Evidence map›Paper›PMID 17343827›Full record

ArticleBiochemical and biophysical research communications2007

Oxidation of calmodulin alters activation and regulation of CaMKII.

A J Robison, Danny G Winder, Roger J Colbran, Ryan K Bartlett

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.4field-weighted citation impact, top 23% 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

24 citing papers in PubMed, 48 citations in OpenAlex.

  1. Toxicogenomics of the Freshwater Oligochaete,International journal of molecular sciences · 2024
    Article
  2. Article
  3. Review
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  10. Review
  11. Article
  12. Article
  13. Article
  14. Impact of methionine oxidation on calmodulin structural dynamics.Biochemical and biophysical research communications · 2015
    Article
  15. Article
  16. Methionine oxidation activates a transcription factor in response to oxidative stress.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  17. Article
  18. Article
  19. Review
  20. Intracellular redox state alters NMDA receptor response during aging through Ca2+/calmodulin-dependent protein kinase II.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    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

4 authors at 1 institution in 1 country.

A J RobisonDepartment of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, TN 37232-0615, USA.
Danny G Winder
Roger J Colbran
Ryan K Bartlett
Vanderbilt University Medical Center · US

Funding

Mechanisms of CaM Kinase II Signal TransductionR01MH063232 · NIMH · VANDERBILT UNIVERSITY · PI COLBRAN, ROGER J · 2001 to 2015
$5.4M
NIMH NIH HHS MH63232NIMH NIH HHS R01 MH063232
6 · The paper itself

Abstract

Increases in reactive oxygen species and mis-regulation of calcium homeostasis are associated with various physiological conditions and disease states including aging, ischemia, exposure to drugs of abuse, and neurodegenerative diseases. In aged animals, this is accompanied by a reduction in oxidative repair mechanisms resulting in increased methionine oxidation of the calcium signaling protein calmodulin in the brain. Here, we show that oxidation of calmodulin results in an inability to: (1) activate CaMKII; (2) support Thr(286) autophosphorylation of CaMKII; (3) prevent Thr(305/6) autophosphorylation of CaMKII; (4) support binding of CaMKII to the NR2B subunit of the NMDA receptor; and (5) compete with alpha-actinin for binding to CaMKII. Moreover, oxidized calmodulin does not efficiently bind calcium/calmodulin-dependent protein kinase II (CaMKII) in rat brain lysates or in vitro. These observations contrast from past experiments performed with oxidized calmodulin and the plasma membrane calcium ATPase, where oxidized calmodulin binds to, and partially activates the PMCA. When taken together, these data suggest that oxidative stress may perturb neuronal and cardiac function via a decreased ability of oxidized calmodulin to bind, activate, and regulate the interactions of CaMKII.

Indexed as

Adenosine TriphosphateAnimalsBlotting, WesternCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2CalmodulinEnzyme ActivationHydrogen PeroxideMagnesiumMutationOxidation-ReductionPhosphorylationProtein BindingRatsReceptors, N-Methyl-D-AspartateAdenosine TriphosphateCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2CalmodulinHydrogen PeroxideMagnesiumReceptors, N-Methyl-D-Aspartate

Identifiers

PMID17343827
PMCPMC1899527
OpenAlexW1984841129

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.