Evidence map›Paper›PMID 22669976›Full record

ArticleThe Journal of biological chemistry2012

Human axonal survival of motor neuron (a-SMN) protein stimulates axon growth, cell motility, C-C motif ligand 2 (CCL2), and insulin-like growth factor-1 (IGF1) production.

Denise Locatelli, Mineko Terao, Maddalena Fratelli, Adriana Zanetti, Mami Kurosaki, Monica Lupi, Maria Monica Barzago, Andrea Uggetti, Silvia Capra, Paolo D'Errico and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. 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
1.1field-weighted citation impact, top 24% 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, 27 citations in OpenAlex.

  1. Review
  2. Article
  3. Boosting the peripheral immune response in the skeletal muscles improved motor function in ALS transgenic mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  4. Article
  5. The role of survival motor neuron protein (SMN) in protein homeostasis.Cellular and molecular life sciences : CMLS · 2018
    Review
  6. Article
  7. Article
  8. Diverse role of survival motor neuron protein.Biochimica et biophysica acta. Gene regulatory mechanisms · 2017
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. 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

12 authors at 2 institutions in 1 country.

Denise LocatelliMolecular Neuroanatomy Laboratory, Department of Experimental Neurophysiology and Epileptology, Istituto Neurologico "C. Besta," via Celoria 11, 20133 Milano, Italy.
Mineko Terao
Maddalena Fratelli
Adriana Zanetti
Mami Kurosaki
Monica Lupi
Maria Monica Barzago
Andrea Uggetti
Silvia Capra
Paolo D'Errico
Giorgio S Battaglia
Enrico Garattini
Mario Negri Institute for Pharmacological Research · ITFondazione IRCCS Istituto Neurologico Carlo Besta · IT

Funding

Telethon GGP07223
6 · The paper itself

Abstract

Spinal muscular atrophy is a fatal genetic disease of motoneurons due to loss of full-length survival of motor neuron protein, the main product of the disease gene SMN1. Axonal SMN (a-SMN) is an alternatively spliced isoform of SMN1, generated by retention of intron 3. To study a-SMN function, we generated cellular clones for the expression of the protein in mouse motoneuron-like NSC34 cells. The model was instrumental in providing evidence that a-SMN decreases cell growth and plays an important role in the processes of axon growth and cellular motility. In our conditions, low levels of a-SMN expression were sufficient to trigger the observed biological effects, which were not modified by further increasing the amounts of the expressed protein. Differential transcriptome analysis led to the identification of novel a-SMN-regulated factors, i.e. the transcripts coding for the two chemokines, C-C motif ligands 2 and 7 (CCL2 and CCL7), as well as the neuronal and myotrophic factor, insulin-like growth factor-1 (IGF1). a-SMN-dependent induction of CCL2 and IGF1 mRNAs resulted in increased intracellular levels and secretion of the respective protein products. Induction of CCL2 contributes to the a-SMN effects, mediating part of the action on axon growth and random cell motility, as indicated by chemokine knockdown and re-addition studies. Our results shed new light on a-SMN function and the underlying molecular mechanisms. The data provide a rational framework to understand the role of a-SMN deficiency in the etiopathogenesis of spinal muscular atrophy.

Indexed as

Cell MovementAxonsCell LineCell ProliferationCell ShapeChemokine CCL2Chemokine CCL7Gene Expression ProfilingGene Expression RegulationHumansInsulin-Like Growth Factor INeuronsProtein TransportSurvival of Motor Neuron 1 ProteinTranscription, GeneticTranscriptomeCCL2 protein, humanCCL7 protein, humanChemokine CCL2Chemokine CCL7Insulin-Like Growth Factor ISMN1 protein, humanSurvival of Motor Neuron 1 Protein

Identifiers

PMID22669976
PMCPMC3406665
OpenAlexW1992439336

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.