ArticleCirculation research2008
Cytoskeletal protein 4.1R affects repolarization and regulates calcium handling in the heart.
Article in Circulation research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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.
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Who cites it
31 citing papers in PubMed, 52 citations in OpenAlex.
- Reducing Granules Without Splicing Restoration Alleviates RBM20 Cardiomyopathy.Circulation research · 2025Article
- PKR associates with 4.1R to promote anchorage-independent growth of hepatocellular carcinoma and lead to poor prognosis.Scientific reports · 2024Article
- Cytoskeletal Protein 4.1R in Health and Diseases.Biomolecules · 2024Review
- Verteporfin treatment controls morphology, phenotype, and global gene expression for cells of the human nucleus pulposus.JOR spine · 2020Article
- Cytoskeleton protein 4.1R regulates B-cell fate by modulating the canonical NF-κB pathway.Immunology · 2020Article
- Supporting the heart: Functions of the cardiomyocyte's non-sarcomeric cytoskeleton.Journal of molecular and cellular cardiology · 2019Review
- Cytoskeletal Protein 4.1R Is a Positive Regulator of the FcεRI Signaling and Chemotaxis in Mast Cells.Frontiers in immunology · 2019Article
- Riding the waves of the intercalated disc of the heart.Biophysical reviews · 2018Review
- Spectrin-based pathways underlying electrical and mechanical dysfunction in cardiac disease.Expert review of cardiovascular therapy · 2018Article
- Protein 4.1R Influences Myogenin Protein Stability and Skeletal Muscle Differentiation.The Journal of biological chemistry · 2016Article
- Repression of the Central Splicing Regulator RBFox2 Is Functionally Linked to Pressure Overload-Induced Heart Failure.Cell reports · 2015Article
- Dysfunction in the βII spectrin-dependent cytoskeleton underlies human arrhythmia.Circulation · 2015Article
- Comprehensive characterization of protein 4.1 expression in epithelium of large intestine.Histochemistry and cell biology · 2014Article
- A 130-kDa protein 4.1B regulates cell adhesion, spreading, and migration of mouse embryo fibroblasts by influencing actin cytoskeleton organization.The Journal of biological chemistry · 2014Article
- Cardiomyocyte growth and sarcomerogenesis at the intercalated disc.Cellular and molecular life sciences : CMLS · 2014Article
- Article
- Impaired intestinal calcium absorption in protein 4.1R-deficient mice due to altered expression of plasma membrane calcium ATPase 1b (PMCA1b).The Journal of biological chemistry · 2013Article
- The effect of microgrooved culture substrates on calcium cycling of cardiac myocytes derived from human induced pluripotent stem cells.Biomaterials · 2013Article
- Ankyrin-B reduction enhances Ca spark-mediated SR Ca release promoting cardiac myocyte arrhythmic activity.Journal of molecular and cellular cardiology · 2012Article
- Reduced Na(+) and higher K(+) channel expression and function contribute to right ventricular origin of arrhythmias in Scn5a+/- mice.Open biology · 2012Article
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
The 4.1 proteins are a family of multifunctional adaptor proteins. They promote the mechanical stability of plasma membranes by interaction with the cytoskeletal proteins spectrin and actin and are required for the cell surface expression of a number of transmembrane proteins. Protein 4.1R is expressed in heart and upregulated in deteriorating human heart failure, but its functional role in myocardium is unknown. To investigate the role of protein 4.1R on myocardial contractility and electrophysiology, we studied 4.1R-deficient (knockout) mice (4.1R KO). ECG analysis revealed reduced heart rate with prolonged Q-T interval in 4.1R KO. No changes in ejection fraction and fractional shortening, assessed by echocardiography, were found. The action potential duration in isolated ventricular myocytes was prolonged in 4.1R KO. Ca(2+) transients were larger and slower to decay in 4.1R KO. The sarcoplasmic reticulum Ca(2+) content and Ca(2+) sparks frequency were increased. The Na(+)/Ca(2+) exchanger current density was reduced in 4.1R KO. The transient inward current inactivation was faster and the persistent Na(+) current density was increased in the 4.1R KO group, with possible effects on action potential duration. Although no major morphological changes were noted, 4.1R KO hearts showed reduced expression of NaV1.5alpha and increased expression of protein 4.1G. Our data indicate an unexpected and novel role for the cytoskeletal protein 4.1R in modulating the functional properties of several cardiac ion transporters with consequences on cardiac electrophysiology and with possible significant roles during normal cardiac function and disease.
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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.