Evidence map›Paper›PMID 36006469›Full record

ReviewCellular and molecular life sciences : CMLS2022

The phospho-landscape of the survival of motoneuron protein (SMN) protein: relevance for spinal muscular atrophy (SMA).

Nora Tula Detering, Tobias Schüning, Niko Hensel, Peter Claus

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Single NucleotideNeurology. Genetics · 2025
    Article
  5. Review
  6. Patient-specific responses toMolecular therapy. Methods & clinical development · 2024
    Article
  7. Review
  8. Review
  9. Review
  10. 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

4 authors at 3 institutions in 3 countries.

Nora Tula Detering *SMATHERIA gGmbH - Non-Profit Biomedical Research Institute, Hannover, Germany.
Tobias Schüning *SMATHERIA gGmbH - Non-Profit Biomedical Research Institute, Hannover, Germany.
Niko HenselOttawa Hospital Research Institute (OHRI), Ottawa, Canada.
Peter ClausSMATHERIA gGmbH - Non-Profit Biomedical Research Institute, Hannover, Germany. peter.claus@smatheria.org.ORCID http://orcid.org/0000-0003-3824-9445
Research Institute for Philosophy Hannover · DENOAA National Weather Service · USOttawa Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spinal muscular atrophy (SMA) is caused by low levels of the survival of motoneuron (SMN) Protein leading to preferential degeneration of lower motoneurons in the ventral horn of the spinal cord and brain stem. However, the SMN protein is ubiquitously expressed and there is growing evidence of a multisystem phenotype in SMA. Since a loss of SMN function is critical, it is important to decipher the regulatory mechanisms of SMN function starting on the level of the SMN protein itself. Posttranslational modifications (PTMs) of proteins regulate multiple functions and processes, including activity, cellular trafficking, and stability. Several PTM sites have been identified within the SMN sequence. Here, we map the identified SMN PTMs highlighting phosphorylation as a key regulator affecting localization, stability and functions of SMN. Furthermore, we propose SMN phosphorylation as a crucial factor for intracellular interaction and cellular distribution of SMN. We outline the relevance of phosphorylation of the spinal muscular atrophy (SMA) gene product SMN with regard to basic housekeeping functions of SMN impaired in this neurodegenerative disease. Finally, we compare SMA patient mutations with putative and verified phosphorylation sites. Thus, we emphasize the importance of phosphorylation as a cellular modulator in a clinical perspective as a potential additional target for combinatorial SMA treatment strategies.

Indexed as

Muscular Atrophy, SpinalNeurodegenerative DiseasesAnimalsDisease Models, AnimalMotor NeuronsPhenotypeSurvival of Motor Neuron 1 ProteinSurvival of Motor Neuron 1 ProteinPhosphorylationPosttranslational modification (PTM)Spinal muscular atrophy (sMA)Survival of motoneuron (SMN) protein

Identifiers

PMID36006469
PMCPMC11071818
OpenAlexW4293034650

What OpenQuestion holds

Textmetadata
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.