Evidence map›Paper›PMID 20824174›Full record

ArticlePLoS neglected tropical diseases2010

Functional genome annotation by combined analysis across microarray studies of Trypanosoma brucei.

Hamed Shateri Najafabadi, Reza Salavati

Abstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

5 citing papers in PubMed.

  1. Article
  2. A Protein Complex Map of Trypanosoma brucei.PLoS neglected tropical diseases · 2016
    Article
  3. Article
  4. Article
  5. 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.

Hamed Shateri NajafabadiInstitute of Parasitology, McGill University, Ste Anne de Bellevue, Quebec, Canada.
Reza Salavati

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFunctional annotation of trypanosomatid genomes has been a daunting task due to the low similarity of their genes with annotated genes of other organisms. Three recent studies have provided gene expression profiles in several different conditions and life stages for one of the main disease-causing trypanosomatids, Trypanosoma brucei. These data can be used to study the gene functions and regulatory mechanisms in this organism. METHODOLOGY/PRINCIPAL

findingsCombining the data from three different microarray studies of T. brucei, we show that functional linkages among T. brucei genes can be identified based on gene coexpression, leading to a powerful approach for gene function prediction. These predictions can be further improved by considering the expression profiles of orthologous genes from other trypanosomatids. Furthermore, gene expression profiles can be used to discover potential regulatory elements within 3' untranslated regions. CONCLUSIONS/SIGNIFICANCE: These results suggest that although trypanosomatids do not regulate genes at transcription level, trypanosomatid genes with related functions are coregulated post-transcriptionally via modulation of mRNA stability, implying the presence of complex regulatory networks in these organisms. Our analysis highlights the demand for a thorough transcript profiling of T. brucei genome in parallel with other trypanosomatid genomes, which can provide a powerful means to improve their functional annotation.

Indexed as

Gene Expression ProfilingGenes, ProtozoanGenomicsMicroarray AnalysisGene Expression RegulationProtozoan ProteinsRNA StabilityTrypanosoma brucei bruceiProtozoan Proteins

Identifiers

PMID20824174
PMCPMC2930875

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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.