ArticleThe Journal of clinical investigation1996
Regulation of human heart contractility by essential myosin light chain isoforms.
Article in The Journal of clinical investigation, 1996. 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, 135 citations in OpenAlex.
- Gene expression analysis of primary graft dysfunction in adult heart transplant recipients: A cohort study.JHLT open · 2025Article
- Article
- Fine tuning contractility: atrial sarcomere function in health and disease.American journal of physiology. Heart and circulatory physiology · 2024Review
- Developmental, physiologic and phylogenetic perspectives on the expression and regulation of myosin heavy chains in mammalian skeletal muscles.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2023Review
- Decreased left heart flow in fetal lambs causes left heart hypoplasia and pro-fibrotic tissue remodeling.Communications biology · 2023Article
- Myosin light-chain 4 gene-transfer attenuates atrial fibrosis while correcting autophagic flux dysregulation.Redox biology · 2023Article
- Prenatal phenotypes and pregnancy outcomes of fetuses with recurrent 1q21.1 microdeletions and microduplications.Frontiers in medicine · 2023Article
- NIMA-related kinase 9 regulates the phosphorylation of the essential myosin light chain in the heart.Nature communications · 2022Article
- Alpha and beta myosin isoforms and human atrial and ventricular contraction.Cellular and molecular life sciences : CMLS · 2021Review
- Expression of atrial‑fetal light chains in cultured human cardiomyocytes after chemical ischemia‑reperfusion injury.Molecular medicine reports · 2021Article
- Insights into myosin regulatory and essential light chains: a focus on their roles in cardiac and skeletal muscle function, development and disease.Journal of muscle research and cell motility · 2020Article
- Tissue Expression of Atrial and Ventricular Myosin Light Chains in the Mechanism of Adaptation to Oxidative Stress.International journal of molecular sciences · 2020Article
- Human cardiac myosin light chain 4 (MYL4) mosaic expression patterns vary by sex.Scientific reports · 2019Article
- Atrial-like Engineered Heart Tissue: An In Vitro Model of the Human Atrium.Stem cell reports · 2018Article
- Determining the Pathogenicity of a Genomic Variant of Uncertain Significance Using CRISPR/Cas9 and Human-Induced Pluripotent Stem Cells.Circulation · 2018Article
- Thick Filament Protein Network, Functions, and Disease Association.Comprehensive Physiology · 2018Review
- A Cardiomyopathy Mutation in the Myosin Essential Light Chain Alters Actomyosin Structure.Biophysical journal · 2017Article
- Dynamic changes in the mouse skeletal muscle proteome during denervation-induced atrophy.Disease models & mechanisms · 2017Article
- Altered Right Ventricular Mechanical Properties Are Afterload Dependent in a Rodent Model of Bronchopulmonary Dysplasia.Frontiers in physiology · 2017Article
- S100A1 transgenic treatment of acute heart failure causes proteomic changes in rats.Molecular medicine reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most of the patients with congenital heart diseases express the atrial myosin light chain 1 (ALC-1) in the right ventricle. We investigated the functional consequences of ALC-1 expression on the myosin cycling kinetics in the intact sarcomeric structure using multicellular demembranated fibers ("skinned fibers") from the right ventricular infundibulum of patients with Tetralogy of Fallot (TOF), double outlet right ventricle (DORV), and infundibular pulmonary stenosis (IPS), Force-velocity relation was analyzed by the constant-load technique at maximal Ca2+ activation (pCa 4.5). Half-time of tension development (t1/2) was investigated by monitoring contraction initiation upon photolytic release of ATP from caged-ATP in rigor. The patients investigated here expressed between 0 and 27% ALC-1. There was a statistically significant correlation between ALC-l and maximal shortening velocity (Vmax) which rose 1.87-fold from 1.2 muscle length per second (ML/s) to 2.25 ML/s in a normal (0% ALC-1) and diseased (19.9% ALC-1) ventricle. Half-time of tension development decreased 1.85-fold with increasing ALC-1 expression (t1/2) was 0.252 s and 0.136 s at 2 and 18.4% ALC-1, respectively). We conclude that the expression of ALC-1 in the human heart modulates cross-bridge cycling kinetics accelerating shortening velocity and isometric tension production.
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.