Evidence map›Paper›PMID 25700840›Full record

ReviewBiochimica et biophysica acta2015

Distinct roles of multiple isoforms of CaMKII in signaling to the nucleus.

Huan Ma, Boxing Li, Richard W Tsien

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Genetic mechanisms for impaired synaptic plasticity in schizophrenia revealed by computational modeling.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Review
  4. Functional implications of CaMKII alternative splicing.The European journal of neuroscience · 2021
    Review
  5. Article
  6. Review
  7. GABAFrontiers in neuroscience · 2020
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Bilobal architecture is a requirement for calmodulin signaling to CaProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  13. Article
  14. From Gene to Behavior: L-Type Calcium Channel Mechanisms Underlying Neuropsychiatric Symptoms.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017
    Review
  15. 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
  16. Review
  17. Review
  18. Article
  19. 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

3 authors at 1 institution in 1 country.

Huan MaNYU Neuroscience Institute, NYU Langone Medical Center, New York, NY 10016, USA. Electronic address: mahuan@gmail.com.
Boxing LiNYU Neuroscience Institute, NYU Langone Medical Center, New York, NY 10016, USA.
Richard W TsienNYU Neuroscience Institute, NYU Langone Medical Center, New York, NY 10016, USA. Electronic address: richard.tsien@nyumc.org.
NYU Langone Health · US

Funding

Neuronal Adaptation and Plasticity after Chronic DisuseR01MH071739 · NIMH · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI TSIEN, RICHARD W · 2015 to 2024
$5.5M
NEURONAL FUNCTIONS OF MULTIPLE TYPES OF CALCIUM CHANNELSR01NS024067 · NINDS · YALE UNIVERSITY · PI TSIEN, RICHARD W · 1986 to 2014
$5.0M
Synaptic Adaptation and Plasticity After Chronic DisuseR37MH071739 · NIMH · STANFORD UNIVERSITY · PI TSIEN, RICHARD W · 2004 to 2013
$3.8M
CALCIUM CHANNELS, CALMODULIN AND NUCLEAR CREB SIGNALINGR01GM058234 · NIGMS · STANFORD UNIVERSITY · PI TSIEN, RICHARD W · 1998 to 2010
$3.0M
Calcium Channels, Calmodulin and Nuclear CREB SignalingR01DA040484 · NIDA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI TSIEN, RICHARD W · 2015 to 2019
$2.0M
NIDA NIH HHS R01 DA040484NIGMS NIH HHS GM058234NIGMS NIH HHS R01 GM058234NIMH NIH HHS R01 MH071739NIMH NIH HHS R37 MH071739NINDS NIH HHS NS024067NINDS NIH HHS R01 NS024067
6 · The paper itself

Abstract

Long-lasting synaptic changes following information acquisition are critical steps for memory. In this process, long-term potentiation (LTP) is widely considered as one of the major cellular mechanisms modifying synaptic strength. It can be classified into early phase LTP (E-LTP) and late phase LTP (L-LTP) based on its duration. Using genetically modified mice, investigators have recognized the critical role of CaMKII in E-LTP and memory. However, its function in L-LTP, which is strongly dependent on gene transcription and protein synthesis, is still unclear. In this review, we discuss how different isoforms of CaMKII are coordinated to regulate gene expression in an activity-dependent manner, and thus contribute to L-LTP and memory. This article is part of a Special Issue entitled: 13th European Symposium on Calcium.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell NucleusGene Expression RegulationHumansIsoenzymesLong-Term PotentiationMemoryMiceProtein BiosynthesisSignal TransductionTranscription, GeneticCalcium-Calmodulin-Dependent Protein Kinase Type 2IsoenzymesCaM translocationExcitation–transcription couplingLong-term potentiation (LTP)αCaMKIIβCaMKIIγCaMKII

Identifiers

PMID25700840
PMCPMC4522395
OpenAlexW2034137610

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.