Evidence map›Paper›PMID 28575377›Full record

ArticleNucleic acids research2017

Major hnRNP proteins act as general TDP-43 functional modifiers both in Drosophila and human neuronal cells.

Chiara Appocher, Fatemeh Mohagheghi, Sara Cappelli, Cristiana Stuani, Maurizio Romano, Fabian Feiguin, Emanuele Buratti

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. TDP-43: [GU]-ardian of the transcriptome.Molecular neurodegeneration · 2026
    Review
  3. RNArchitects: how hnRNPs shape neuronal landscapes.Brain : a journal of neurology · 2026
    Review
  4. Article
  5. Article
  6. From development to disease: the neuronal role of hnRNPs through the lens ofFrontiers in cell and developmental biology · 2026
    Review
  7. Article
  8. Article
  9. Review
  10. Context-dependent Interactors Regulate TDP-43 Dysfunction in ALS/FTLD.bioRxiv : the preprint server for biology · 2025
    Article
  11. Review
  12. Article
  13. Article
  14. TDP-43 Epigenetic Facets and Their Neurodegenerative Implications.International journal of molecular sciences · 2023
    Review
  15. A Novel Drosophila-based Drug Repurposing Platform Identified Fingolimod As a Potential Therapeutic for TDP-43 Proteinopathy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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

7 authors at 2 institutions in 1 country.

Chiara AppocherInternational Centre for Genetic Engineering and Biotechnology (ICGEB), 34149 Trieste, Italy.
Fatemeh MohagheghiInternational Centre for Genetic Engineering and Biotechnology (ICGEB), 34149 Trieste, Italy.
Sara CappelliInternational Centre for Genetic Engineering and Biotechnology (ICGEB), 34149 Trieste, Italy.
Cristiana StuaniInternational Centre for Genetic Engineering and Biotechnology (ICGEB), 34149 Trieste, Italy.
Maurizio RomanoDepartment of Life Sciences, University of Trieste, Via A. Valerio 28, 34127 Trieste, Italy.
Fabian FeiguinInternational Centre for Genetic Engineering and Biotechnology (ICGEB), 34149 Trieste, Italy.
Emanuele BurattiInternational Centre for Genetic Engineering and Biotechnology (ICGEB), 34149 Trieste, Italy.
International Centre for Genetic Engineering and Biotechnology · ITUniversity of Trieste · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear factor TDP-43 is known to play an important role in several neurodegenerative pathologies. In general, TDP-43 is an abundant protein within the eukaryotic nucleus that binds to many coding and non-coding RNAs and influence their processing. Using Drosophila, we have performed a functional screening to establish the ability of major hnRNP proteins to affect TDP-43 overexpression/depletion phenotypes. Interestingly, we observed that lowering hnRNP and TDP-43 expression has a generally harmful effect on flies locomotor abilities. In parallel, our study has also identified a distinct set of hnRNPs that is capable of powerfully rescuing TDP-43 toxicity in the fly eye (Hrb27c, CG42458, Glo and Syp). Most importantly, removing the human orthologs of Hrb27c (DAZAP1) in human neuronal cell lines can correct several pre-mRNA splicing events altered by TDP-43 depletion. Moreover, using RNA sequencing analysis we show that DAZAP1 and TDP-43 can co-regulate an extensive number of biological processes and molecular functions potentially important for the neuron/motor neuron pathophysiology. Our results suggest that changes in hnRNP expression levels can significantly modulate TDP-43 functions and affect pathological outcomes.

Indexed as

Amyotrophic Lateral SclerosisAnimalsAnimals, Genetically ModifiedCell LineDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsEyeGene Knockdown TechniquesHeLa CellsHeterogeneous-Nuclear RibonucleoproteinsHumansNeuronsRNA-Binding ProteinsRNA, MessengerRNA SplicingDAZAP1 protein, humanDNA-Binding ProteinsDrosophila ProteinsHeterogeneous-Nuclear RibonucleoproteinsRNA-Binding ProteinsRNA, MessengerTARDBP protein, humanTBPH protein, Drosophila

Identifiers

PMID28575377
PMCPMC5570092
OpenAlexW2619571880

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.