Evidence map›Paper›PMID 39305312›Full record

ArticleActa neuropathologica2024

TDP-43 regulates LC3ylation in neural tissue through ATG4B cryptic splicing inhibition.

Pascual Torres, Santiago Rico-Rios, Miriam Ceron-Codorniu, Marta Santacreu-Vilaseca, David Seoane-Miraz, Yahya Jad, Victòria Ayala, Guillermo Mariño, Maria Beltran, Maria P Miralles and 11 more

Abstract read
In one paragraph

Article in Acta neuropathologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Review
  2. Article
  3. Autophagy · 2026
    Review
  4. TDP-43: [GU]-ardian of the transcriptome.Molecular neurodegeneration · 2026
    Review
  5. Article
  6. Article
  7. Review
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

21 authors.

Pascual TorresMetabolic Pathophysiology Research Group, Department of Experimental Medicine, University of Lleida (UdL), Lleida Biomedical Research Institute (IRBLleida), 25198, Lleida, Spain.
Santiago Rico-RiosMetabolic Pathophysiology Research Group, Department of Experimental Medicine, University of Lleida (UdL), Lleida Biomedical Research Institute (IRBLleida), 25198, Lleida, Spain.
Miriam Ceron-CodorniuMetabolic Pathophysiology Research Group, Department of Experimental Medicine, University of Lleida (UdL), Lleida Biomedical Research Institute (IRBLleida), 25198, Lleida, Spain.
Marta Santacreu-VilasecaMetabolic Pathophysiology Research Group, Department of Experimental Medicine, University of Lleida (UdL), Lleida Biomedical Research Institute (IRBLleida), 25198, Lleida, Spain.
David Seoane-MirazDepartment of Paediatrics, Institute of Developmental and Regenerative Medicine (IDRM), University of Oxford, Roosevelt Dr, Oxford, OX3 7TY, UK.
Yahya JadDepartment of Paediatrics, Institute of Developmental and Regenerative Medicine (IDRM), University of Oxford, Roosevelt Dr, Oxford, OX3 7TY, UK.
Victòria AyalaMetabolic Pathophysiology Research Group, Department of Experimental Medicine, University of Lleida (UdL), Lleida Biomedical Research Institute (IRBLleida), 25198, Lleida, Spain.
Guillermo MariñoDepartamento de Biología Funcional, Facultad de Medicina, Universidad de Oviedo, 33006, Oviedo, Spain.
Maria BeltranNeuronal Signaling Unit, Department of Experimental Medicine, Lleida Biomedical Research Institute (IRBLleida), University of Lleida (UdL), 25198, Lleida, Spain.
Maria P MirallesNeuronal Signaling Unit, Department of Experimental Medicine, Lleida Biomedical Research Institute (IRBLleida), University of Lleida (UdL), 25198, Lleida, Spain.
Pol Andrés-BenitoNeurologic Diseases and Neurogenetics Group, Bellvitge Institute for Biomedical Research (IDIBELL), 08907, L'Hospitalet de Llobregat, Spain.
Joaquin Fernandez-IrigoyenClinical Neuroproteomics Unit, Proteomics Platform, Proteored-ISCIII, Navarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), diSNA, 31008, Pamplona, Spain.
Enrique SantamariaClinical Neuroproteomics Unit, Proteomics Platform, Proteored-ISCIII, Navarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), diSNA, 31008, Pamplona, Spain.
Carlos López-OtínDepartamento de Biología Funcional, Facultad de Medicina, Universidad de Oviedo, 33006, Oviedo, Spain.
Rosa M SolerNeuronal Signaling Unit, Department of Experimental Medicine, Lleida Biomedical Research Institute (IRBLleida), University of Lleida (UdL), 25198, Lleida, Spain.
Monica PovedanoNeurologic Diseases and Neurogenetics Group, Bellvitge Institute for Biomedical Research (IDIBELL), 08907, L'Hospitalet de Llobregat, Spain.
Isidro FerrerCIBERNED (Network Centre of Biomedical Research of Neurodegenerative Diseases), Institute of Health Carlos III, 08907, L'Hospitalet de Llobregat, Barcelona, Spain.
Reinald PamplonaMetabolic Pathophysiology Research Group, Department of Experimental Medicine, University of Lleida (UdL), Lleida Biomedical Research Institute (IRBLleida), 25198, Lleida, Spain.
Matthew J A WoodDepartment of Paediatrics, Institute of Developmental and Regenerative Medicine (IDRM), University of Oxford, Roosevelt Dr, Oxford, OX3 7TY, UK.
Miguel A VarelaDepartment of Paediatrics, Institute of Developmental and Regenerative Medicine (IDRM), University of Oxford, Roosevelt Dr, Oxford, OX3 7TY, UK. miguel.varela@paediatrics.ox.ac.uk.
Manuel Portero-OtinMetabolic Pathophysiology Research Group, Department of Experimental Medicine, University of Lleida (UdL), Lleida Biomedical Research Institute (IRBLleida), 25198, Lleida, Spain. manuel.portero@udl.cat.ORCID 0000-0002-1823-0299

Funding

Departament d'Innovació, Universitats i Empresa, Generalitat de Catalunya SGRFundación Luzon Ayuda UnzueInstituto de Salud Carlos III 23-00176Instituto de Salud Carlos III PI 20-00155Ministerio de Universidades Programa Margarita Salas
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is an adult-onset motor neuron disease with a mean survival time of three years. The 97% of the cases have TDP-43 nuclear depletion and cytoplasmic aggregation in motor neurons. TDP-43 prevents non-conserved cryptic exon splicing in certain genes, maintaining transcript stability, including ATG4B, which is crucial for autophagosome maturation and Microtubule-associated proteins 1A/1B light chain 3B (LC3B) homeostasis. In ALS mice (G93A), Atg4b depletion worsens survival rates and autophagy function. For the first time, we observed an elevation of LC3ylation in the CNS of both ALS patients and atg4b

Indexed as

Amyotrophic Lateral SclerosisAutophagy-Related ProteinsCysteine EndopeptidasesDNA-Binding ProteinsMicrotubule-Associated ProteinsAnimalsAutophagyFemaleHumansMaleMiceMice, KnockoutMice, TransgenicMotor NeuronsOligonucleotides, AntisenseRNA SplicingATG4B protein, humanAtg4b protein, mouseAutophagy-Related ProteinsCysteine EndopeptidasesDNA-Binding ProteinsMicrotubule-Associated ProteinsOligonucleotides, AntisenseTARDBP protein, humanTardbp protein, mouseALSAntisense oligonucleotidesAutophagyDigital PCRPost-translational modification

Identifiers

PMID39305312
PMCPMC11416411

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.