Evidence map›Paper›PMID 19302474›Full record

ArticleJournal of neurochemistry2009

The atypical protein kinase C in Aplysia can form a protein kinase M by cleavage.

Joanna K Bougie, Travis Lim, Carole Abi Farah, Varsha Manjunath, Ikue Nagakura, Gino B Ferraro, Wayne S Sossin

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.9field-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

45 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Pattern detection in the TGFβ cascade controls the induction of long-term synaptic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  3. The evolution of synaptic and cognitive capacity: Insights from the nervous system transcriptome ofProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  4. Article
  5. Isoform Specificity of PKMs during Long-Term Facilitation inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Memory Takes Time.Neuron · 2017
    Review
  12. Article
  13. Cell-Specific PKM Isoforms Contribute to the Maintenance of Different Forms of Persistent Long-Term Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Mechanisms of polarity protein expression control.Current opinion in cell biology · 2016
    Review
  19. Article
  20. Nonassociative learning in invertebrates.Cold Spring Harbor perspectives in biology · 2015
    Review
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

7 authors at 2 institutions in 1 country.

Joanna K BougieDepartment of Psychology, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada.
Travis Lim
Carole Abi Farah
Varsha Manjunath
Ikue Nagakura
Gino B Ferraro
Wayne S Sossin
Montreal Neurological Institute and Hospital · CAMcGill University · CA

Funding

CIHR 12046
6 · The paper itself

Abstract

In vertebrates, a brain-specific transcript from the atypical protein kinase C (PKC) zeta gene encodes protein kinase M (PKM) zeta, a constitutively active kinase implicated in the maintenance of synaptic plasticity and memory. We have cloned the atypical PKC from Aplysia, PKC Apl III. We did not find a transcript in Aplysia encoding PKMzeta, and evolutionary analysis of atypical PKCs suggests formation of this transcript is restricted to vertebrates. Instead, over-expression of PKC Apl III in Aplysia sensory neurons leads to production of a PKM fragment of PKC Apl III. This cleavage was induced by calcium and blocked by calpain inhibitors. Moreover, nervous system enriched spliced forms of PKC Apl III show enhanced cleavage. PKC Apl III could also be activated through phosphorylation downstream of phosphoinositide 3-kinase. We suggest that PKM forms of atypical PKCs play a conserved role in memory formation, but the mechanism of formation of these kinases has changed over evolution.

Indexed as

Alternative SplicingAmino Acid SequenceAnimalsAplysiaCalpainCells, CulturedCloning, MolecularDNAGene Expression Regulation, EnzymologicImage Processing, Computer-AssistedImmunohistochemistryMicroinjectionsMicroscopy, ConfocalMolecular Sequence DataNeuronal PlasticityPhosphorylationCalpainDNAProtein Kinase CSerotonin

Identifiers

PMID19302474
PMCPMC5154740
OpenAlexW1985927272

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.