Evidence map›Paper›PMID 28178525›Full record

ArticleCell reports2017

Single-Cell Analysis of SMN Reveals Its Broader Role in Neuromuscular Disease.

Natalia Rodriguez-Muela, Nadia K Litterman, Erika M Norabuena, Jesse L Mull, Maria José Galazo, Chicheng Sun, Shi-Yan Ng, Nina R Makhortova, Andrew White, Maureen M Lynes and 4 more

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

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 52 citations in OpenAlex.

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  15. Spinal muscular atrophy.Nature reviews. Disease primers · 2022
    Review
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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

14 authors at 3 institutions in 1 country.

Natalia Rodriguez-MuelaDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA. Electronic address: natalia_rodriguezmuela@harvard.edu.
Nadia K LittermanDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA.
Erika M NorabuenaDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA.
Jesse L MullDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA.
Maria José GalazoDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA.
Chicheng SunDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA.
Shi-Yan NgDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA.
Nina R MakhortovaDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA.
Andrew WhiteDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA.
Maureen M LynesDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA.
Wendy K ChungDepartment of Pediatrics, Columbia University, New York, NY 10032, USA.
Lance S DavidowDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA.
Jeffrey D MacklisDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA; Center for Brain Science, Harvard University, Cambridge, MA 02138, USA.
Lee L RubinDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA; Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA. Electronic address: lee_rubin@harvard.edu.
Harvard University · USHarvard Stem Cell Institute · USColumbia University · US

Funding

Smn Regulation of Neuromuscular Morphogenesis in DrosophilaP01NS066888 · NINDS · HARVARD MEDICAL SCHOOL · PI ARTAVANIS-TSAKONAS, SPYRIDON · 2010 to 2014
$6.7M
Molecular Controls over Neurogenesis, Subtype Development, and Diversity of Cortical Output Projection NeuronsR01NS045523 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI MACKLIS, JEFFREY D · 2002 to 2020
$5.4M
Molecular Mechanisms of CTIP2 Function in Corticospinal Motor Neuron DevelopmentR01NS075672 · NINDS · HARVARD UNIVERSITY · PI MACKLIS, JEFFREY D · 2012 to 2016
$1.8M
NINDS NIH HHS P01 NS066888NINDS NIH HHS R01 NS045523NINDS NIH HHS R01 NS075672
6 · The paper itself

Abstract

The mechanism underlying selective motor neuron (MN) death remains an essential question in the MN disease field. The MN disease spinal muscular atrophy (SMA) is attributable to reduced levels of the ubiquitous protein SMN. Here, we report that SMN levels are widely variable in MNs within a single genetic background and that this heterogeneity is seen not only in SMA MNs but also in MNs derived from controls and amyotrophic lateral sclerosis (ALS) patients. Furthermore, cells with low SMN are more susceptible to cell death. These findings raise the important clinical implication that some SMN-elevating therapeutics might be effective in MN diseases besides SMA. Supporting this, we found that increasing SMN across all MN populations using an Nedd8-activating enzyme inhibitor promotes survival in both SMA and ALS-derived MNs. Altogether, our work demonstrates that examination of human neurons at the single-cell level can reveal alternative strategies to be explored in the treatment of degenerative diseases.

Indexed as

Amyotrophic Lateral SclerosisAnimalsDisease Models, AnimalHumansMiceMotor NeuronsMuscular Atrophy, SpinalNeuromuscular DiseasesSingle-Cell AnalysisSMN Complex ProteinsSpinal CordSMN Complex Proteinsamyotrophic lateral sclerosiscell deathcell heterogeneityprotein degradationsingle cell analysisspinal muscular atrophysurvival of motor neurontherapeutics

Identifiers

PMID28178525
PMCPMC5463539
OpenAlexW2586338189

What OpenQuestion holds

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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.