Evidence map›Paper›PMID 11549715›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Mitogen-activated protein kinase regulates early phosphorylation and delayed expression of Ca2+/calmodulin-dependent protein kinase II in long-term potentiation.

M G Giovannini, R D Blitzer, T Wong, K Asoma, P Tsokas, J H Morrison, R Iyengar, E M Landau

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Role of CaFrontiers in molecular neuroscience · 2022
    Review
  7. Review
  8. Transfer of complex regional pain syndrome to mice via human autoantibodies is mediated by interleukin-1-induced mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  9. Memory-Related Synaptic Plasticity Is Sexually Dimorphic in Rodent Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Insulin resistance in Alzheimer's disease.Neurobiology of disease · 2014
    Review
  17. Article
  18. Article
  19. Review
  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

8 authors at 2 institutions in 2 countries.

M G GiovanniniDepartment of Pharmacology, Mount Sinai School of Medicine, New York, New York 10029, USA.
R D Blitzer
T Wong
K Asoma
P Tsokas
J H Morrison
R Iyengar
E M Landau
Icahn School of Medicine at Mount Sinai · USUniversity of Florence · IT

Funding

Glutamate receptors in aging cortical circuitsR37AG006647 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI MORRISON, JOHN H · 2007 to 2015
$4.8M
GLUTAMATE receptors in aging cortical circuitsR01AG006647 · NIA · SCRIPPS CLINIC AND RESEARCH FOUNDATION · PI MORRISON, JOHN HENRY · 1987 to 2005
$2.2M
CAMP AND PHOSPHATASE CASCADE AND LTPR01NS033646 · NINDS · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI LANDAU, EMMANUEL M · 1997 to 1999
–
NIA NIH HHS AG06647NIA NIH HHS R01 AG006647NIA NIH HHS R37 AG006647NIGMS NIH HHS GM5408NINDS NIH HHS NS33646
6 · The paper itself

Abstract

Activation of mitogen-activated protein kinase (MAPK) and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) are required for numerous forms of neuronal plasticity, including long-term potentiation (LTP). We induced LTP in rat hippocampal area CA1 using theta-pulse stimulation (TPS) paired with beta-adrenergic receptor activation [isoproterenol (ISO)], a protocol that may be particularly relevant to normal patterns of hippocampal activity during learning. This stimulation resulted in a transient phosphorylation of p42 MAPK, and the resulting LTP was MAPK dependent. In addition, CaMKII was regulated in two, temporally distinct ways after TPS-ISO: a transient rise in the fraction of phosphorylated CaMKII and a subsequent persistent increase in CaMKII expression. The increases in MAPK and CaMKII phosphorylation were strongly colocalized in the dendrites and cell bodies of CA1 pyramidal cells, and both the transient phosphorylation and delayed expression of CaMKII were prevented by inhibiting p42/p44 MAPK. These results establish a novel bimodal regulation of CaMKII by MAPK, which may contribute to both post-translational modification and increased gene expression.

Indexed as

Adrenergic beta-AgonistsAnimalsCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Electric StimulationEnzyme InhibitorsExcitatory Postsynaptic PotentialsGrowth SubstancesHeLa CellsHippocampusHumansIn Vitro TechniquesIsoproterenolLong-Term PotentiationMaleMitogen-Activated Protein Kinase 1Adrenergic beta-AgonistsCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Enzyme InhibitorsGrowth SubstancesIsoproterenolMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinase 7Mitogen-Activated Protein KinasesReceptors, Adrenergic, beta

Identifiers

PMID11549715
PMCPMC6762991
OpenAlexW1848864628

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.