ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2012
α-Actinin-2 deficiency results in sarcomeric defects in zebrafish that cannot be rescued by α-actinin-3 revealing functional differences between sarcomeric isoforms.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- The Effect of ACTN3 Gene Doping on Skeletal Muscle Performance.American journal of human genetics · 2018Pooled it
- Transcriptomic adaptation during skeletal muscle habituation to eccentric or concentric exercise training.Scientific reports · 2021Trial
- Klhl41b orchestrates sarcomere assembly and growth to drive skeletal muscle hypertrophy in vivo.Skeletal muscle · 2026Article
- Metabolic Health and Fitness Do Not Differ Substantially Between Overweight Adults With and Without α-Actinin-3 Deficiency.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Nonmuscle α-Actinin-4 Couples Sarcomere Function to Cardiac Remodeling.Circulation research · 2026Article
- Developmental exposure to ethylbenzene: Elucidating the effects of volatile organic compounds on phenotypic and transcriptomic endpoints using zebrafish (Danio rerio).Journal of hazardous materials · 2026Article
- Biological properties of α-actinin-2 and its role and mechanisms in disease development.Frontiers in physiology · 2026Review
- Integrative Transcriptomic and Proteomic Analysis RevealsAnimals : an open access journal from MDPI · 2025Article
- IGFBP2 Mediates Human iPSC-Cardiomyocyte Proliferation in a Cellular Contact-Dependent Manner.Circulation research · 2025Article
- Deciphering European Sea Bass (International journal of molecular sciences · 2025Article
- Actn2 defects accelerates H9c2 hypertrophy via ERK phosphorylation under chronic stress.Genes & genomics · 2024Article
- Recurring homozygous ACTN2 variant (p.Arg506Gly) causes a recessive myopathy.Annals of clinical and translational neurology · 2024Article
- Cardiomyopathy-associated variants alter the structure and function of the α-actinin-2 actin-binding domain.Biochemical and biophysical research communications · 2023Article
- Using Zebrafish Animal Model to Study the Genetic Underpinning and Mechanism of Arrhythmogenic Cardiomyopathy.International journal of molecular sciences · 2023Review
- Mutation update for the ACTN2 gene.Human mutation · 2022Review
- Animal Models to Study Cardiac Arrhythmias.Circulation research · 2022Review
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- Panorama of the distal myopathies.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2020Review
- Genome-wide association and multi-omic analyses reveal ACTN2 as a gene linked to heart failure.Nature communications · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
α-Actinins are actin-binding proteins that can be broadly divided into Ca(2+)-sensitive cytoskeletal and Ca(2+)-insensitive sarcomeric isoforms. To date, little is known about functional differences between the isoforms due to their indistinguishable activities in most in vitro assays. To identify functional differences in vivo between sarcomeric isoforms, we employed computational and molecular approaches to characterize the zebrafish (Danio rerio) genome, which contains orthologoues of each human α-actinin gene, including duplicated copies of actn3. Each isoform exhibits a distinct and unique pattern of gene expression as assessed by mRNA in situ hybridization, largely sharing similar expression profiles as seen in humans. The spatial conservation of expression of these genes from lower invertebrates to humans suggests that regulation and subsequent functions of these genes are conserved during evolution. Morpholino-based knockdown of the sarcomeric isoform, actn2, leads to skeletal muscle, cardiac, and ocular defects evident over the first week of development. Remarkably, despite the high degree of sequence conservation between actn2 and actn3, the phenotypes of α-actinin-2 deficient zebrafish can be rescued by overexpression of α-actinin-2 but not by α-actinin-3 mRNAs from zebrafish or human. These data provide functional evidence that the primary sequences of α-actinin-2 and α-actinin-3 evolved differences to optimize their functions.
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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.