Evidence map›Paper›PMID 35399514›Full record

ArticleFrontiers in cell and developmental biology2022

c-Abl Activation Linked to Autophagy-Lysosomal Dysfunction Contributes to Neurological Impairment in Niemann-Pick Type A Disease.

Tamara Marín, Andrés E Dulcey, Fabián Campos, Catalina de la Fuente, Mariana Acuña, Juan Castro, Claudio Pinto, María José Yañez, Cristian Cortez, David W McGrath and 8 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 18 citations in OpenAlex.

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  15. Neuronopathic Gaucher disease: Beyond lysosomal dysfunction.Frontiers in molecular neuroscience · 2022
    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

18 authors at 9 institutions in 4 countries.

Tamara MarínDepartment of Gastroenterology, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
Andrés E DulceyEarly Translation Branch, National Center for Advancing Translational Sciences (NCATS), NIH, Rockville, MD, United States.
Fabián CamposDepartment of Gastroenterology, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
Catalina de la FuenteLaboratory of Cell Signaling, Center for Aging and Regeneration (CARE), Millennium Institute on Immunology and Immunotherapy (IMII), Department of Cellular and Molecular Biology, Biological Sciences Faculty, Pontificia Universidad Católica de Chile, Santiago, Chile.
Mariana AcuñaDepartment of Gastroenterology, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
Juan CastroDepartment of Gastroenterology, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
Claudio PintoLaboratory of Cell Signaling, Center for Aging and Regeneration (CARE), Millennium Institute on Immunology and Immunotherapy (IMII), Department of Cellular and Molecular Biology, Biological Sciences Faculty, Pontificia Universidad Católica de Chile, Santiago, Chile.
María José YañezSchool of Medical Technology, Health Sciences Faculty, Universidad San Sebastián, Santiago, Chile.
Cristian CortezCenter for Genomics and Bioinformatics, Faculty of Science, Universidad Mayor, Santiago, Chile.
David W McGrathCell Communication and Migration Laboratory, Institute of Biochemistry and Molecular Cell Biology, Center for Experimental Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Pablo J SáezCell Communication and Migration Laboratory, Institute of Biochemistry and Molecular Cell Biology, Center for Experimental Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Kirill GorshkovEarly Translation Branch, National Center for Advancing Translational Sciences (NCATS), NIH, Rockville, MD, United States.
Wei ZhengEarly Translation Branch, National Center for Advancing Translational Sciences (NCATS), NIH, Rockville, MD, United States.
Noel SouthallEarly Translation Branch, National Center for Advancing Translational Sciences (NCATS), NIH, Rockville, MD, United States.
Maria Carmo-FonsecaInstituto de Medicina Molecular Joȧo Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal.
Juan MarugánEarly Translation Branch, National Center for Advancing Translational Sciences (NCATS), NIH, Rockville, MD, United States.
Alejandra R AlvarezLaboratory of Cell Signaling, Center for Aging and Regeneration (CARE), Millennium Institute on Immunology and Immunotherapy (IMII), Department of Cellular and Molecular Biology, Biological Sciences Faculty, Pontificia Universidad Católica de Chile, Santiago, Chile.
Silvana ZanlungoDepartment of Gastroenterology, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
National Center for Advancing Translational Sciences · USPontificia Universidad Católica de Chile · CLMillennium Institute on Immunology and Immunotherapy · CLHarvard University · USSan Sebastián University · CLUniversidad Mayor · CLUniversität Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DEUniversity of Lisbon · PT

Funding

Drug Repurposing Screening for Rare and Neglected DiseasesZIATR000018 · NCATS · NATIONAL CENTER FOR ADVANCING TRANSLATIONAL SCIENCES · PI ZHENG, WEI · 2015 to 2025
$24.6M
6 · The paper itself

Abstract

Niemann-Pick type A (NPA) disease is a fatal lysosomal neurodegenerative disorder caused by the deficiency in acid sphingomyelinase (ASM) activity. NPA patients present severe and progressive neurodegeneration starting at an early age. Currently, there is no effective treatment for this disease and NPA patients die between 2 and 3 years of age. NPA is characterized by an accumulation of sphingomyelin in lysosomes and dysfunction in the autophagy-lysosomal pathway. Recent studies show that c-Abl tyrosine kinase activity downregulates autophagy and the lysosomal pathway. Interestingly, this kinase is also activated in other lysosomal neurodegenerative disorders. Here, we describe that c-Abl activation contributes to the mechanisms of neuronal damage and death in NPA disease. Our data demonstrate that: 1) c-Abl is activated

Indexed as

autophay-lysosomal pathwayc-Abl kinaselysosomal storage disorder (LSD)neurodegenerationNiemann-Pick disease

Identifiers

PMID35399514
PMCPMC8985125
OpenAlexW4220694702

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.