ArticleActa neuropathologica communications2019
Heterogeneous nuclear ribonucleoproteins R and Q accumulate in pathological inclusions in FTLD-FUS.
Article in Acta neuropathologica communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Preclinical serum alterations and tissue changes in protein and gene expression of early cerebrospinal fluid-validated biomarkers in scrapie.Veterinary research · 2026Article
- Transcriptomic and pathological analysis of the hnRNP network reveals glial involvement in frontotemporal lobar degeneration pathological subtypes.Brain communications · 2026Article
- Brain transcriptomics highlight abundant gene expression and splicing alterations in non-neuronal cells in aFTLD-U.Acta neuropathologica · 2025Article
- hnRNP R promotes O-GlcNAcylation of eIF4G and facilitates axonal protein synthesis.Nature communications · 2024Article
- The Roles of hnRNP Family in the Brain and Brain-Related Disorders.Molecular neurobiology · 2024Review
- Deregulated circRNAs in Epithelial Ovarian Cancer With Activity in PreclinicalCancer genomics & proteomics · 2024Review
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- hnRNP R negatively regulates transcription by modulating the association of P-TEFb with 7SK and BRD4.EMBO reports · 2022Article
- Deciphering therapeutic options for neurodegenerative diseases: insights from SIRT1.Journal of molecular medicine (Berlin, Germany) · 2022Review
- NOS1AP is a novel molecular target and critical factor in TDP-43 pathology.Brain communications · 2022Article
- Loss of full-length hnRNP R isoform impairs DNA damage response in motoneurons by inhibiting Yb1 recruitment to chromatin.Nucleic acids research · 2021Article
- HnRNP K mislocalisation is a novel protein pathology of frontotemporal lobar degeneration and ageing and leads to cryptic splicing.Acta neuropathologica · 2021Article
- RNA-Binding Proteins and the Complex Pathophysiology of ALS.International journal of molecular sciences · 2021Review
- The multifaceted role of PARP1 in RNA biogenesis.Wiley interdisciplinary reviews. RNA · 2021Review
- Divergent FUS phosphorylation in primate and mouse cells following double-strand DNA damage.Neurobiology of disease · 2020Article
- The role of hnRNPs in frontotemporal dementia and amyotrophic lateral sclerosis.Acta neuropathologica · 2020Review
- The role of DNA damage response in amyotrophic lateral sclerosis.Essays in biochemistry · 2020Review
- Traffic jam at the nuclear pore: All roads lead to nucleocytoplasmic transport defects in ALS/FTD.Neurobiology of disease · 2020Review
- The Hitchhiker's Guide to Nucleocytoplasmic Trafficking in Neurodegeneration.Neurochemical research · 2020Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Frontotemporal lobar degeneration (FTLD) is pathologically subdivided based on the presence of particular pathological proteins that are identified in inclusion bodies observed post-mortem. The FTLD-FUS subgroup is defined by the presence of the fused in sarcoma protein (FUS) in pathological inclusions. FUS is a heterogeneous nuclear ribonucleoprotein (hnRNP) protein and a member of the FET (FUS, EWS, TAF15) protein family. It shuttles between the nucleus and cytoplasm, and has been implicated in many cellular functions including translation, splicing, and RNA transport. EWS, TAF15 and the nuclear import receptor transportin have been shown to co-accumulate with FUS in neuronal inclusions specifically in FTLD-FUS, with transportin-positive inclusions most frequently observed. Here, we report the identification of hnRNP R and hnRNP Q in neuronal cytoplasmic and intranuclear inclusions in the frontal cortex and hippocampus of FTLD-FUS patients, as frequently as transportin. hnRNP R and hnRNP Q were not found in the characteristic pathological inclusions observed in FTLD-TDP (subtypes A-C). Additionally, we studied the expression of hnRNP R in the frontal and temporal cortices from patients with FTLD and found significantly increased expression of the heterogeneous nuclear ribonucleoprotein R in several FTLD disease groups. Our identification of the frequent presence of hnRNP R and hnRNP Q in FTLD-FUS inclusions suggests a potential role for these hnRNPs in FTLD-FUS pathogenesis and supports the role of dysfunctional RNA metabolism in FTLD.
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