Evidence map›Paper›PMID 31319884›Full record

ReviewActa neuropathologica communications2019

Key role of UBQLN2 in pathogenesis of amyotrophic lateral sclerosis and frontotemporal dementia.

Laurence Renaud, Vincent Picher-Martel, Philippe Codron, Jean-Pierre Julien

Open access · goldAbstract readReview
In one paragraph

Review in Acta neuropathologica communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
10.0field-weighted citation impact, top 1% 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

79 citing papers in PubMed, 124 citations in OpenAlex.

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19 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Laurence RenaudDepartment of Psychiatry and Neuroscience, Laval University, Quebec, Canada.
Vincent Picher-MartelDepartment of Psychiatry and Neuroscience, Laval University, Quebec, Canada. vincent.picher-martel.1@ulaval.ca.ORCID 0000-0001-5620-6938
Philippe CodronUMR CNRS 6015, INSERM U1083, University of Angers, Angers, France.
Jean-Pierre JulienDepartment of Psychiatry and Neuroscience, Laval University, Quebec, Canada.
Université Laval · CACentre National de la Recherche Scientifique · FR

Funding

CIHR
6 · The paper itself

Abstract

Ubiquilin-2 (UBQLN2) is a member of the ubiquilin family, actively implicated in the degradation of misfolded and redundant proteins through the ubiquitin-proteasome system and macroautophagy. UBQLN2 received much attention after the discovery of gene mutations in amyotrophic lateral sclerosis and frontotemporal dementia (ALS/FTD). The abnormal presence of positive UBQLN2 inclusion in the cytosol of degenerating motor neurons of familial and sporadic forms of ALS patients has been newly related to neurodegeneration. Only recently, data have emerged on its role in liquid-liquid phase separation, in stress granule development and in the formation of secondary amyloid structures. Furthermore, several animal models are available to investigate its involvement in TDP-43 pathology and neuroinflammation in ALS. This review addresses the molecular pathogenetic pathways involving UBQLN2 abnormalities which are converging toward defects in clearance mechanisms. UBQLN2.

Indexed as

Adaptor Proteins, Signal TransducingAmyotrophic Lateral SclerosisAnimalsAutophagy-Related ProteinsDNA-Binding ProteinsFrontotemporal DementiaHumansInclusion BodiesAdaptor Proteins, Signal TransducingAutophagy-Related ProteinsDNA-Binding ProteinsUBQLN2 protein, humanAmyotrophic lateral sclerosis (ALS)Animal modelsAutophagyTAR DNA-binding protein 43 (TDP-43)Ubiquilin-2 (UBQLN2)Ubiquitin-proteasome system (UPS)

Identifiers

PMID31319884
PMCPMC6889556
OpenAlexW2959318704

What OpenQuestion 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 OpenQuestion graph.