ArticleNeurobiology of aging2011
Association of AICD and Fe65 with Hirano bodies reduces transcriptional activation and initiation of apoptosis.
Article in Neurobiology of aging, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 17 citations in OpenAlex.
- R5 and R7 positions on fluoroquinolone scaffolds drive F-actin filament disruption.Scientific reports · 2026Article
- APP-C31 pathology as a target in neurodegenerative diseases.Journal of biomedical science · 2026Review
- De novo actin polymerization is required for model Hirano body formation in Dictyostelium.Biology open · 2016Article
- Apoptosis in Alzheimer's disease: an understanding of the physiology, pathology and therapeutic avenues.Neurochemical research · 2014Review
- 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
- Article
- Transgenic mouse model for the formation of Hirano bodies.BMC neuroscience · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hirano bodies are cytoplasmic inclusions predominantly found in the central nervous system associated with various conditions including aging and Alzheimer's disease (AD). Since most studies of Hirano bodies have been performed in post-mortem samples, the physiological roles of Hirano bodies have not been investigated. Astrocytoma H4 cells were employed to test the hypothesis that Hirano bodies interact with and modulate signaling by the C-terminal fragment of amyloid-β precursor protein (AICD). We demonstrated by immunofluorescence and immunoprecipitation that model Hirano bodies accumulate AICD. Since stimulation of transcription by AICD is dependent on its interaction with the nuclear adaptor protein Fe65, we examined localization of Fe65, and employed a dual luciferase reporter assay to test the effects of Hirano bodies on AICD- and Fe65-dependent modulation of gene expression. We find that both AICD and Fe65 are co-localized in model Hirano bodies. Model Hirano bodies also down-regulate both AICD-dependent apoptosis and AICD- and Fe65-dependent transcriptional activity. Thus, association of AICD and Fe65 with Hirano bodies impedes their function in promoting apoptosis and modulating transcription.
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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.