INTERFEROME v2.0: an updated database of annotated interferon-regulated genes
By I. Rusinova, S. Forster, Simon Yu, Anitha Kannan, M. Masse, Helen Cumming, Ross Chapman, P. Hertzog. Nucleic Acids Res., 2012
876 citations recorded by the source corpus.
Interferome v2.0 (http://interferome.its.monash.edu.au/interferome/) is an update of an earlier version of the Interferome DB published in the 2009 NAR database edition. Vastly improved computational infrastructure now enables more complex and faster queries, and supports more data sets from types I, II and III interferon (IFN)-treated cells, mice or humans. Quantitative, MIAME compliant data are collected, subjected to thorough, standardized, quantitative and statistical analyses and then significant changes in gene expression are uploaded. Comprehensive manual collection of metadata in v2.0 allows flexible, detailed search capacity including the parameters: range of -fold change, IFN type, concentration and time, and cell/tissue type. There is no limit to the number of genes that can be used to search the database in a single query. Secondary analysis such as gene ontology, regulatory factors, chromosomal location or tissue expression plots of IFN-regulated genes (IRGs) can be performed in Interferome v2.0, or data can be downloaded in convenient text formats compatible with common secondary analysis programs. Given the importance of IFN to innate immune responses in infectious, inflammatory diseases and cancer, this upgrade of the Interferome to version 2.0 will facilitate the identification of gene signatures of importance in the pathogenesis of these diseases.
Subfields: Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/e5356a85ade974359411232a6add4873a909ff86
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Citations in the corpus
- SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues (2020, positive): “Altogether, our own and publicly available data highlight that ACE2 might have been missed as a canonical ISG because of its notable absence in peripheral blood mononuclear cell datasets and in lung-derived transformed cell lines such as the A549 cell line (Butler et al., 2018; Letko et al., 2020; R”
- Transcriptome-wide isoform-level dysregulation in ASD, schizophrenia, and bipolar disorder (2018, positive): “The IFN-response module (geneM32) contains critical components of the IFN-stimulated gene factor 3 (ISGF3) complex that activates the transcription of downstream IFN-stimulated genes, which comprise 59 of the 61 genes in this module (71).”