ArticleEukaryotic cell2003
Formation of Hirano bodies induced by expression of an actin cross-linking protein with a gain-of-function mutation.
Article in Eukaryotic cell, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 39 citations in OpenAlex.
- Dictyostelium discoideum as a non-mammalian biomedical model.Microbial biotechnology · 2021Review
- Ofloxacin as a Disruptor of Actin Aggresome "Hirano Bodies": A Potential Repurposed Drug for the Treatment of Neurodegenerative Diseases.Frontiers in aging neuroscience · 2020Article
- Actin-Interacting Protein 1 Contributes to Intranuclear Rod Assembly in Dictyostelium discoideum.Scientific reports · 2017Article
- De novo actin polymerization is required for model Hirano body formation in Dictyostelium.Biology open · 2016Article
- Hirano body expression impairs spatial working memory in a novel mouse model.Acta neuropathologica communications · 2014Article
- Hirano bodies differentially modulate cell death induced by tau and the amyloid precursor protein intracellular domain.BMC neuroscience · 2014Article
- Requirements for Hirano body formation.Eukaryotic cell · 2014Article
- Article
- Association of AICD and Fe65 with Hirano bodies reduces transcriptional activation and initiation of apoptosis.Neurobiology of aging · 2011Article
- Transgenic mouse model for the formation of Hirano bodies.BMC neuroscience · 2011Article
- Dictyostelium discoideum--a model for many reasons.Molecular and cellular biochemistry · 2009Review
- Formation of Hirano bodies after inducible expression of a modified form of an actin-cross-linking protein.Eukaryotic cell · 2009Article
- Autophagy contributes to degradation of Hirano bodies.Autophagy · 2009Article
- Molecular and biochemical characterization of a novel actin bundling protein in Acanthamoeba.The Korean journal of parasitology · 2006Article
- Cofilin expression induces cofilin-actin rod formation and disrupts synaptic structure and function in Aplysia synapses.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hirano bodies are paracrystalline actin filament-containing structures reported to be associated with a variety of neurodegenerative diseases. However, the biological function of Hirano bodies remains poorly understood, since nearly all prior studies of these structures were done with postmortem samples of tissue. In the present study, we generated a full-length form of a Dictyostelium 34-kDa actin cross-linking protein with point mutations in the first putative EF hand, termed 34-kDa DeltaEF1. The 34-kDa DeltaEF1 protein binds calcium normally but has activated actin binding that is unregulated by calcium. The expression of the 34-kDa DeltaEF1 protein in Dictyostelium induces the formation of Hirano bodies, as assessed by both fluorescence microscopy and transmission electron microscopy. Dictyostelium cells bearing Hirano bodies grow normally, indicating that Hirano bodies are not associated with cell death and are not deleterious to cell growth. Moreover, the expression of the 34-kDa DeltaEF1 protein rescues the phenotypes of cells lacking the 34-kDa protein and cells lacking both the 34-kDa protein and alpha-actinin. Finally, the expression of the 34-kDa DeltaEF1 protein also initiates the formation of Hirano bodies in cultured mouse fibroblasts. These results show that the failure to regulate the activity and/or affinity of an actin cross-linking protein can provide a signal for the formation of Hirano bodies. More generally, the formation of Hirano bodies is a cellular response to or a consequence of aberrant function of the actin cytoskeleton.
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