ArticleMolecular and cellular biology1993
Developmental analysis of tropomyosin gene expression in embryonic stem cells and mouse embryos.
Article in Molecular and cellular biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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.
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Who cites it
35 citing papers in PubMed, 127 citations in OpenAlex.
- Dilated Cardiomyopathy - Exploring the Underlying Causes.Medical research archives · 2024Article
- Tropomyosin 3 (TPM3) function in skeletal muscle and in myopathy.Skeletal muscle · 2023Review
- The Oxidative Balance Orchestrates the Main Keystones of the Functional Activity of Cardiomyocytes.Oxidative medicine and cellular longevity · 2022Review
- Tropomyosin pseudo-phosphorylation results in dilated cardiomyopathy.The Journal of biological chemistry · 2019Article
- Pre-mRNA mis-splicing of sarcomeric genes in heart failure.Biochimica et biophysica acta. Molecular basis of disease · 2017Review
- Overview of the Muscle Cytoskeleton.Comprehensive Physiology · 2017Review
- Differences in Contractile Function of Myofibrils within Human Embryonic Stem Cell-Derived Cardiomyocytes vs. Adult Ventricular Myofibrils Are Related to Distinct Sarcomeric Protein Isoforms.Frontiers in physiology · 2017Article
- Cloning, Sequencing, and the Expression of the Elusive Sarcomeric TPM4Molecular biology international · 2016Article
- Repression of the Central Splicing Regulator RBFox2 Is Functionally Linked to Pressure Overload-Induced Heart Failure.Cell reports · 2015Article
- cDNA clone and expression analysis of α-Tropomyosin during Japanese flounder (Paralichthys olivaceus) metamorphosis.Dong wu xue yan jiu = Zoological research · 2014Article
- Mutation update and genotype-phenotype correlations of novel and previously described mutations in TPM2 and TPM3 causing congenital myopathies.Human mutation · 2014Article
- Tropomyosin is required for cardiac morphogenesis, myofibril assembly, and formation of adherens junctions in the developing mouse embryo.Developmental dynamics : an official publication of the American Association of Anatomists · 2014Article
- Multifaceted roles of miR-1s in repressing the fetal gene program in the heart.Cell research · 2014Article
- Decreasing tropomyosin phosphorylation rescues tropomyosin-induced familial hypertrophic cardiomyopathy.The Journal of biological chemistry · 2013Article
- A study of tropomyosin's role in cardiac function and disease using thin-filament reconstituted myocardium.Journal of muscle research and cell motility · 2013Review
- Tropomyosin isoform expression and phosphorylation in the human heart in health and disease.Journal of muscle research and cell motility · 2013Article
- Polymorphism in tropomyosin structure and function.Journal of muscle research and cell motility · 2013Review
- Tropomyosin de-phosphorylation in the heart: what are the consequences?Journal of muscle research and cell motility · 2013Review
- Identification of two new regions in the N-terminus of cardiac troponin T that have divergent effects on cardiac contractile function.The Journal of physiology · 2013Article
- Derivation of es Cells From Early Stage Preimplantation Embryos and Characterisation of their Cardiac Differentiation Potential in Mice.Journal of stem cells & regenerative medicine · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Tropomyosins (TMs) comprise a family of actin-binding proteins which play an important role in the regulation of contractility in muscle (cardiac, skeletal, and smooth) and nonmuscle cells. Although they are present in all cells, different isoforms are characteristic of specific cell types. In vertebrates, there are four different TM genes (alpha-TM, beta-TM, TM30, and TM4), three of which generate alternatively spliced isoforms. This study defines the expression patterns of these isoforms during murine embryogenesis, using both in vivo and in vitro conditions. The embryonic stem cell culture system, which has been shown to mimic different stages of mouse embryonic development, including the differentiation of primitive organ systems such as the myocardium, is used for our in vitro analysis. Our results demonstrate that several TM isoforms are expressed in specific developmental patterns, often correlated with the differentiation of particular tissues or organs. Surprisingly, other TMs, such as the striated muscle beta-TM and smooth muscle alpha-TM, are expressed constitutively. This study also demonstrates that there is an excellent correlation between the expression patterns of the TM isoforms observed in developing embryonic stem cells and mouse embryos. In addition, a quantitative molecular analysis of TM isoforms was conducted in embryonic, neonatal, and adult cardiac tissue. Our results show for the first time that the alpha- and beta-TM striated muscle transcripts are present in the earliest functional stages of the heart, and these TM isoforms are identical to those present throughout cardiac development.
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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.