Evidence map›Paper›PMID 23445784›Full record

ReviewGenome medicine2013

Functional decorations: post-translational modifications and heart disease delineated by targeted proteomics.

Kiersten A Liddy, Melanie Y White, Stuart J Cordwell

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Genome medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
3.6field-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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Guideline
  2. Article
  3. Review
  4. Review
  5. Precision Profiling of the Cardiovascular Post-Translationally Modified Proteome.Journal of cardiovascular development and disease · 2026
    Review
  6. Review
  7. Article
  8. New Types of Post-Translational Modification of Proteins in Cardiovascular Diseases.Journal of cardiovascular translational research · 2025
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. ABRO1 arrests cardiomyocyte proliferation and myocardial repair by suppressing PSPH.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  16. Article
  17. Review
  18. Review
  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

3 authors at 1 institution in 1 country.

Kiersten A LiddySchool of Molecular Bioscience, The University of Sydney, 2006 Sydney, Australia.
Melanie Y WhiteSchool of Molecular Bioscience, The University of Sydney, 2006 Sydney, Australia ; Discipline of Pathology, School of Medical Sciences, The University of Sydney, 2006 Sydney, Australia.
Stuart J CordwellSchool of Molecular Bioscience, The University of Sydney, 2006 Sydney, Australia ; Discipline of Pathology, School of Medical Sciences, The University of Sydney, 2006 Sydney, Australia.
University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The more than 300 currently identified post-translational modifications (PTMs) provides great scope for subtle or dramatic alteration of protein structure and function. Furthermore, the rapid and transient nature of many PTMs allows efficient signal transmission in response to internal and environmental stimuli. PTMs are predominantly added by enzymes, and the enzymes responsible (such as kinases) are thus attractive targets for therapeutic interventions. Modifications can be grouped according to their stability or transience (reversible versus irreversible): irreversible types (such as irreversible redox modifications or protein deamidation) are often associated with aging or tissue injury, whereas transient modifications are associated with signal propagation and regulation. This is particularly important in the setting of heart disease, which comprises a diverse range of acute (such as ischemia/reperfusion), chronic (such as heart failure, dilated cardiomyopathy) and genetic (such as hypertrophic cardiomyopathy) disease states, all of which have been associated with protein PTM. Recently the interplay between diverse PTMs has been suggested to also influence cellular function, with cooperation or competition for sites of modification possible. Here we discuss the utility of proteomics for examining PTMs in the context of the molecular mechanisms of heart disease.

Identifiers

PMID23445784
PMCPMC3706772
OpenAlexW2130944775

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.