling of muscarinic receptors in the atria of mouse hearts.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Cantharidin increases the force of contraction and protein phosphorylation in isolated human atria.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Protein Phosphatase 2A Improves Cardiac Functional Response to Ischemia and Sepsis.International journal of molecular sciences · 2022Article
- Study on diverse pathological characteristics of heart failure in different stages based on proteomics.Journal of cellular and molecular medicine · 2022Article
- Transcriptional, Post-Transcriptional, and Post-Translational Mechanisms Rewrite the Tubulin Code During Cardiac Hypertrophy and Failure.Frontiers in cell and developmental biology · 2022Article
- Kv7 channel trafficking by the microtubule network in vascular smooth muscle.Acta physiologica (Oxford, England) · 2021Review
- MAP4 as a New Candidate in Cardiovascular Disease.Frontiers in physiology · 2020Review
- Cardiac microtubules in health and heart disease.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- Supporting the heart: Functions of the cardiomyocyte's non-sarcomeric cytoskeleton.Journal of molecular and cellular cardiology · 2019Review
- RNA binding protein 24 deletion disrupts global alternative splicing and causes dilated cardiomyopathy.Protein & cell · 2019Article
- WIPI1 is a conserved mediator of right ventricular failure.JCI insight · 2019Article
- Age-Dependent Protein Expression of Serine/Threonine Phosphatases and Their Inhibitors in the Human Cardiac Atrium.Advances in medicine · 2019Article
- Suppression of detyrosinated microtubules improves cardiomyocyte function in human heart failure.Nature medicine · 2018Article
- ISGylation - a key to lock the cell gates for preventing the spread of threats.Journal of cell science · 2017Review
- Microtubule-associated protein-4 controls nanovesicle dynamics and T cell activation.Journal of cell science · 2017Article
- Proteasome failure promotes positioning of lysosomes around the aggresome via local block of microtubule-dependent transport.Molecular and cellular biology · 2014Article
- Unique catalytic activities and scaffolding of p21 activated kinase-1 in cardiovascular signaling.Frontiers in pharmacology · 2013Review
- X-ROS signaling in the heart and skeletal muscle: stretch-dependent local ROS regulates [Ca²⁺]i.Journal of molecular and cellular cardiology · 2013Review
- AMPK attenuates microtubule proliferation in cardiac hypertrophy.American journal of physiology. Heart and circulatory physiology · 2013Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Increased activity of Ser/Thr protein phosphatases types 1 (PP1) and 2A (PP2A) during maladaptive cardiac hypertrophy contributes to cardiac dysfunction and eventual failure, partly through effects on calcium metabolism. A second maladaptive feature of pressure overload cardiac hypertrophy that instead leads to heart failure by interfering with cardiac contraction and intracellular transport is a dense microtubule network stabilized by decoration with microtubule-associated protein 4 (MAP4). In an earlier study we showed that the major determinant of MAP4-microtubule affinity, and thus microtubule network density and stability, is site-specific MAP4 dephosphorylation at Ser-924 and to a lesser extent at Ser-1056; this was found to be prominent in hypertrophied myocardium. Therefore, in seeking the etiology of this MAP4 dephosphorylation, we looked here at PP2A and PP1, as well as the upstream p21-activated kinase 1, in maladaptive pressure overload cardiac hypertrophy. The activity of each was increased persistently during maladaptive hypertrophy, and overexpression of PP2A or PP1 in normal hearts reproduced both the microtubule network phenotype and the dephosphorylation of MAP4 Ser-924 and Ser-1056 seen in hypertrophy. Given the major microtubule-based abnormalities of contractile and transport function in maladaptive hypertrophy, these findings constitute a second important mechanism for phosphatase-dependent pathology in the hypertrophied and failing heart.
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Registered trials
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