ArticleBiochemical and biophysical research communications2012
Disease-drug pairs revealed by computational genomic connectivity mapping on GBA1 deficient, Gaucher disease mice.
Article in Biochemical and biophysical research communications, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Beyond bone biology: Lessons from team science.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2020Article
- A review of connectivity map and computational approaches in pharmacogenomics.Briefings in bioinformatics · 2018Review
- FSIP1 binds HER2 directly to regulate breast cancer growth and invasiveness.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Mining the transcriptome for rare disease therapies: a comparison of the efficiencies of two data mining approaches and a targeted cell-based drug screen.NPJ genomic medicine · 2017Article
- A Next Generation Multiscale View of Inborn Errors of Metabolism.Cell metabolism · 2016Review
- Glucocerebrosidase 2 gene deletion rescues type 1 Gaucher disease.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
We have reported that, in addition to recapitulating the classical human Gaucher disease (GD1) phenotype, deletion of the glucocerebrosidase (GBA1) gene in mice results in the dysfunction of a diverse population of immune cells. Most of immune-related, non-classical features of GD1, including gammopathies and autoimmune diathesis, are resistant to macrophage-directed therapies. This has prompted a search for newer agents for human GD1. Here, we used high-density microarray on splenic and liver cells from affected GBA1(-/-) mice to establish a gene "signature", which was then utilized to interrogate the Broad Institute database, CMAP. Computational connectivity mapping of disease and drug pairs through CMAP revealed several highly enriched, non-null, mimic and anti-mimic hits. Most notably, two compounds with anti-helminthic properties, namely albendazole and oxamniquine, were identified; these are particularly relevant for future testing as the expression of chitinases is enhanced in GD1.
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Registered trials
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