Evidence map›Paper›PMID 18095372›Full record

ArticleProteomics2008

Use of 2-D DIGE analysis reveals altered phosphorylation in a tropomyosin mutant (Glu54Lys) linked to dilated cardiomyopathy.

Chad M Warren, Grace M Arteaga, Sudarsan Rajan, Rafeeq P H Ahmed, David F Wieczorek, R John Solaro

Open access · greenAbstract read
In one paragraph

Article in Proteomics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  6. β-Arrestin mediates the Frank-Starling mechanism of cardiac contractility.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
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  15. Article
  16. Phosphorylation of tropomyosin in striated muscle.Journal of muscle research and cell motility · 2013
    Review
  17. Tropomyosin de-phosphorylation in the heart: what are the consequences?Journal of muscle research and cell motility · 2013
    Review
  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

6 authors at 3 institutions in 1 country.

Chad M WarrenDepartment of Physiology and Biophysics, Center for Cardiovascular Research, College of Medicine, University of Illinois at Chicago, 835 E. Wolcott Avenue, Chicago, IL 60612, USA.
Grace M Arteaga
Sudarsan Rajan
Rafeeq P H Ahmed
David F Wieczorek
R John Solaro
University of Cincinnati · USUniversity of Illinois Chicago · USUniversity of Cincinnati Medical Center · US

Funding

Sarcomeric Modifications and Progressive Cardiac MaladaptationP01HL062426 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI AI, XUN · 2000 to 2020
$42.4M
MODULATION OF CALCIUM CONTROL OF CARDIAC MYOFIBRILSR01HL022231 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GUPTA, MADHU, SOLARO, R JOHN · 1985 to 2014
$2.9M
MODULATION OF CALCIUM CONTROL OF CARDIAC MYOFIBRILSR37HL022231 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SOLARO, R JOHN · 1999 to 2006
$2.2M
Mechanisms of Tropomyosin Induced HypertrophyR01HL071952 · NHLBI · UNIVERSITY OF CINCINNATI · PI WIECZOREK, DAVID F · 2003 to 2006
$2.0M
Ischemia/Reperfusion Injury and Cardiac MyofilamentsK01HL067709 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ARTEAGA, GRACE M. · 2001 to 2005
$718k
NHLBI NIH HHS HL 71952NHLBI NIH HHS K01 HL067709NHLBI NIH HHS K01 HL 67709NHLBI NIH HHS P01 HL062426NHLBI NIH HHS P01 HL 62426NHLBI NIH HHS R01 HL022231NHLBI NIH HHS R01 HL071952NHLBI NIH HHS R37 HL022231NHLBI NIH HHS R37 HL 22231
6 · The paper itself

Abstract

Current electrophoretic methods have not been optimized to fully separate post-translationally modified mutant forms of tropomyosin (Tm) from wild-type cardiac samples. We describe here a method employing a modified 2-D PAGE/2-D DIGE protocol, to fully separate native, mutant (E54K), and phosphorylated forms of Tm. Our data demonstrate the first evidence of a significant (approximately 40%) decrease in Tm phosphorylation in transgenic compared to non-transgenic mouse hearts, and indicate that altered phosphorylation may be a significant factor in the linkage of the E54K mutation to dilated cardiomyopathy.

Indexed as

Amino Acid SubstitutionAnimalsCardiomyopathy, DilatedElectrophoresis, Gel, Two-DimensionalGlutamic AcidImmunoblottingLysineMiceMice, TransgenicPhosphorylationPoint MutationTropomyosinGlutamic AcidLysineTropomyosin

Identifiers

PMID18095372
PMCPMC2586826
OpenAlexW1975805588

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.