ArticlePloS one2015
Repeat Associated Non-AUG Translation (RAN Translation) Dependent on Sequence Downstream of the ATXN2 CAG Repeat.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- Autophagy at the Crossroads of Protein and RNA Toxicity in Repeat Expansion Cerebellar Ataxias.Cells · 2026Review
- Bioinformatic Analyses of the Ataxin-2 Family Since Algae Emphasize Its Small Isoforms, Large Chimerisms, and the Importance of Human Exon 1B as Target of Therapies to Prevent Neurodegeneration.International journal of molecular sciences · 2026Article
- Molecular hallmarks of neurodegeneration in polyglutamine spinocerebellar ataxias.Cell death & disease · 2025Review
- Stability of the CAG Tract in theBiomedicines · 2024Article
- CAG repeat expansions create splicing acceptor sites and produce aberrant repeat-containing RNAs.Molecular cell · 2024Article
- CAG repeat expansions create splicing acceptor sites and produce aberrant repeat-containing RNAs.bioRxiv : the preprint server for biology · 2023Article
- TR-FRET-Based Immunoassay to Measure Ataxin-2 as a Target Engagement Marker in Spinocerebellar Ataxia Type 2.Molecular neurobiology · 2023Article
- Cell-based therapeutic strategies for treatment of spinocerebellar ataxias: an update.Neural regeneration research · 2023Review
- ATXN2 is a target of N-terminal proteolysis.PloS one · 2023Article
- Between Order and Chaos: Understanding the Mechanism and Pathology of RAN Translation.Biological & pharmaceutical bulletin · 2023Review
- Repeat RNA Toxicity Drives Ribosomal RNA Processing Defects in SCA2.Movement disorders : official journal of the Movement Disorder Society · 2021Article
- RNA Toxicity and Perturbation of rRNA Processing in Spinocerebellar Ataxia Type 2.Movement disorders : official journal of the Movement Disorder Society · 2021Article
- Polyglutamine Ataxias: Our Current Molecular Understanding and What the Future Holds for Antisense Therapies.Biomedicines · 2021Review
- Toxicity of pathogenic ataxin-2 in Drosophila shows dependence on a pure CAG repeat sequence.Human molecular genetics · 2021Article
- Mechanisms of repeat-associated non-AUG translation in neurological microsatellite expansion disorders.Biochemical Society transactions · 2021Review
- Lack of RAN-mediated toxicity in Huntington's disease knock-in mice.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Structural Variants May Be a Source of Missing Heritability in sALS.Frontiers in neuroscience · 2020Article
- New pathologic mechanisms in nucleotide repeat expansion disorders.Neurobiology of disease · 2019Review
- RAN translation down.Nature neuroscience · 2019Article
- Repeat-Associated Non-ATG Translation in Neurological Diseases.Cold Spring Harbor perspectives in biology · 2018Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Spinocerebellar ataxia type 2 (SCA2) is a progressive autosomal dominant disorder caused by the expansion of a CAG tract in the ATXN2 gene. The SCA2 disease phenotype is characterized by cerebellar atrophy, gait ataxia, and slow saccades. ATXN2 mutation causes gains of toxic and normal functions of the ATXN2 gene product, ataxin-2, and abnormally slow Purkinje cell firing frequency. Previously we investigated features of ATXN2 controlling expression and noted expression differences for ATXN2 constructs with varying CAG lengths, suggestive of repeat associated non-AUG translation (RAN translation). To determine whether RAN translation occurs for ATXN2 we assembled various ATXN2 constructs with ATXN2 tagged by luciferase, HA or FLAG tags, driven by the CMV promoter or the ATXN2 promoter. Luciferase expression from ATXN2-luciferase constructs lacking the ATXN2 start codon was weak vs AUG translation, regardless of promoter type, and did not increase with longer CAG repeat lengths. RAN translation was detected on western blots by the anti-polyglutamine antibody 1C2 for constructs driven by the CMV promoter but not the ATXN2 promoter, and was weaker than AUG translation. Strong RAN translation was also observed when driving the ATXN2 sequence with the CMV promoter with ATXN2 sequence downstream of the CAG repeat truncated to 18 bp in the polyglutamine frame but not in the polyserine or polyalanine frames. Our data demonstrate that ATXN2 RAN translation is weak compared to AUG translation and is dependent on ATXN2 sequences flanking the CAG repeat.
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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.