Evidence map›Paper›PMID 19343312›Full record

ArticleResults and problems in cell differentiation2009

Spinal muscular atrophy and a model for survival of motor neuron protein function in axonal ribonucleoprotein complexes.

Wilfried Rossoll, Gary J Bassell

Open access · greenAbstract read
In one paragraph

Article in Results and problems in cell differentiation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
31.8field-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

43 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Journal of clinical medicine · 2024
    Article
  5. Article
  6. Gene Therapy in ALS and SMA: Advances, Challenges and Perspectives.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. A newRNA (New York, N.Y.) · 2017
    Article
  15. Article
  16. Article
  17. Dysregulation of mRNA Localization and Translation in Genetic Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Review
  18. Deficiency of the Survival of Motor Neuron Protein Impairs mRNA Localization and Local Translation in the Growth Cone of Motor Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  19. Article
  20. Article
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

2 authors at 1 institution in 1 country.

Wilfried RossollDepartments of Cell Biology and Neurology, Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, GA 30322, USA. wrossol@emory.edu
Gary J Bassell
Emory University · US

Funding

Spinal Muscular Atrophy: SMNs role in MRNA localization and local translationR01HD055835 · NICHD · EMORY UNIVERSITY · PI BASSELL, GARY J · 2007 to 2011
$1.8M
Spinal muscular atrophy: a novel role of SMN in axonal ribonucleoprotein complexeR21HD056130 · NICHD · EMORY UNIVERSITY · PI ROSSOLL, WILFRIED · 2007 to 2008
$416k
NICHD NIH HHS HD055835NICHD NIH HHS HD56130NICHD NIH HHS R01 HD055835NICHD NIH HHS R21 HD056130
6 · The paper itself

Abstract

Spinal muscular atrophy (SMA) is a neurodegenerative disease that results from loss of function of the SMN1 gene, encoding the ubiquitously expressed survival of motor neuron (SMN) protein, a protein best known for its housekeeping role in the SMN-Gemin multiprotein complex involved in spliceosomal small nuclear ribonucleoprotein (snRNP) assembly. However, numerous studies reveal that SMN has many interaction partners, including mRNA binding proteins and actin regulators, suggesting its diverse role as a molecular chaperone involved in mRNA metabolism. This review focuses on studies suggesting an important role of SMN in regulating the assembly, localization, or stability of axonal messenger ribonucleoprotein (mRNP) complexes. Various animal models for SMA are discussed, and phenotypes described that indicate a predominant function for SMN in neuronal development and synapse formation. These models have begun to be used to test different therapeutic strategies that have the potential to restore SMN function. Further work to elucidate SMN mechanisms within motor neurons and other cell types involved in neuromuscular circuitry hold promise for the potential treatment of SMA.

Indexed as

Models, BiologicalMuscular Atrophy, SpinalRNA, MessengerActinsAnimalsAxonsCaenorhabditis elegansDisease Models, AnimalDrosophilaHumansMiceSMN Complex ProteinsSurvival of Motor Neuron 1 ProteinZebrafishActinsRNA, MessengerSMN Complex ProteinsSurvival of Motor Neuron 1 Protein

Identifiers

PMID19343312
PMCPMC3718852
OpenAlexW2118334335

What OpenQuestion 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 OpenQuestion graph.