Evidence map›Paper›PMID 30917850›Full record

ArticleMolecular neurodegeneration2019

Network approach identifies Pacer as an autophagy protein involved in ALS pathogenesis.

S Beltran, M Nassif, E Vicencio, J Arcos, L Labrador, B I Cortes, C Cortez, C A Bergmann, S Espinoza, M F Hernandez and 9 more

Open access · goldAbstract read
In one paragraph

Article in Molecular neurodegeneration, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

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  16. Homeostatic Roles of the Proteostasis Network in Dendrites.Frontiers in cellular neuroscience · 2020
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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

19 authors at 6 institutions in 3 countries.

S BeltranCenter for Integrative Biology, Faculty of Science, Universidad Mayor, Camino la Piramide 5750, P.O.BOX 70086, Santiago, Chile.
M NassifCenter for Integrative Biology, Faculty of Science, Universidad Mayor, Camino la Piramide 5750, P.O.BOX 70086, Santiago, Chile.
E VicencioCenter for Integrative Biology, Faculty of Science, Universidad Mayor, Camino la Piramide 5750, P.O.BOX 70086, Santiago, Chile.
J ArcosCenter for Integrative Biology, Faculty of Science, Universidad Mayor, Camino la Piramide 5750, P.O.BOX 70086, Santiago, Chile.
L LabradorCenter for Integrative Biology, Faculty of Science, Universidad Mayor, Camino la Piramide 5750, P.O.BOX 70086, Santiago, Chile.
B I CortesCenter for Integrative Biology, Faculty of Science, Universidad Mayor, Camino la Piramide 5750, P.O.BOX 70086, Santiago, Chile.
C CortezCenter for Genomics and Bioinformatics, Faculty of Science, Universidad Mayor, Camino la Piramide, 5750, Santiago, Chile.
C A BergmannCenter for Integrative Biology, Faculty of Science, Universidad Mayor, Camino la Piramide 5750, P.O.BOX 70086, Santiago, Chile.
S EspinozaCenter for Integrative Biology, Faculty of Science, Universidad Mayor, Camino la Piramide 5750, P.O.BOX 70086, Santiago, Chile.
M F HernandezCenter for Integrative Biology, Faculty of Science, Universidad Mayor, Camino la Piramide 5750, P.O.BOX 70086, Santiago, Chile.
J M MatamalaDepartment of Neurological Sciences, Faculty of Medicine, University of Chile, Santiago, Chile.
L BargstedBiomedical Neuroscience Institute, Faculty of Medicine, University of Chile, Independencia, 1027, Santiago, Chile.
S MatusBiomedical Neuroscience Institute, Faculty of Medicine, University of Chile, Independencia, 1027, Santiago, Chile.
D Rojas-RiveraCenter for Integrative Biology, Faculty of Science, Universidad Mayor, Camino la Piramide 5750, P.O.BOX 70086, Santiago, Chile.
M J M BertrandVIB Center for Inflammation Research, Technologiepark 927, Zwijnaarde, 9052, Ghent, Belgium.
D B MedinasBiomedical Neuroscience Institute, Faculty of Medicine, University of Chile, Independencia, 1027, Santiago, Chile.
C HetzBiomedical Neuroscience Institute, Faculty of Medicine, University of Chile, Independencia, 1027, Santiago, Chile.
P A ManqueCenter for Integrative Biology, Faculty of Science, Universidad Mayor, Camino la Piramide 5750, P.O.BOX 70086, Santiago, Chile. patricio.manque@umayor.cl.
U WoehlbierCenter for Integrative Biology, Faculty of Science, Universidad Mayor, Camino la Piramide 5750, P.O.BOX 70086, Santiago, Chile. ute.woehlbier@umayor.cl.ORCID 0000-0003-3114-9708
Universidad Mayor · CLUniversity of Chile · CLBuck Institute for Research on Aging · USCenter for Climate and Resilience Research · CLFundación Ciencia and Vida · CLGhent University · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAmyotrophic lateral sclerosis (ALS) is a multifactorial fatal motoneuron disease without a cure. Ten percent of ALS cases can be pointed to a clear genetic cause, while the remaining 90% is classified as sporadic. Our study was aimed to uncover new connections within the ALS network through a bioinformatic approach, by which we identified C13orf18, recently named Pacer, as a new component of the autophagic machinery and potentially involved in ALS pathogenesis.

methodsInitially, we identified Pacer using a network-based bioinformatic analysis. Expression of Pacer was then investigated in vivo using spinal cord tissue from two ALS mouse models (SOD1

resultsUsing an unbiased network-based approach, we integrated all available ALS data to identify new functional interactions involved in ALS pathogenesis. We found that Pacer associates to an ALS-specific subnetwork composed of components of the autophagy pathway, one of the main cellular processes affected in the disease. Interestingly, we found that Pacer levels are significantly reduced in spinal cord tissue from sporadic ALS patients and in tissues from two ALS mouse models. In vitro, Pacer deficiency lead to impaired autophagy and accumulation of ALS-associated protein aggregates, which correlated with the induction of cell death.

conclusionsThis study, therefore, identifies Pacer as a new regulator of proteostasis associated with ALS pathology.

Indexed as

Amyotrophic Lateral SclerosisAnimalsAutophagyDisease Models, AnimalDNA-Binding ProteinsHumansMice, TransgenicMotor NeuronsSpinal CordSuperoxide DismutaseDNA-Binding ProteinsSuperoxide DismutaseALSAutophagyBeclin1C13orf18, KIAA0226-likePacerRubiconRubicon-likeSOD1TDP43

Identifiers

PMID30917850
PMCPMC6437924
OpenAlexW2943684516

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.