ArticleProceedings of the National Academy of Sciences of the United States of America1997
Rescue of cardiac alpha-actin-deficient mice by enteric smooth muscle gamma-actin.
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 67 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
67 citing papers in PubMed, 191 citations in OpenAlex.
- Dilated Cardiomyopathy - Exploring the Underlying Causes.Medical research archives · 2024Article
- Actin Alpha 2, Smooth Muscle (ACTA2) Is Involved in the Migratory Potential of Malignant Gliomas, and Its Increased Expression at Recurrence Is a Significant Adverse Prognostic Factor.Brain sciences · 2023Article
- Actin polymerization and depolymerization in developing vertebrates.Frontiers in physiology · 2023Review
- Human deafness-associated variants alter the dynamics of key molecules in hair cell stereocilia F-actin cores.Human genetics · 2022Review
- The Oxidative Balance Orchestrates the Main Keystones of the Functional Activity of Cardiomyocytes.Oxidative medicine and cellular longevity · 2022Review
- The remodelling of actin composition as a hallmark of cancer.Translational oncology · 2021Review
- Article
- Age-Onset Phosphorylation of a Minor Actin Variant Promotes Intestinal Barrier Dysfunction.Developmental cell · 2019Article
- Extracellular Matrix in Regulation of Contractile System in Cardiomyocytes.International journal of molecular sciences · 2019Review
- High-throughput screen, using time-resolved FRET, yields actin-binding compounds that modulate actin-myosin structure and function.The Journal of biological chemistry · 2018Article
- The makings of the 'actin code': regulation of actin's biological function at the amino acid and nucleotide level.Journal of cell science · 2018Review
- Biomechanical defects and rescue of cardiomyocytes expressing pathologic nuclear lamins.Cardiovascular research · 2018Article
- Absence of the Drosophila jump muscle actin Act79B is compensated by up-regulation of Act88F.Developmental dynamics : an official publication of the American Association of Anatomists · 2018Article
- Impaired muscle relaxation and mitochondrial fission associated with genetic ablation of cytoplasmic actin isoforms.The FEBS journal · 2018Article
- Misato underlies visceral myopathy in Drosophila.Scientific reports · 2017Article
- Overview of the Muscle Cytoskeleton.Comprehensive Physiology · 2017Review
- Differential roles of α-, β-, and γ-actin in axon growth and collateral branch formation in motoneurons.The Journal of cell biology · 2017Article
- Myocardial transcription factors in diastolic dysfunction: clues for model systems and disease.Heart failure reviews · 2016Review
- A gain-of-function ACTC1 3'UTR mutation that introduces a miR-139-5p target site may be associated with a dominant familial atrial septal defect.Scientific reports · 2016Article
- Localizations of γ-Actins in Skin, Hair, Vibrissa, Arrector Pili Muscle and Other Hair Appendages of Developing Rats.Acta histochemica et cytochemica · 2016Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The muscle actins in higher vertebrates display highly conserved amino acid sequences, yet they show distinct expression patterns. Thus, cardiac alpha-actin, skeletal alpha-actin, vascular smooth muscle alpha-actin, and enteric smooth muscle gamma-actin comprise the major actins in their respective tissues. To assess the functional and developmental significance of cardiac alpha-actin, the murine (129/SvJ) cardiac alpha-actin gene was disrupted by homologous recombination. The majority ( approximately 56%) of the mice lacking cardiac alpha-actin do not survive to term, and the remainder generally die within 2 weeks of birth. Increased expression of vascular smooth muscle and skeletal alpha-actins is observed in the hearts of newborn homozygous mutants and also heterozygotes but apparently is insufficient to maintain myofibrillar integrity in the homozygous mutants. Mice lacking cardiac alpha-actin can be rescued to adulthood by the ectopic expression of enteric smooth muscle gamma-actin using the cardiac alpha-myosin heavy chain promoter. However, the hearts of such rescued cardiac alpha-actin-deficient mice are extremely hypodynamic, considerably enlarged, and hypertrophied. Furthermore, the transgenically expressed enteric smooth muscle gamma-actin reduces cardiac contractility in wild-type and heterozygous mice. These results demonstrate that alterations in actin composition in the fetal and adult heart are associated with severe structural and functional perturbations.
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