Evidence map›Paper›PMID 18048055›Full record

ArticleJournal of molecular and cellular cardiology2008

Calmodulin kinase II inhibition disrupts cardiomyopathic effects of enhanced green fluorescent protein.

Michelle S C Khoo, Chad E Grueter, Mesut Eren, Jinying Yang, Rong Zhang, Martha A Bass, Seint T Lwin, Lisa A Mendes, Douglas E Vaughan, Roger J Colbran and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of molecular and cellular cardiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 40% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. 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

11 authors at 3 institutions in 1 country.

Michelle S C KhooDepartment of Internal Medicine, University of Colorado at Denver and Health Sciences Center, Aurora, CO 80045, USA.
Chad E Grueter
Mesut Eren
Jinying Yang
Rong Zhang
Martha A Bass
Seint T Lwin
Lisa A Mendes
Douglas E Vaughan
Roger J Colbran
Mark E Anderson
Vanderbilt University · USUniversity of Iowa · USUniversity of Colorado Denver · US

Funding

Mechanisms of CaM Kinase II Signal TransductionR01MH063232 · NIMH · VANDERBILT UNIVERSITY · PI COLBRAN, ROGER J · 2001 to 2015
$5.4M
Mitochondrial Calmodulin Kinase II in Physiology and DiseaseR01HL070250 · NHLBI · VANDERBILT UNIVERSITY · PI ANDERSON, MARK E · 2002 to 2017
$5.2M
Methionine sulfoxide reductase A and oxidized CaMKII in structural heart diseaseR01HL079031 · NHLBI · UNIVERSITY OF IOWA · PI ANDERSON, MARK E · 2006 to 2015
$3.3M
CALMODULIN KINASE II AND EARLY AFTERDEPOLARIZATIONSR01HL062494 · NHLBI · VANDERBILT UNIVERSITY · PI ANDERSON, MARK E · 1999 to 2007
$1.8M
NHLBI NIH HHS R01 HL062494NHLBI NIH HHS R01 HL070250NHLBI NIH HHS R01 HL 079031NHLBI NIH HHS R01 HL079031NHLBI NIH HHS R01 HL 62494NHLBI NIH HHS R01 HL 70250NIMH NIH HHS R01 MH063232
6 · The paper itself

Abstract

Transgenic expression of enhanced green fluorescent protein (eGFP) in myocardium can result in cardiac dysfunction and cardiomyopathy, presumably through toxic effects that disrupt normal cellular signaling. The multifunctional Ca(2+)- and calmodulin-dependent protein kinase II (CaMKII) is widely expressed in myocardium and CaMKII activity is increased in human and animal models of cardiomyopathy, so we hypothesized that increased CaMKII activity is important for cardiomyopathy due to transgenic expression of eGFP. Here we report that cardiomyocyte-delimited eGFP over-expression causes increased CaMKII activity that predicts left ventricular dilation and dysfunction. On the other hand, transgenic co-expression of a CaMKII inhibitory peptide with eGFP prevents eGFP-mediated left ventricular dilation and dysfunction. These findings suggest that increased CaMKII activity is a critical pathological signal in transgenic cardiomyopathy due to eGFP over-expression.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2CardiomyopathiesGreen Fluorescent ProteinsHeart VentriclesHypertrophyMiceMice, TransgenicOrgan SizePeptidesVentricular Function, Leftautocamtide 3Calcium-Calmodulin-Dependent Protein Kinase Type 2enhanced green fluorescent proteinGreen Fluorescent ProteinsPeptides

Identifiers

PMID18048055
PMCPMC2695824
OpenAlexW2002923854

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.