Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
43
pubmed:dateCreated
2004-10-18
pubmed:abstractText
The interferon regulatory factors (IRF) are transcriptional mediators of cellular response to viral invasion that play a critical role in the innate antiviral defense. Two of these factors, IRF-5 and IRF-7, play a critical role in the induction of interferon (IFNA) genes in infected cells; they are expressed constitutively in monocytes, B cells, and precursors of dendritic cells (pDC2) that are high producers of interferon alpha, and their expression can be further stimulated by type I interferon. The goal of the present study was to identify and analyze expression of cellular genes that are modulated by IRF-5 and IRF-7 during the innate response to viral infection. The transcription profiles of infected BJAB cells overexpressing IRF-5 or IRF-7 were determined by using oligonucleotide arrays with probe sets representing about 6800 human genes. This analysis shows that IRF-5 and IRF-7 activate a broad profile of heterologous genes encoding not only antiviral, inflammatory, and pro-apoptotic proteins but also proteins of other functional categories. The number of IRF-5- and IRF-7-modulated genes was significantly higher in infected than in uninfected cells, and the transcription signature was predominantly positive. Although IRF-5 and IRF-7 stimulated a large number of common genes, a distinct functional profile was associated with each of these IRFs. The noted difference was a broad antiviral and early inflammatory transcriptional profile in infected BJAB/IRF-5 cells, whereas the IRF-7-induced transcripts were enriched for the group of mitochondrial genes and genes affecting the DNA structure. Taken together, these data indicate that IRF-5 and IRF-7 act primarily as transcriptional activators and that IRF-5-and IRF-7-induced innate antiviral response results in a broad alteration of the transcriptional profile of cellular genes.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/CXCL11 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Carbon Tetrachloride, http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL11, http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CXC, http://linkedlifedata.com/resource/pubmed/chemical/DNA, http://linkedlifedata.com/resource/pubmed/chemical/DNA, Complementary, http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/IRF5 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/IRF7 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Interferon Regulatory Factor-7, http://linkedlifedata.com/resource/pubmed/chemical/Interferon Regulatory Factors, http://linkedlifedata.com/resource/pubmed/chemical/Interferon-beta, http://linkedlifedata.com/resource/pubmed/chemical/Interferons, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Complementary, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
22
pubmed:volume
279
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
45194-207
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:15308637-Blotting, Western, pubmed-meshheading:15308637-Carbon Tetrachloride, pubmed-meshheading:15308637-Cell Line, pubmed-meshheading:15308637-Cell Line, Tumor, pubmed-meshheading:15308637-Chemokine CXCL11, pubmed-meshheading:15308637-Chemokines, CXC, pubmed-meshheading:15308637-DNA, pubmed-meshheading:15308637-DNA, Complementary, pubmed-meshheading:15308637-DNA-Binding Proteins, pubmed-meshheading:15308637-Dendritic Cells, pubmed-meshheading:15308637-Electrophoresis, Polyacrylamide Gel, pubmed-meshheading:15308637-Gene Expression Regulation, pubmed-meshheading:15308637-Humans, pubmed-meshheading:15308637-Inflammation, pubmed-meshheading:15308637-Interferon Regulatory Factor-7, pubmed-meshheading:15308637-Interferon Regulatory Factors, pubmed-meshheading:15308637-Interferon-beta, pubmed-meshheading:15308637-Interferons, pubmed-meshheading:15308637-Kinetics, pubmed-meshheading:15308637-Mitochondria, pubmed-meshheading:15308637-Monocytes, pubmed-meshheading:15308637-Nucleic Acid Hybridization, pubmed-meshheading:15308637-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:15308637-Phosphorylation, pubmed-meshheading:15308637-RNA, Complementary, pubmed-meshheading:15308637-RNA, Messenger, pubmed-meshheading:15308637-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:15308637-Time Factors, pubmed-meshheading:15308637-Transcription, Genetic, pubmed-meshheading:15308637-Transcription Factors, pubmed-meshheading:15308637-Up-Regulation
pubmed:year
2004
pubmed:articleTitle
Global and distinct targets of IRF-5 and IRF-7 during innate response to viral infection.
pubmed:affiliation
The Sidney Kimmel Comprehensive Cancer Center, University of Michigan, Ann Arbor 48109, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't