ArticleNeuron2011
CTCF regulates ataxin-7 expression through promotion of a convergently transcribed, antisense noncoding RNA.
Article in Neuron, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 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
87 citing papers in PubMed, 130 citations in OpenAlex.
- RAN proteins and RNA foci from antisense transcripts in C9ORF72 ALS and frontotemporal dementia.Proceedings of the National Academy of Sciences of the United States of America · 2013Trial
- Regulation of PHOX2B gene expression by the long non-coding natural antisense RNA PHOX2B-AS1.The FEBS journal · 2026Article
- Metformin improves RAN protein pathology, alternative splicing, and behavioral phenotypes in SCA8 mice.Life science alliance · 2026Article
- Repeat-associated non-AUG translation as a common mechanism for the polyGln ataxias.Cell reports · 2026Article
- A review of post-GWAS studies in schizophrenia.Translational psychiatry · 2025Review
- YTHDC1-Mediated lncRNA MSC-AS1 m6A Modification Potentiates Laryngeal Squamous Cell Carcinoma Development via Repressing ATXN7 Transcription.Molecular biotechnology · 2025Article
- Retinal degeneration in spinocerebellar ataxia type 7: an overview of the current knowledge.Arquivos brasileiros de oftalmologia · 2025Review
- Spinocerebellar ataxias: from pathogenesis to recent therapeutic advances.Frontiers in neuroscience · 2024Review
- Bidirectional Transcription at the PPP2R2B Gene Locus in Spinocerebellar Ataxia Type 12.Movement disorders : official journal of the Movement Disorder Society · 2023Article
- Functional implications of paralog genes in polyglutamine spinocerebellar ataxias.Human genetics · 2023Review
- Human Induced Pluripotent Stem Cell-Based Modelling of Spinocerebellar Ataxias.Stem cell reviews and reports · 2022Review
- RNA Toxicity and Perturbation of rRNA Processing in Spinocerebellar Ataxia Type 2.Movement disorders : official journal of the Movement Disorder Society · 2021Article
- Natural antisense transcript ofGenes & development · 2021Article
- Molecular landscape of long noncoding RNAs in brain disorders.Molecular psychiatry · 2021Review
- Variant-selective stereopure oligonucleotides protect against pathologies associated with C9orf72-repeat expansion in preclinical models.Nature communications · 2021Article
- Molecular and electrophysiological features of spinocerebellar ataxia type seven in induced pluripotent stem cells.PloS one · 2021Article
- Review
- On the wrong DNA track: Molecular mechanisms of repeat-mediated genome instability.The Journal of biological chemistry · 2020Review
- Non-coding RNAs in Nervous System Development and Disease.Frontiers in cell and developmental biology · 2020Review
- Antisense Transcription in Loci Associated to Hereditary Neurodegenerative Diseases.Molecular neurobiology · 2019Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 1 country.
Funding
Abstract
Spinocerebellar ataxia type 7 (SCA7) is a neurodegenerative disorder caused by CAG/polyglutamine repeat expansions in the ataxin-7 gene. Ataxin-7 is a component of two different transcription coactivator complexes, and recent work indicates that disease protein normal function is altered in polyglutamine neurodegeneration. Given this, we studied how ataxin-7 gene expression is regulated. The ataxin-7 repeat and translation start site are flanked by binding sites for CTCF, a highly conserved multifunctional transcription regulator. When we analyzed this region, we discovered an adjacent alternative promoter and a convergently transcribed antisense noncoding RNA, SCAANT1. To understand how CTCF regulates ataxin-7 gene expression, we introduced ataxin-7 mini-genes into mice, and found that CTCF is required for SCAANT1 expression. Loss of SCAANT1 derepressed ataxin-7 sense transcription in a cis-dependent fashion and was accompanied by chromatin remodeling. Discovery of this pathway underscores the importance of altered epigenetic regulation for disease pathology at repeat loci exhibiting bidirectional transcription.
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.