ArticleCell2025
DNA binding and mitotic phosphorylation protect polyglutamine proteins from assembly formation.
Article in Cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed.
- ATRX Condensates as Candidate Organizers of Enhancer-Centered Nuclear Microenvironments in Neural Progenitors: A Hypothesis for Enhancer-Associated ATRX Function in Neural Progenitors.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- MLL3 and MLL4 sustain hematopoietic stem cell multipotency by opposing a B-cell default state.Blood · 2026Article
- Core clock protein subcellular dynamics coordinate local and global circadian control in syncytia.The Journal of cell biology · 2026Article
- In Depth Characterization of the Promoter Proximal Proteome of Single Copy Locus FOXP2.Molecular & cellular proteomics : MCP · 2026Article
- Unstructured transcription factor interactions enable emergent specificity.Science (New York, N.Y.) · 2026Article
- Multimerizing transcription factors FOXP3 and AIRE as chromatin architectural regulators.Nature immunology · 2026Review
- BRD2 bridges TFIID and MOF-H4K16ac-containing nucleosomes to promote transcriptional initiation.Molecular cell · 2026Article
- DNA binding and mitotic phosphorylation: native mechanisms preventing polyglutamine protein aggregation.Science China. Life sciences · 2026Article
- Core Clock Protein Subcellular Dynamics Coordinate Local and Global Circadian Control in Syncytia.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Polyglutamine (polyQ) expansion is associated with pathogenic protein aggregation in neurodegenerative disorders. However, long polyQ tracts are also found in many transcription factors (TFs), such as FOXP2, a TF implicated in human speech. Here, we explore how FOXP2 and other glutamine-rich TFs avoid unscheduled assembly. Throughout interphase, DNA binding, irrespective of sequence specificity, has a solubilizing effect. During mitosis, multiple phosphorylation events promote FOXP2's eviction from chromatin and supplant the solubilizing function of DNA. Further, human-specific amino acid substitutions linked to the evolution of speech map to a mitotic phospho-patch, the "EVO patch," and reduce the propensity of the human FOXP2 to assemble. Fusing the pathogenic form of Huntingtin to either a DNA-binding domain, a phosphomimetic variant of this EVO patch, or a negatively charged peptide is sufficient to diminish assembly formation, suggesting that hijacking mechanisms governing solubility of glutamine-rich TFs may offer new strategies for treatment of polyQ expansion diseases.
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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.