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      INTERFEROME v2.0: an updated database of annotated interferon-regulated genes

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          Abstract

          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.

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          Most cited references25

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          Gene Ontology: tool for the unification of biology

          Genomic sequencing has made it clear that a large fraction of the genes specifying the core biological functions are shared by all eukaryotes. Knowledge of the biological role of such shared proteins in one organism can often be transferred to other organisms. The goal of the Gene Ontology Consortium is to produce a dynamic, controlled vocabulary that can be applied to all eukaryotes even as knowledge of gene and protein roles in cells is accumulating and changing. To this end, three independent ontologies accessible on the World-Wide Web (http://www.geneontology.org) are being constructed: biological process, molecular function and cellular component.
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            Normalization of cDNA microarray data.

            Normalization means to adjust microarray data for effects which arise from variation in the technology rather than from biological differences between the RNA samples or between the printed probes. This paper describes normalization methods based on the fact that dye balance typically varies with spot intensity and with spatial position on the array. Print-tip loess normalization provides a well-tested general purpose normalization method which has given good results on a wide range of arrays. The method may be refined by using quality weights for individual spots. The method is best combined with diagnostic plots of the data which display the spatial and intensity trends. When diagnostic plots show that biases still remain in the data after normalization, further normalization steps such as plate-order normalization or scale-normalization between the arrays may be undertaken. Composite normalization may be used when control spots are available which are known to be not differentially expressed. Variations on loess normalization include global loess normalization and two-dimensional normalization. Detailed commands are given to implement the normalization techniques using freely available software.
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              Identification of genes differentially regulated by interferon alpha, beta, or gamma using oligonucleotide arrays.

              The pleiotropic activities of interferons (IFNs) are mediated primarily through the transcriptional regulation of many downstream effector genes. The mRNA profiles from IFN-alpha, -beta, or -gamma treatments of the human fibrosarcoma cell line, HT1080, were determined by using oligonucleotide arrays with probe sets corresponding to more than 6,800 human genes. Among these were transcripts for known IFN-stimulated genes (ISGs), the expression of which were consistent with previous studies in which the particular ISG was characterized as responsive to either Type I (alpha, beta) or Type II (gamma) IFNs, or both. Importantly, many novel IFN-stimulated genes were identified that were diverse in their known biological functions. For instance, several novel ISGs were identified that are implicated in apoptosis (including RAP46/Bag-1, phospholipid scramblase, and hypoxia inducible factor-1alpha). Furthermore, several IFN-repressed genes also were identified. These results demonstrate the usefulness of oligonucleotide arrays in monitoring mammalian gene expression on a broad and unprecedented scale. In particular, these findings provide insights into the basic mechanisms of IFN actions and ultimately may contribute to better therapeutic uses for IFNs.
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                Author and article information

                Journal
                Nucleic Acids Res
                Nucleic Acids Res
                nar
                nar
                Nucleic Acids Research
                Oxford University Press
                0305-1048
                1362-4962
                January 2013
                January 2013
                29 November 2012
                29 November 2012
                : 41
                : D1 , Database issue
                : D1040-D1046
                Affiliations
                1Centre for Innate Immunity and Infectious Diseases, Monash Institute of Medical Research, 2ARC Centre of Excellence for Structural and Functional Microbial Genomics, 3Monash e-Research, Monash University, Clayton, Victoria, Australia and 4Universite Paris Descartes, Paris, France
                Author notes
                *To whom correspondence should be addressed. Tel: +61 3 95 94 72 06/99 02 48 27; Fax: +61 3 95 94 72 11; Email: paul.hertzog@ 123456monash.edu

                The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors.

                Article
                gks1215
                10.1093/nar/gks1215
                3531205
                23203888
                da070f4c-811e-47d3-800f-71c10211c744
                © The Author(s) 2012. Published by Oxford University Press.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by-nc/3.0/), which permits non-commercial reuse, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com.

                History
                : 1 October 2012
                : 26 October 2012
                : 30 October 2012
                Page count
                Pages: 7
                Categories
                Articles

                Genetics
                Genetics

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