Evidence map›Paper›PMID 30532008›Full record

ArticleNature communications2018

Modeling genome-wide enzyme evolution predicts strong epistasis underlying catalytic turnover rates.

David Heckmann, Daniel C Zielinski, Bernhard O Palsson

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Weakest link epistasis and the geometry of genetic load.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Principles of metabolome conservation in animals.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  6. Article
  7. Kinetic profiling of metabolic specialists demonstrates stability and consistency of in vivo enzyme turnover numbers.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  8. 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 2 institutions in 2 countries.

David HeckmannDepartment of Bioengineering, University of California, San Diego, La Jolla, CA, 92093-0412, USA.
Daniel C ZielinskiDepartment of Bioengineering, University of California, San Diego, La Jolla, CA, 92093-0412, USA.
Bernhard O PalssonDepartment of Bioengineering, University of California, San Diego, La Jolla, CA, 92093-0412, USA. palsson@ucsd.edu.ORCID http://orcid.org/0000-0003-2357-6785
University of California San Diego · USNovo Nordisk Foundation · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systems biology describes cellular phenotypes as properties that emerge from the complex interactions of individual system components. Little is known about how these interactions have affected the evolution of metabolic enzymes. Here, we combine genome-scale metabolic modeling with population genetics models to simulate the evolution of enzyme turnover numbers (k

Indexed as

Epistasis, GeneticEvolution, MolecularAlgorithmsBiocatalysisEnzymesEscherichia coli K12Escherichia coli ProteinsGenome, BacterialKineticsModels, GeneticEnzymesEscherichia coli Proteins

Identifiers

PMID30532008
PMCPMC6288127
OpenAlexW2902333319

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.