Evidence map›Paper›PMID 33382987›Full record

ArticleExperimental neurology2021

Spinal motor neuron loss occurs through a p53-and-p21-independent mechanism in the Smn

Emily J Reedich, Martin Kalski, Nicholas Armijo, Gregory A Cox, Christine J DiDonato

Open access · hybridAbstract read
In one paragraph

Article in Experimental neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. 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

5 authors at 3 institutions in 1 country.

Emily J ReedichHuman Molecular Genetics and Physiology Program, Stanley Manne Children's Research Institute at Ann & Robert H. Lurie Children's Hospital, Chicago, IL, USA; Department of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Martin KalskiHuman Molecular Genetics and Physiology Program, Stanley Manne Children's Research Institute at Ann & Robert H. Lurie Children's Hospital, Chicago, IL, USA.
Nicholas ArmijoHuman Molecular Genetics and Physiology Program, Stanley Manne Children's Research Institute at Ann & Robert H. Lurie Children's Hospital, Chicago, IL, USA.
Gregory A CoxThe Jackson Laboratory, Bar Harbor, ME, USA; Graduate School of Biomedical Sciences and Engineering, University of Maine, Orono, ME, USA.
Christine J DiDonatoHuman Molecular Genetics and Physiology Program, Stanley Manne Children's Research Institute at Ann & Robert H. Lurie Children's Hospital, Chicago, IL, USA; Department of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. Electronic address: c-didonato@northwestern.edu.
Lurie Children's Hospital · USNorthwestern University · USJackson Laboratory · US

Funding

General Motor Control Mechanisms and Disease Training ProgramT32NS041234 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BEVAN, MARK D · 2001 to 2022
$6.0M
Spinal Muscular Atrophy: Inducing SMN Expression: Administrative SupplementR01NS060926 · NINDS · LURIE CHILDREN'S HOSPITAL OF CHICAGO · PI DIDONATO, CHRISTINE J. · 2007 to 2017
$3.4M
Long-term effect of troponin activators for spinal muscular atrophyR21NS103107 · NINDS · LURIE CHILDREN'S HOSPITAL OF CHICAGO · PI DIDONATO, CHRISTINE J. · 2017 to 2018
$429k
NINDS NIH HHS R01 NS060926NINDS NIH HHS R21 NS103107NINDS NIH HHS T32 NS041234
6 · The paper itself

Abstract

Spinal muscular atrophy (SMA) is a pediatric neuromuscular disease caused by genetic deficiency of the survival motor neuron (SMN) protein. Pathological hallmarks of SMA are spinal motor neuron loss and skeletal muscle atrophy. The molecular mechanisms that elicit and drive preferential motor neuron degeneration and death in SMA remain unclear. Transcriptomic studies consistently report p53 pathway activation in motor neurons and spinal cord tissue of SMA mice. Recent work has identified p53 as an inducer of spinal motor neuron loss in severe Δ7 SMA mice. Additionally, the cyclin-dependent kinase inhibitor P21 (Cdkn1a), an inducer of cell cycle arrest and mediator of skeletal muscle atrophy, is consistently increased in motor neurons, spinal cords, and other tissues of various SMA models. p21 is a p53 transcriptional target but can be independently induced by cellular stressors. To ascertain whether p53 and p21 signaling pathways mediate spinal motor neuron death in milder SMA mice, and how they affect the overall SMA phenotype, we introduced Trp53 and P21 null alleles onto the Smn

Indexed as

AnimalsCell DeathCell SurvivalCyclin-Dependent Kinase Inhibitor p21Disease Models, AnimalFemaleImmunohistochemistryLife ExpectancyMaleMiceMice, KnockoutMotor NeuronsMuscular Atrophy, SpinalSignal TransductionSpinal CordSurvival AnalysisCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21SMN2 protein, mouseSurvival of Motor Neuron 2 ProteinTrp53 protein, mouseTumor Suppressor Protein p53Motor neuronMousep21 (cdkn1a)p53Smn(2B/−)Spinal muscular atrophy (SMA)Survival motor neuron (SMN)

Identifiers

PMID33382987
PMCPMC7870563
OpenAlexW3114679522

What Socratic holds

Textmetadata
LicenceTDM
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.