ArticleThe Journal of biological chemistry2018
RNA-binding proteins with basic-acidic dipeptide (BAD) domains self-assemble and aggregate in Alzheimer's disease.
Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Dissecting Detergent-Insoluble Proteome in Alzheimer's Disease by TMTc-Corrected Quantitative Mass Spectrometry.Molecular & cellular proteomics : MCP · 2023Pooled it
- Aβ Aggregates Bind the U1 Spliceosomal Ribonucleoprotein in Alzheimer Disease Brain.bioRxiv : the preprint server for biology · 2026Article
- Roles of RNA-Binding Nuclear Proteins in Alzheimer's Disease Pathophysiology.ACS pharmacology & translational science · 2026Review
- Pharmacologic inhibition of PCBP2 biomolecular condensates relieves Alzheimer's disease.Nature communications · 2025Article
- Alzheimer's disease brain-derived tau extracts show differential processing and transcriptional effects in human astrocytes.iScience · 2025Article
- Cannabinerol Restores mRNA Splicing Defects Induced by β-Amyloid in an In Vitro Model of Alzheimer's Disease: A Transcriptomic Study.International journal of molecular sciences · 2025Article
- Benchmarking residue-resolution protein coarse-grained models for simulations of biomolecular condensates.PLoS computational biology · 2025Article
- Effects of the therapeutic correction of U1 snRNP complex on Alzheimer's disease.Scientific reports · 2024Article
- RBM25 is required to restrain inflammation via ACLY RNA splicing-dependent metabolism rewiring.Cellular & molecular immunology · 2024Article
- Proteomic networks of gray and white matter reveal tissue-specific changes in human tauopathy.Annals of clinical and translational neurology · 2024Article
- Expression and Purification of Human U1-70K (snRNP70) and its BAD Domains Using an E. coli Expression System.Current protocols · 2024Article
- Native-state proteomics of Parvalbumin interneurons identifies unique molecular signatures and vulnerabilities to early Alzheimer's pathology.Nature communications · 2024Article
- Liquid-liquid phase separation in Alzheimer's disease.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Tau-RNA complexes inhibit microtubule polymerization and drive disease-relevant conformation change.Brain : a journal of neurology · 2023Article
- RBM25 induces trophoblast epithelial-mesenchymal transition and preeclampsia disorder by enhancing the positive feedback loop between Grhl2 and RBM25.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Moving beyond amyloid and tau to capture the biological heterogeneity of Alzheimer's disease.Trends in neurosciences · 2023Review
- Differential splicing of neuronal genes in a Trem2*R47H mouse model mimics alterations associated with Alzheimer's disease.BMC genomics · 2023Article
- Light, Water, and Melatonin: The Synergistic Regulation of Phase Separation in Dementia.International journal of molecular sciences · 2023Review
- Analyzing alternative splicing in Alzheimer's disease postmortem brain: a cell-level perspective.Frontiers in molecular neuroscience · 2023Article
- U1 snRNP proteins promote proximal alternative polyadenylation sites by directly interacting with 3' end processing core factors.Journal of molecular cell biology · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The U1 small nuclear ribonucleoprotein 70 kDa (U1-70K) and other RNA-binding proteins (RBPs) are mislocalized to cytoplasmic neurofibrillary Tau aggregates in Alzheimer's disease (AD), yet the co-aggregation mechanisms are incompletely understood. U1-70K harbors two disordered low-complexity domains (LC1 and LC2) that are necessary for aggregation in AD brain extracts. The LC1 domain contains highly repetitive basic (Arg/Lys) and acidic (Asp/Glu) residues, referred to as a basic-acidic dipeptide (BAD) domain. We report here that this domain shares many of the properties of the Gln/Asn-rich LC domains in RBPs that also aggregate in neurodegenerative disease. These properties included self-assembly into oligomers and localization to nuclear granules. Co-immunoprecipitations of recombinant U1-70K and deletions lacking the LC domain(s) followed by quantitative proteomic analyses were used to resolve functional classes of U1-70K-interacting proteins that depend on the BAD domain for their interaction. Within this interaction network, we identified a class of RBPs with BAD domains nearly identical to that found in U1-70K. Two members of this class, LUC7L3 and RBM25, required their respective BAD domains for reciprocal interactions with U1-70K and nuclear granule localization. Strikingly, a significant proportion of RBPs with BAD domains had elevated insolubility in the AD brain proteome. Furthermore, we show that the BAD domain of U1-70K can interact with Tau from AD brains but not from other tauopathies. These findings highlight a mechanistic role for BAD domains in stabilizing RBP interactions and in potentially mediating co-aggregation with the pathological AD-specific Tau isoforms.
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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 Socratic graph.