Linked Life Data

20631312

Source:http://linkedlifedata.com/resource/pubmed/id/20631312

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-8-5
pubmed:abstractText
Interferon-gamma is crucial for the noncytopathic clearance of hepatitis B virus. In our previous study, we demonstrated that an IFN-gamma-inducible molecule, tripartite motif (TRIM) 22, played an important role in antiviral immunity against hepatitis B virus. However, the molecular mechanism of TRIM22 induction by IFN-gamma is still unclear. In this study, we identified a novel cis-element termed 5' extended IFN-stimulating response element (5' eISRE) that was crucial for IFN-gamma inducibility of TRIM22 through transfection assays with luciferase reporter constructs and EMSAs. The 5' eISRE consists of an ISRE-like motif (ACTTTCGTTTCTC) and a 6-bp sequence (AATTTA) upstream of it, and all three thymine triplets of this cis-element (AATTTAACTTTCGTTTCTC) were revealed to contribute to the IFN-gamma inducibility of TRIM22 by site-directed mutagenesis. Further studies showed that upon IFN-gamma stimulation, the 5' eISRE could be bound by IFN regulatory factor-1 (IRF-1), but not by STAT1, as demonstrated by supershift analysis and an ELISA-based transcription factor assay. Moreover, overexpression of IRF-1 significantly induced TRIM22 expression, whereas silencing of IRF-1 with specific short interference RNA abolished IFN-gamma-induced TRIM22 expression in HepG2 cells, indicating an IRF-1-dependent expression of TRIM22. Taken together, it was demonstrated in this study that a novel cis-element, 5' eISRE, was crucial for the IFN-gamma-induced transcriptional activity of the TRIM22 gene via interaction with IRF-1.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
185
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2314-23
pubmed:meshHeading
pubmed-meshheading:20631312-5' Flanking Region, pubmed-meshheading:20631312-Base Sequence, pubmed-meshheading:20631312-Binding Sites, pubmed-meshheading:20631312-Blotting, Western, pubmed-meshheading:20631312-Cycloheximide, pubmed-meshheading:20631312-Electrophoretic Mobility Shift Assay, pubmed-meshheading:20631312-Gene Expression Regulation, Neoplastic, pubmed-meshheading:20631312-Hep G2 Cells, pubmed-meshheading:20631312-Humans, pubmed-meshheading:20631312-Interferon Regulatory Factor-1, pubmed-meshheading:20631312-Interferon-gamma, pubmed-meshheading:20631312-Luciferases, pubmed-meshheading:20631312-Mutation, pubmed-meshheading:20631312-Protein Binding, pubmed-meshheading:20631312-Protein Synthesis Inhibitors, pubmed-meshheading:20631312-RNA Interference, pubmed-meshheading:20631312-Recombinant Fusion Proteins, pubmed-meshheading:20631312-Repressor Proteins, pubmed-meshheading:20631312-Response Elements, pubmed-meshheading:20631312-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:20631312-Transfection
pubmed:year
2010
pubmed:articleTitle
A 5' extended IFN-stimulating response element is crucial for IFN-gamma-induced tripartite motif 22 expression via interaction with IFN regulatory factor-1.
pubmed:affiliation
Institute for Immunobiology, Department of Immunology, Shanghai Medical College of Fudan University, Shanghai, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't