ArticleScience (New York, N.Y.)2013
A role for Drosophila ATX2 in activation of PER translation and circadian behavior.
Article in Science (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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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.
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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
92 citing papers in PubMed, 142 citations in OpenAlex.
- Conserved role of Atx2 in JNK pathway activation.Cell death & disease · 2026Article
- Article
- A role for the cholinergic neuron circadian clock in RNA metabolism and mediating neurodegeneration.Life science alliance · 2026Article
- SWI/SNF nuclear foci scaffold peripheral gene hubs for circadian chromatin control.bioRxiv : the preprint server for biology · 2026Article
- 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
- Remote and partial clocks expand the circadian neuronal network, driving widespread molecular rhythmicity inbioRxiv : the preprint server for biology · 2025Article
- Genomic Organization, Evolutionary Conservation and Expression ofBiomedicines · 2025Article
- A rapid and dynamic role for FMRP in the plasticity of adult neurons.Nature communications · 2025Article
- Article
- Fbxo42 promotes the degradation of Ataxin-2 granules to trigger terminal Xbp1 signaling.Nature communications · 2025Article
- Upstream open reading frames dynamically modulate CLOCK protein translation to regulate circadian rhythms and sleep.PLoS biology · 2025Article
- The polyglutamine protein ATXN2: from its molecular functions to its involvement in disease.Cell death & disease · 2024Review
- Greatwall-Endos-PP2A/B55Open biology · 2024Article
- Structured and disordered regions of Ataxin-2 contribute differently to the specificity and efficiency of mRNP granule formation.PLoS genetics · 2024Article
- TDP-43 impairs sleep inScience advances · 2024Article
- Circadian regulation of translation.RNA biology · 2024Review
- Poly(A)-binding protein is an ataxin-2 chaperone that regulates biomolecular condensates.Molecular cell · 2023Article
- CLOCK and TIMELESS regulate rhythmic occupancy of the BRAHMA chromatin-remodeling protein at clock gene promoters.PLoS genetics · 2023Article
- ATXN2 is a target of N-terminal proteolysis.PloS one · 2023Article
- Targeting RTN4/NoGo-Receptor reduces levels of ALS protein ataxin-2.Cell reports · 2022Article
32 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
5 authors at 1 institution in 1 country.
Funding
Abstract
A negative transcriptional feedback loop generates circadian rhythms in Drosophila. PERIOD (PER) is a critical state-variable in this mechanism, and its abundance is tightly regulated. We found that the Drosophila homolog of ATAXIN-2 (ATX2)--an RNA-binding protein implicated in human neurodegenerative diseases--was required for circadian locomotor behavior. ATX2 was necessary for PER accumulation in circadian pacemaker neurons and thus determined period length of circadian behavior. ATX2 was required for the function of TWENTY-FOUR (TYF), a crucial activator of PER translation. ATX2 formed a complex with TYF and promoted its interaction with polyadenylate-binding protein (PABP). Our work uncovers a role for ATX2 in circadian timing and reveals that this protein functions as an activator of PER translation in circadian neurons.
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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.