Evidence map›Paper›PMID 20676303›Full record

ArticleHFSP journal2010

Systems genetics: the added value of gene expression.

Peter M Visscher, Michael E Goddard

Open access · hybridAbstract read
In one paragraph

Article in HFSP journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 48% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Identifying genetic modulators of the connectivity between transcription factors and their transcriptional targets.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  2. Article
  3. 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

2 authors at 2 institutions in 1 country.

Peter M Visscher
Michael E Goddard
QIMR Berghofer Medical Research Institute · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Understanding causal relationships between genotypes and phenotypes is a long-standing aim in genetics. In addition to high-throughput technologies that allow the measurement of many DNA variants it is possible to measure gene expression in specific tissues using array technology. "Systems genetics" is an emerging discipline that combines dense data on genotypes, gene expression, and outcome phenotypes to answer fundamental questions about causal pathways from genotype to phenotype. A recent paper by Chen et al. [Mol. Syst. Biol. 5, 310 (2009)] addressed the question of whether relative levels of mRNA expression help to elucidate causal paths from genotype to phenotype, using drug resistance in yeast as a model. The authors show that data on genetic markers and on gene expression, measured in a drug-free environment, can be combined to predict the growth of a yeast strain in the presence of a drug. They argue that their prediction can be used to identify causal pathways and for a subset of the genes used in prediction, the authors demonstrate that these genes cause an effect on drug sensitivity by deleting the gene or overexpressing it or swapping alleles between strains of yeast. This approach can also be applied to other species, including humans, and may become a tool in the study of personalized medicine.

Identifiers

PMID20676303
PMCPMC2880025
OpenAlexW1974616228

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.