Cited by 19Bioinformatics and Genomic NetworksAlzheimer's disease research and treatmentsComputational Drug Discovery Methods

A portal to visualize transcriptome profiles in mouse models of neurological disorders

Open access
Al-Ouran, Rami, Wan, Ying-Wooi, Mangleburg, Carl Grant, Lee, Tom V., Allison, Katherine, Shulman, Joshua M., Liu, Zhandong·2019·Genes

Abstract

Target nomination for drug development has been a major challenge in the path to finding a cure for several neurological disorders. Comprehensive transcriptome profiles have revealed brain gene expression changes associated with many neurological disorders, and the functional validation of these changes is a critical next step. Model organisms are a proven approach for the elucidation of disease mechanisms, including screening of gene candidates as therapeutic targets. Frequently, multiple models exist for a given disease, creating a challenge to select the optimal model for validation and functional follow-up. To help in nominating the best mouse models for studying neurological diseases, we developed a web portal to visualize mouse transcriptomic data related to neurological disorders. Users can examine gene expression changes across mouse model studies to help select the optimal mouse model for further investigation. The portal provides access to mouse studies related to Alzheimer’s diseases (AD), Parkinson’s disease (PD), Huntington’s disease (HD), Amyotrophic Lateral Sclerosis (ALS), Spinocerebellar ataxia (SCA), and models related to aging.

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  • The output of the mouse neurological disorders RNA-seq portal showed a downregulation of Signature C genes within studies designated "other cell types".

    “Notably, the output of this portal showed a downregulation of Signature C genes within studies designated “other cell types” (Fig. S5 C).”

    From Network analysis identifies strain-dependent response to tau and tau seeding-associated genes (2023) · cites this paper as Al-Ouran et al., 2019

    The Results and Discussion section describes this portal and shows downregulated genes in mouse models studying different cell types. Those results concern the paper’s yellow-module gene set, however; our copy does not report an analysis of Signature C genes or a category designated “other cell types.” (LLM, conf=0.82)

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  • The gene lists can be used with external databases like the mouse neurological disorders RNA-seq portal to probe similar signatures across mouse models.

    “We demonstrated the ability to use our gene lists with external databases like the mouse neurological disorders RNA-seq portal (Al-Ouran et al., 2019) to probe similar signatures across mouse models.”
  • Among 26 mouse transcriptomic cohorts where Abi3 and Gngt2 were both differentially regulated, their expression changes were concordant in 24 studies.

    “In addition, we investigated 96 additional mouse transcriptomic datasets [33, 34] and in 26 of these cohorts, we found that Abi3 and Gngt2 were both differentially regulated. Among these 26 cohorts, Abi3 and Gngt2 expression changes were concordant in 24 studies (Additional File 6: Table S4), showing that these genes are consistently co-regulated across different mouse models and experimental”

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Research works printed but not linked: 11

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Authors
Al-Ouran, R., Wan, Y.-W., Mangleburg, C. G., Lee, T. V., Allison, K., Shulman, J. M., & Liu, Z.
Affiliations
  • Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030, USA
  • Baylor College of Medicine (US)
Corresponding author
  • Wan, Ying-Wooi
  • Liu, Zhandong
Venue
Genes
Publisher
MDPI AG
Published
2019-09-26
Volume
10
Issue
10
Pages
759
ISSN
2073-4425 (ISSN-L)
OpenAlex
W2977066221
Cited by
19
References
2
Citations by year
2023: 2 · 2022: 13 · 2021: 2 · 2020: 1 · 2019: 1
FWCI
1.41
Type
journal article
Language
en
Open access
Locations
  • Genes (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Huffington Foundation
  • National Institutes of Health (5r01gm120033-05)
  • National Institute on Aging (F31AG067677, R01AG057339)
  • National Institute of General Medical Sciences (R01-GM120033)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bioinformatics and Genomic Networks
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Physical Sciences › Computer Science › Computational Theory and Mathematics › Computational Drug Discovery Methods
Keywords
gene expression profiling, web portal, gene expression changes, drug target validation, Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, spinocerebellar ataxia, aging, brain gene expression, model selection
MeSH terms
Animals, Disease Models, Animal, Nervous System Diseases, Software, Databases, Genetic, Mice, Transcriptome

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