ArticleCell reports2026
Repeat-associated non-AUG translation as a common mechanism for the polyGln ataxias.
Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Discovery of a mutation-containing circRNA in polyglutamine disease through systematic analysis of RNAs with CAG repeats.RNA biology · 2026Article
- Autophagy at the Crossroads of Protein and RNA Toxicity in Repeat Expansion Cerebellar Ataxias.Cells · 2026Review
- Metformin improves RAN protein pathology, alternative splicing, and behavioral phenotypes in SCA8 mice.Life science alliance · 2026Article
Corrections and comments
- Update of
Authors and funding
17 authors.
Funding
Abstract
Determining if repeat-associated non-AUG (RAN) proteins contribute to the CAG-polyglutamine (polyGln)-encoding spinocerebellar ataxias (CAG-SCAs) is critical for understanding disease mechanisms and for therapy development. Immunohistochemistry shows that sense polyserine (polySer) (AGC frame) and antisense polyleucine (polyLeu) (CUG frame) RAN protein aggregates accumulate throughout the cerebellum and pons, in SCA1, SCA2, SCA3, SCA6, and SCA7 autopsy brains, and in damaged neurons. Cerebellar white matter regions, with prominent polySer and polyLeu but minimal polyGln, show neuroinflammation and demyelination. In SCA3 mice, RAN protein aggregates increase with age. SCA1 Pcp2-ATXN1[82Q] (Pcp2-82Q) mice designed to express ataxin-1 (ATXN1)-polyGln in Purkinje cells show sense and antisense RAN protein aggregates throughout the cerebellum. Disrupting the ATXN182Q:capicua binding, which improves behavior and neuropathology, also reduces RAN protein aggregates. In neural cells, toxic polySer and polyLeu proteins impair autophagy, and reducing RAN protein levels with metformin reduces cytotoxicity. These data identify sense and antisense RAN proteins as a common molecular mechanism shared by the CAG-SCAs.
Indexed as
Identifiers
What OpenQuestion holds
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.