Evidence map›Paper›PMID 29138296›Full record

ReviewScience signaling2017

The genetics of PKMζ and memory maintenance.

Todd Charlton Sacktor, Johannes W Hell

Open access · greenAbstract readReview
In one paragraph

Review in Science signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. A Necessary Role for PKC-2 and TPA-1 in Olfactory Memory and Synaptic AMPAR Trafficking inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Glutamatergic Systems and Memory Mechanisms Underlying Opioid Addiction.Cold Spring Harbor perspectives in medicine · 2021
    Review
  14. Multiple signaling pathways are essential for synapse formation induced by synaptic adhesion molecules.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  15. Review
  16. Article
  17. Article
  18. 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 2 institutions in 1 country.

Todd Charlton SacktorDepartments of Physiology & Pharmacology, Anesthesiology, and Neurology, Robert F. Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, NY 11203, USA. tsacktor@downstate.edu jwhell@ucdavis.edu.ORCID http://orcid.org/0000-0002-8625-8701
Johannes W HellDepartment of Pharmacology, University of California, Davis, Davis, CA 95615, USA. tsacktor@downstate.edu jwhell@ucdavis.edu.ORCID http://orcid.org/0000-0001-7960-7531
SUNY Downstate Health Sciences University · USUniversity of California, Davis · US

Funding

Regulation and Neural Function of Atypical PKCR37MH057068 · NIMH · SUNY DOWNSTATE MEDICAL CENTER · PI SACKTOR, TODD C · 2011 to 2020
$4.0M
CRCNS: PKMzeta-Dependent Protein Synthesis Maintains Synaptic PlasticityR01DA034970 · NIDA · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI SHOUVAL, HAREL ZEEV · 2012 to 2016
$1.4M
NIDA NIH HHS R01 DA034970NIMH NIH HHS R37 MH057068
6 · The paper itself

Abstract

Elucidating the molecular mechanisms that maintain long-term memory is a fundamental goal of neuroscience. Accumulating evidence suggests that persistent signaling by the atypical protein kinase C (PKC) isoform protein kinase Mζ (PKMζ) might maintain synaptic long-term potentiation (LTP) and long-term memory. However, the role of PKMζ has been challenged by genetic data from PKMζ-knockout mice showing intact LTP and long-term memory. Moreover, the PKMζ inhibitor peptide ζ inhibitory peptide (ZIP) reverses LTP and erases memory in both wild-type and knockout mice. Data from four papers using additional isoform-specific genetic approaches have helped to reconcile these conflicting findings. First, a PKMζ-antisense approach showed that LTP and long-term memory in PKMζ-knockout mice are mediated through a compensatory mechanism that depends on another ZIP-sensitive atypical isoform, PKCι/λ. Second, short hairpin RNAs decreasing the amounts of individual atypical isoforms without inducing compensation disrupted memory in different temporal phases. PKCι/λ knockdown disrupted short-term memory, whereas PKMζ knockdown specifically erased long-term memory. Third, conditional PKCι/λ knockout induced compensation by rapidly activating PKMζ to preserve short-term memory. Fourth, a dominant-negative approach in the model system

Indexed as

AnimalsHumansLong-Term PotentiationMemoryProtein Kinase CProtein Kinase C zetaSignal TransductionProtein Kinase CProtein Kinase C zeta

Identifiers

PMID29138296
PMCPMC6171341
OpenAlexW2768847639

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.