Evidence map›Paper›PMID 32586831›Full record

ArticleDisease models & mechanisms2020

Mitochondrial damage and senescence phenotype of cells derived from a novel frataxin G127V point mutation mouse model of Friedreich's ataxia.

Daniel Fil, Balu K Chacko, Robbie Conley, Xiaosen Ouyang, Jianhua Zhang, Victor M Darley-Usmar, Aamir R Zuberi, Cathleen M Lutz, Marek Napierala, Jill S Napierala

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Disease models & mechanisms, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Daniel FilDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, 1825 University Boulevard, Birmingham, AL 35294, USA.
Balu K ChackoDepartment of Pathology, University of Alabama at Birmingham, 901 19th Street South, Birmingham, AL 35294, USA.
Robbie ConleyDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, 1825 University Boulevard, Birmingham, AL 35294, USA.
Xiaosen OuyangDepartment of Pathology, University of Alabama at Birmingham, 901 19th Street South, Birmingham, AL 35294, USA.
Jianhua ZhangDepartment of Pathology, University of Alabama at Birmingham, 901 19th Street South, Birmingham, AL 35294, USA.
Victor M Darley-UsmarDepartment of Pathology, University of Alabama at Birmingham, 901 19th Street South, Birmingham, AL 35294, USA.
Aamir R ZuberiThe Rare and Orphan Disease Center, JAX Center for Precision Genetics, 600 Main Street, Bar Harbor, ME 04609, USA.
Cathleen M LutzThe Rare and Orphan Disease Center, JAX Center for Precision Genetics, 600 Main Street, Bar Harbor, ME 04609, USA.
Marek NapieralaDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, 1825 University Boulevard, Birmingham, AL 35294, USA.
Jill S NapieralaDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, 1825 University Boulevard, Birmingham, AL 35294, USA jsbutler@uab.edu.ORCID 0000-0002-5141-0822
University of Alabama at Birmingham · US

Funding

Sex hormones and arthritis in a long lived animal modelP30AG050886 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DAVID B ALLISON · 2015 to 2026
$11.3M
GAA REPEATS INDUCED EPIGENETIC SILENCING IN FRIEDREICH'S ATAXIAR01NS081366 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI NAPIERALA, MAREK · 2012 to 2021
$3.7M
New GAA expansion mouse for efficacy studies of treatments for Friedreich ataxiaR21NS101145 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI NAPIERALA, MAREK · 2017 to 2018
$715k
Developing models to define the Frataxin G130V-specific pathogenic mechanism in Friedreich's ataxiaR03NS099953 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI NAPIERALA, JILL SERGESKETTER · 2017 to 2018
$149k
NIA NIH HHS P30 AG050886NINDS NIH HHS R01 NS081366NINDS NIH HHS R03 NS099953NINDS NIH HHS R21 NS101145
6 · The paper itself

Abstract

Friedreich's ataxia (FRDA) is an autosomal recessive neurodegenerative disease caused by reduced expression of the mitochondrial protein frataxin (FXN). Most FRDA patients are homozygous for large expansions of GAA repeat sequences in intron 1 of

Indexed as

Cell ProliferationCellular SenescencePoint MutationAnimalsCell LineDisease Models, AnimalEnergy MetabolismFatty AcidsFibroblastsFrataxinFriedreich AtaxiaGenetic Predisposition to DiseaseIron-Binding ProteinsMice, Inbred C57BLMice, TransgenicMitochondriaFatty AcidsFrataxinIron-Binding ProteinsNfe2l2 protein, mouseNF-E2-Related Factor 2FrataxinFriedreich's ataxiaMitochondriaOxidative stressPoint mutationSenescence

Identifiers

PMID32586831
PMCPMC7406325
OpenAlexW3037204047

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.