Evidence map›Paper›PMID 24298140›Full record

ArticlePhilosophical transactions of the Royal Society of London. Series B, Biological sciences2014

Alternative polyadenylation and differential expression of Shank mRNAs in the synaptic neuropil.

Irina Epstein, Georgi Tushev, Tristan J Will, Irena Vlatkovic, Iván J Cajigas, Erin M Schuman

Open access · bronzeAbstract read
In one paragraph

Article in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. GABA Neuronal Deletion ofFrontiers in cellular neuroscience · 2018
    Article
  9. Transcriptomic Analysis of Ribosome-Bound mRNA in Cortical NeuritesThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  10. Review
  11. Article
  12. Article
  13. Synaptic plasticity in health and disease: introduction and overview.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014
    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

6 authors at 1 institution in 1 country.

Irina EpsteinMax Planck Institute for Brain Research, , Max-von-Laue Strasse 4, Frankfurt am Main 60438, Germany.
Georgi Tushev
Tristan J Will
Irena Vlatkovic
Iván J Cajigas
Erin M Schuman
Max Planck Institute for Brain Research · DE

Funding

European Research Council 294376
6 · The paper itself

Abstract

The stability and dynamics of synapses rely on tight regulation of the synaptic proteome. Shank proteins, encoded by the three genes Shank1, Shank2 and Shank3 are scaffold molecules in the postsynaptic density of excitatory neurons that contribute to activity-dependent neuronal signalling. Mutations in the Shank genes are associated with neurological diseases. Using state-of-the-art technologies, we investigated the levels of expression of the Shank family messenger RNAs (mRNAs) within the synaptic neuropil of the rat hippocampus. We detected all three Shank transcripts in the neuropil of CA1 pyramidal neurons. We found Shank1 to be the most abundantly expressed among the three Shank mRNA homologues. We also examined the turnover of Shank mRNAs and predict the half-lives of Shank1, Shank2 and Shank3 mRNAs to be 18-28 h. Using 3'-end sequencing, we identified novel 3' ends for the Shank1 and Shank2 3' untranslated regions (3' UTRs) that may contribute to the diversity of alternative polyadenylation (APA) for the Shank transcripts. Our findings consolidate the view that the Shank molecules play a central role at the postsynaptic density. This study may shed light on synaptopathologies associated with disruption of local protein synthesis, perhaps linked to mutations in mRNA 3' UTRs or inappropriate 3' end processing.

Indexed as

Models, NeurologicalAnimalsBase SequenceCA1 Region, HippocampalDNA PrimersGene Expression RegulationHalf-LifeImmunoblottingIn Situ HybridizationMicrodissectionMolecular Sequence DataNerve Tissue ProteinsNeuropilPolyadenylationRatsReal-Time Polymerase Chain ReactionDNA PrimersNerve Tissue ProteinsRNA, MessengerShank1 protein, rat3′ untranslated regionalternative polyadenylationhippocampusShank mRNAsynaptic neuropil

Identifiers

PMID24298140
PMCPMC3843870
OpenAlexW2067647220

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.