ArticleCell reports2016
Atypical Protein Kinase C-Dependent Polarized Cell Division Is Required for Myocardial Trabeculation.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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
19 citing papers in PubMed, 37 citations in OpenAlex.
- β1 integrins regulate cellular behaviour and cardiomyocyte organization during ventricular wall formation.Cardiovascular research · 2024Article
- Epigenetic determinants and non-myocardial signaling pathways contributing to heart growth and regeneration.Pharmacology & therapeutics · 2024Review
- Nrg1 Regulates Cardiomyocyte Migration and Cell Cycle in Ventricular Development.Circulation research · 2023Article
- Left Ventricular Noncompaction Is Associated with Valvular Regurgitation and a Variety of Arrhythmias.Journal of cardiovascular development and disease · 2022Article
- The Endocardium and Heart Valves.Cold Spring Harbor perspectives in biology · 2020Review
- Development of the human heart.American journal of medical genetics. Part C, Seminars in medical genetics · 2020Review
- A susceptibility biomarker identification strategy based on significantly differentially expressed ceRNA triplets for ischemic cardiomyopathy.Bioscience reports · 2020Article
- Bearing My Heart: The Role of Extracellular Matrix on Cardiac Development, Homeostasis, and Injury Response.Frontiers in cell and developmental biology · 2020Review
- PCA via joint graph Laplacian and sparse constraint: Identification of differentially expressed genes and sample clustering on gene expression data.BMC bioinformatics · 2019Article
- Cardiomyocyte orientation modulated by the Numb family proteins-N-cadherin axis is essential for ventricular wall morphogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- YAP Partially Reprograms Chromatin Accessibility to Directly Induce Adult Cardiogenesis In Vivo.Developmental cell · 2019Article
- PKC and PKN in heart disease.Journal of molecular and cellular cardiology · 2019Review
- AFrontiers in pediatrics · 2019Article
- Notch and interacting signalling pathways in cardiac development, disease, and regeneration.Nature reviews. Cardiology · 2018Review
- Transcriptional regulation of cell shape during organ morphogenesis.The Journal of cell biology · 2018Review
- Mechanisms of Trabecular Formation and Specification During Cardiogenesis.Pediatric cardiology · 2018Review
- Recreating the Cardiac Microenvironment in Pluripotent Stem Cell Models of Human Physiology and Disease.Trends in cell biology · 2017Review
- Untangling the Biology of Genetic Cardiomyopathies with Pluripotent Stem Cell Disease Models.Current cardiology reports · 2017Review
- Cardiac Regeneration: Lessons From Development.Circulation research · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
A hallmark of cardiac development is the formation of myocardial trabeculations exclusively from the luminal surface of the primitive heart tube. Although a number of genetic defects in the endocardium and cardiac jelly disrupt myocardial trabeculation, the role of cell polarization remains unclear. Here, we demonstrate that atypical protein kinase C iota (Prkci) and its interacting partners are localized primarily to the luminal side of myocardial cells of early murine embryonic hearts. A subset of these cells undergoes polarized cell division with the cell division plane perpendicular to the heart's lumen. Disruption of the cell polarity complex by targeted gene mutations results in aberrant mitotic spindle alignment, loss of polarized cardiomyocyte division, and loss of normal myocardial trabeculation. Collectively, these results suggest that, in response to inductive signals, Prkci and its downstream partners direct polarized cell division of luminal myocardial cells to drive trabeculation in the nascent heart.
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What Socratic 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 Socratic graph.