ArticleBioarchitecture2011
Functional identity of the gamma tropomyosin gene: Implications for embryonic development, reproduction and cell viability.
Article in Bioarchitecture, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 31 citations in OpenAlex.
- Multiple Mechanisms to Regulate Actin Functions: "Fundamental" Versus Lineage-Specific Mechanisms and Hierarchical Relationships.Biomolecules · 2025Review
- The tropomyosin 3.1/3.2 inhibitor ATM-3507 alters B-cell actin dynamics and impairs the growth and motility of diffuse large B-cell lymphoma cell lines.Frontiers in immunology · 2025Article
- Functional and Structural Properties of Cytoplasmic Tropomyosin Isoforms Tpm1.8 and Tpm1.9.International journal of molecular sciences · 2024Article
- RNF20 Regulates Oocyte Meiotic Spindle Assembly by Recruiting TPM3 to Centromeres and Spindle Poles.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Tropomyosin 3 (TPM3) function in skeletal muscle and in myopathy.Skeletal muscle · 2023Review
- Novel human cell expression method reveals the role and prevalence of posttranslational modification in nonmuscle tropomyosins.The Journal of biological chemistry · 2021Article
- Tropomyosin 3.5 protects the F-actin networks required for tissue biomechanical properties.Journal of cell science · 2018Article
- Tropomyosin 2 heterozygous knockout in mice using CRISPR-Cas9 system displays the inhibition of injury-induced epithelial-mesenchymal transition, and lens opacity.Mechanisms of ageing and development · 2018Article
- On-target action of anti-tropomyosin drugs regulates glucose metabolism.Scientific reports · 2018Article
- Smad4 SUMOylation is essential for memory formation through upregulation of the skeletal myopathy gene TPM2.BMC biology · 2017Article
- Stabilization of F-actin by tropomyosin isoforms regulates the morphology and mechanical behavior of red blood cells.Molecular biology of the cell · 2017Article
- A Large Deletion Affecting TPM3, Causing Severe Nemaline Myopathy.Journal of neuromuscular diseases · 2015Article
- Regulation of cell proliferation by ERK and signal-dependent nuclear translocation of ERK is dependent on Tm5NM1-containing actin filaments.Molecular biology of the cell · 2015Article
- An actin filament population defined by the tropomyosin Tpm3.1 regulates glucose uptake.Traffic (Copenhagen, Denmark) · 2015Article
- Profiling of the embryonic Atlantic halibut (Hippoglossus hippoglossus L.) transcriptome reveals maternal transcripts as potential markers of embryo quality.BMC genomics · 2014Article
- Non-muscle tropomyosin (Tpm3) is crucial for asymmetric cell division and maintenance of cortical integrity in mouse oocytes.Cell cycle (Georgetown, Tex.) · 2014Article
- Cytoskeletal tropomyosins: choreographers of actin filament functional diversity.Journal of muscle research and cell motility · 2013Review
- Tropomyosin isoforms and reagents.Bioarchitecture · 2011Article
- Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The actin filament system is fundamental to cellular functions including regulation of shape, motility, cytokinesis, intracellular trafficking and tissue organization. Tropomyosins (Tm) are highly conserved components of actin filaments which differentially regulate filament stability and function. The mammalian Tm family consists of four genes; αTm, βTm, γTm and δTm. Multiple Tm isoforms (>40) are generated by alternative splicing and expression of these isoforms is highly regulated during development. In order to further identify the role of Tm isoforms during development, we tested the specificity of function of products from the γTm gene family in mice using a series of gene knockouts. Ablation of all γTm gene cytoskeletal products results in embryonic lethality. Elimination of just two cytoskeletal products from the γTm gene (NM1,2) resulted in a 50% reduction in embryo viability. It was also not possible to generate homozygous knockout ES cells for the targets which eliminated or reduced embryo viability in mice. In contrast, homozygous knockout ES cells were generated for a different set of isoforms (NM3,5,6,8,9,11) which were not required for embryogenesis. We also observed that males hemizygous for the knockout of all cytoskeletal products from the γTm gene preferentially transmitted the minus allele with 80-100% transmission. Since all four Tm genes are expressed in early embryos, ES cells and sperm, we conclude that isoforms of the γTm gene are functionally unique in their role in embryogenesis, ES cell viability and sperm function.
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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.