Evidence map›Paper›PMID 18852689›Full record

ReviewPediatric research2009

Modeling molecular and cellular aspects of human disease using the nematode Caenorhabditis elegans.

Gary A Silverman, Cliff J Luke, Sangeeta R Bhatia, Olivia S Long, Anne C Vetica, David H Perlmutter, Stephen C Pak

Open access · bronzeAbstract readReview
In one paragraph

Review in Pediatric research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

48 citing papers in PubMed, 104 citations in OpenAlex.

  1. High-Throughput Toxicity Screening withEnvironmental science & technology · 2026
    Review
  2. Article
  3. TheToxicology reports · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Autumn Olive (International journal of molecular sciences · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Phenotypic Screening inPharmaceuticals (Basel, Switzerland) · 2020
    Review
  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 4 institutions in 1 country.

Gary A SilvermanDepartment of Pediatrics, Children's Hospital of Pittsburgh and Magee-Womens Hospital Research Institute, Department of Cell Biology and Physiology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA. gsilverman@upmc.edu
Cliff J Luke
Sangeeta R Bhatia
Olivia S Long
Anne C Vetica
David H Perlmutter
Stephen C Pak
Children's Hospital of Pittsburgh · USMagee-Womens Hospital · USMagee-Womens Research Institute · USUniversity of Pittsburgh · US

Funding

High Throughput Genetic and Drug Screens for Alph-1-Antitrypsin DeficiencyR01DK079806 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SILVERMAN, GARY ARTHUR · 2008 to 2011
$2.4M
NIDDK NIH HHS DK079806NIDDK NIH HHS R01 DK079806
6 · The paper itself

Abstract

As an experimental system, Caenorhabditis elegans offers a unique opportunity to interrogate in vivo the genetic and molecular functions of human disease-related genes. For example, C. elegans has provided crucial insights into fundamental biologic processes, such as cell death and cell fate determinations, as well as pathologic processes such as neurodegeneration and microbial susceptibility. The C. elegans model has several distinct advantages, including a completely sequenced genome that shares extensive homology with that of mammals, ease of cultivation and storage, a relatively short lifespan and techniques for generating null and transgenic animals. However, the ability to conduct unbiased forward and reverse genetic screens in C. elegans remains one of the most powerful experimental paradigms for discovering the biochemical pathways underlying human disease phenotypes. The identification of these pathways leads to a better understanding of the molecular interactions that perturb cellular physiology, and forms the foundation for designing mechanism-based therapies. To this end, the ability to process large numbers of isogenic animals through automated work stations suggests that C. elegans, manifesting different aspects of human disease phenotypes, will become the platform of choice for in vivo drug discovery and target validation using high-throughput/content screening technologies.

Indexed as

DNA, HelminthGene Expression RegulationGenetic Predisposition to DiseaseModels, AnimalAnimalsAnimals, Genetically ModifiedApoptosisBase SequenceCaenorhabditis elegansConserved SequenceDatabases, GeneticDrug DiscoveryHost-Pathogen InteractionsHumansMutationNecrosisDNA, Helminth

Identifiers

PMID18852689
PMCPMC2731241
OpenAlexW2083924543

What OpenQuestion holds

Textmetadata
LicenceTDM
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.