Evidence map›Paper›PMID 28291226›Full record

ArticleScientific reports2017

Neuronal ELAVL proteins utilize AUF-1 as a co-partner to induce neuron-specific alternative splicing of APP.

Apostolia Fragkouli, Pelagia Koukouraki, Ioannis S Vlachos, Maria D Paraskevopoulou, Artemis G Hatzigeorgiou, Epaminondas Doxakis

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. MRAS: Master Regulator Analysis of Alternative Splicing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
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  8. 1-L Transcription in Alzheimer's Disease.Current issues in molecular biology · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Splicing alterations in healthy aging and disease.Wiley interdisciplinary reviews. RNA · 2021
    Review
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  16. Article
  17. Article
  18. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Apostolia FragkouliCenter for Basic Research, Biomedical Research Foundation Academy of Athens, 4 Soranou Efesiou str, 11527, Athens Greece.
Pelagia KoukourakiCenter for Basic Research, Biomedical Research Foundation Academy of Athens, 4 Soranou Efesiou str, 11527, Athens Greece.
Ioannis S VlachosHellenic Pasteur Institute, 127 Vasilissis Sofias Avenue, 11521 Athens, Greece.
Maria D ParaskevopoulouHellenic Pasteur Institute, 127 Vasilissis Sofias Avenue, 11521 Athens, Greece.
Artemis G HatzigeorgiouHellenic Pasteur Institute, 127 Vasilissis Sofias Avenue, 11521 Athens, Greece.
Epaminondas DoxakisCenter for Basic Research, Biomedical Research Foundation Academy of Athens, 4 Soranou Efesiou str, 11527, Athens Greece.
Academy of Athens · GRPasteur Hellenic Institute · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aβ peptide that accumulates in Alzheimer's disease brain, derives from proteolytic processing of the amyloid precursor protein (APP) that exists in three main isoforms derived by alternative splicing. The isoform APP695, lacking exons 7 and 8, is predominately expressed in neurons and abnormal neuronal splicing of APP has been observed in the brain of patients with Alzheimer's disease. Herein, we demonstrate that expression of the neuronal members of the ELAVL protein family (nELAVLs) correlate with APP695 levels in vitro and in vivo. Moreover, we provide evidence that nELAVLs regulate the production of APP695; by using a series of reporters we show that concurrent binding of nELAVLs to sequences located both upstream and downstream of exon 7 is required for its skipping, whereas nELAVL-binding to a highly conserved U-rich sequence upstream of exon 8, is sufficient for its exclusion. Finally, we report that nELAVLs block APP exon 7 or 8 definition by reducing the binding of the essential splicing factor U2AF65, an effect facilitated by the concurrent binding of AUF-1. Our study provides new insights into the regulation of APP pre-mRNA processing, supports the role for nELAVLs as neuron-specific splicing regulators and reveals a novel function of AUF1 in alternative splicing.

Indexed as

Alternative SplicingAlzheimer DiseaseAmyloid beta-Protein PrecursorBrainELAV-Like Protein 2Gene Expression RegulationHeLa CellsHeterogeneous-Nuclear Ribonucleoprotein DHeterogeneous Nuclear Ribonucleoprotein D0HumansMultigene FamilyNeuronsPeptide FragmentsProtein BindingProtein IsoformsRNA PrecursorsAmyloid beta-Protein Precursoramyloid beta-protein precursor 695 (18-38)ELAVL2 protein, humanELAV-Like Protein 2Heterogeneous-Nuclear Ribonucleoprotein DHeterogeneous Nuclear Ribonucleoprotein D0HNRNPD protein, humanPeptide FragmentsProtein IsoformsRNA PrecursorsSplicing Factor U2AFT-Cell Intracellular Antigen-1TIA1 protein, human

Identifiers

PMID28291226
PMCPMC5349543
OpenAlexW2621758578

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Registered trials

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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.