ArticleProceedings of the National Academy of Sciences of the United States of America1997
Nonmuscle myosin II-B is required for normal development of the mouse heart.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers, 1 of them a synthesis that pooled it.
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
137 citing papers in PubMed, 1 synthesis or guideline pooled it, 305 citations in OpenAlex.
- GGCX-Associated Phenotypes: An Overview in Search of Genotype-Phenotype Correlations.International journal of molecular sciences · 2017Pooled it
- Research progress on the function of non-muscle myosin II during cell division.Frontiers in cell and developmental biology · 2026Review
- Article
- Ventral body wall closure: Mechanistic insights from mouse models and translation to human pathology.Developmental dynamics : an official publication of the American Association of Anatomists · 2025Review
- myh9b is a critical non-muscle myosin II encoding gene that interacts with myh9a and myh10 during zebrafish development in both compensatory and redundant pathways.G3 (Bethesda, Md.) · 2025Article
- Structure, regulation, and mechanisms of nonmuscle myosin-2.Cellular and molecular life sciences : CMLS · 2024Review
- Article
- Molecular Pathways and Animal Models of Tetralogy of Fallot and Double Outlet Right Ventricle.Advances in experimental medicine and biology · 2024Review
- Smoothelin-like protein 1 promotes insulin sensitivity and modulates the contractile properties of endometrial epithelial cells with insulin resistance.Frontiers in endocrinology · 2024Article
- MYH10 activation rescues contractile defects in arrhythmogenic cardiomyopathy (ACM).Nature communications · 2023Article
- Cardiac myofibrillogenesis is spatiotemporally modulated by the molecular chaperone UNC45B.Stem cell reports · 2023Article
- Actomyosin-mediated cellular tension promotes Yap nuclear translocation and myocardial proliferation through α5 integrin signaling.Development (Cambridge, England) · 2023Article
- Force- and cell state-dependent recruitment of Piezo1 drives focal adhesion dynamics and calcium entry.Science advances · 2022Article
- Heterozygous variants in MYH10 associated with neurodevelopmental disorders and congenital anomalies with evidence for primary cilia-dependent defects in Hedgehog signaling.Genetics in medicine : official journal of the American College of Medical Genetics · 2022Article
- Unique and redundant functions of cytoplasmic actins and nonmuscle myosin II isoforms at epithelial junctions.Annals of the New York Academy of Sciences · 2022Review
- Forces in stem cells and cancer stem cells.Cells & development · 2022Review
- MYH10 Governs Adipocyte Function and Adipogenesis through Its Interaction with GLUT4.International journal of molecular sciences · 2022Article
- Interspecies transcriptomics identify genes that underlie disproportionate foot growth in jerboas.Current biology : CB · 2022Article
- Micron-scale supramolecular myosin arrays help mediate cytoskeletal assembly at mature adherens junctions.The Journal of cell biology · 2022Article
- Smoothelin-Like Protein 1 Regulates the Thyroid Hormone-Induced Homeostasis and Remodeling of C2C12 Cells via the Modulation of Myosin Phosphatase.International journal of molecular sciences · 2021Article
77 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We used targeted gene disruption in mice to ablate nonmuscle myosin heavy chain B (NMHC-B), one of the two isoforms of nonmuscle myosin II present in all vertebrate cells. Approximately 65% of the NMHC-B-/- embryos died prior to birth, and those that were born suffered from congestive heart failure and died during the first day. No abnormalities were detected in NMHC-B+/- mice. The absence of NMHC-B resulted in a significant increase in the transverse diameters of the cardiac myocytes from 7.8 +/- 1.8 micron (right ventricle) and 7.8 +/- 1.3 micron (left ventricle) in NMHC-B+/+ and B+/- mice to 14.7 +/- 1.1 micron and 13.8 +/- 2.3 micron, respectively, in NMHC-B-/- mice (in both cases, P < 0.001). The increase in size of the cardiac myocytes was seen as early as embryonic day 12.5 (4.5 +/- 0.2 micron for NMHC-B+/+ and B+/- vs. 7. 2 +/- 0.6 micron for NMHC-B-/- mice (P < 0.01)). Six of seven NMHC-B-/- newborn mice analyzed by serial sectioning also showed structural cardiac defects, including a ventricular septal defect, an aortic root that either straddled the defect or originated from the right ventricle, and muscular obstruction to right ventricular outflow. Some of the hearts of NMHC-B-/- mice showed evidence for up-regulation of NMHC-A protein. These studies suggest that nonmuscle myosin II-B is required for normal cardiac myocyte development and that its absence results in structural defects resembling, in part, two common human congenital heart diseases, tetralogy of Fallot and double outlet right ventricle.
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.