Evidence map›Paper›PMID 23288936›Full record

ArticleGenetics2013

Modeling causality for pairs of phenotypes in system genetics.

Elias Chaibub Neto, Aimee T Broman, Mark P Keller, Alan D Attie, Bin Zhang, Jun Zhu, Brian S Yandell

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.7field-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

21 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  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

7 authors at 2 institutions in 1 country.

Elias Chaibub NetoSage Bionetworks, Seattle, Washington 98109, USA. byandell@wisc.edu
Aimee T Broman
Mark P Keller
Alan D Attie
Bin Zhang
Jun Zhu
Brian S Yandell
University of Wisconsin–Madison · USSage Bionetworks · US

Funding

Integrating cancer datasets for predictive model development and trainingU54CA149237 · NCI · SAGE BIONETWORKS · PI FRIEND, STEPHEN HENRY · 2010 to 2014
$8.9M
Genetic Mapping of Networks Associated with Beta-cell D*R01DK066369 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI ATTIE, ALAN D · 2004 to 2014
$6.3M
The Genetics of Obesity and DiabetesR01DK058037 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI ATTIE, ALAN D · 2001 to 2013
$5.7M
Bayesian Methods for Mapping Complex Epistatic GenesR01GM069430 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YI, NENGJUN · 2005 to 2013
$2.3M
Epistatic and Cross Tissue Analysis for Human Gene Expression TraitsR01MH090948 · NIMH · HARVARD UNIVERSITY · PI LIU, JUN S · 2010 to 2011
$588k
NCI NIH HHS U54 CA149237NCI NIH HHS U54-CA149237NIDDK NIH HHS DK06639NIDDK NIH HHS DK58037NIDDK NIH HHS DK66369NIDDK NIH HHS R01 DK058037NIDDK NIH HHS R01 DK066369NIGMS NIH HHS GM069430-01A2NIGMS NIH HHS R01 GM069430NIMH NIH HHS R01 MH090948NIMH NIH HHS R01MH090948PHS HHS PA02110
6 · The paper itself

Abstract

Current efforts in systems genetics have focused on the development of statistical approaches that aim to disentangle causal relationships among molecular phenotypes in segregating populations. Reverse engineering of transcriptional networks plays a key role in the understanding of gene regulation. However, transcriptional regulation is only one possible mechanism, as methylation, phosphorylation, direct protein-protein interaction, transcription factor binding, etc., can also contribute to gene regulation. These additional modes of regulation can be interpreted as unobserved variables in the transcriptional gene network and can potentially affect its reconstruction accuracy. We develop tests of causal direction for a pair of phenotypes that may be embedded in a more complicated but unobserved network by extending Vuong's selection tests for misspecified models. Our tests provide a significance level, which is unavailable for the widely used AIC and BIC criteria. We evaluate the performance of our tests against the AIC, BIC, and a recently published causality inference test in simulation studies. We compare the precision of causal calls using biologically validated causal relationships extracted from a database of 247 knockout experiments in yeast. Our model selection tests are more precise, showing greatly reduced false-positive rates compared to the alternative approaches. In practice, this is a useful feature since follow-up studies tend to be time consuming and expensive and, hence, it is important for the experimentalist to have causal predictions with low false-positive rates.

Indexed as

Models, GeneticPhenotypeComputer SimulationFalse Positive ReactionsGene DeletionGene Expression RegulationGene Regulatory NetworksProbabilityQuantitative Trait LociYeasts

Identifiers

PMID23288936
PMCPMC3583988
OpenAlexW2120505647

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.