| pubmed-article:16475990 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16475990 | lifeskim:mentions | umls-concept:C0011220 | lld:lifeskim |
| pubmed-article:16475990 | lifeskim:mentions | umls-concept:C0035736 | lld:lifeskim |
| pubmed-article:16475990 | lifeskim:mentions | umls-concept:C1273518 | lld:lifeskim |
| pubmed-article:16475990 | lifeskim:mentions | umls-concept:C1819995 | lld:lifeskim |
| pubmed-article:16475990 | lifeskim:mentions | umls-concept:C1412215 | lld:lifeskim |
| pubmed-article:16475990 | lifeskim:mentions | umls-concept:C0376315 | lld:lifeskim |
| pubmed-article:16475990 | lifeskim:mentions | umls-concept:C0162782 | lld:lifeskim |
| pubmed-article:16475990 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
| pubmed-article:16475990 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:16475990 | pubmed:dateCreated | 2006-2-14 | lld:pubmed |
| pubmed-article:16475990 | pubmed:abstractText | Hepatitis delta virus (HDV) RNA editing controls the formation of hepatitis-delta-antigen-S and -L and therefore indirectly regulates HDV replication. Editing is thought to be catalysed by the adenosine deaminase acting on RNA1 (ADAR1) of which two different forms exist, interferon (IFN)-alpha-inducible ADAR1-L and constitutively expressed ADAR1-S. ADAR1-L is hypothesized to be a part of the innate cellular immune system, responsible for deaminating adenosines in viral dsRNAs. We examined the influence of both forms on HDV RNA editing in IFN-alpha-stimulated and unstimulated hepatoma cells. For gene silencing, an antisense oligodeoxyribonucleotide against a common sequence of both forms of ADAR1 and another one specific for ADAR1-L alone were used. IFN-alpha treatment of host cells led to approximately twofold increase of RNA editing compared with unstimulated controls. If ADAR1-L expression was inhibited, this substantial increase in editing could no longer be observed. In unstimulated cells, ADAR1-L suppression had only minor effects on editing. Inhibition of both forms of ADAR1 simultaneously led to a substantial decrease of edited RNA independently of IFN-alpha-stimulation. In conclusion, the two forms of ADAR1 are responsible almost alone for HDV editing. In unstimulated cells, ADAR1-S is the main editing activity. The increase of edited RNA under IFN-alpha-stimulation is because of induction of ADAR1-L, showing for the first time that this IFN-inducible protein is involved in the base modification of replicating HDV RNA. Thus, induction of ADAR1-L may at least partially cause the antiviral effect of IFN-alpha in natural immune response to HDV as well as in case of therapeutic administration of IFN. | lld:pubmed |
| pubmed-article:16475990 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16475990 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16475990 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16475990 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16475990 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16475990 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16475990 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16475990 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16475990 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16475990 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16475990 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:16475990 | pubmed:issn | 1352-0504 | lld:pubmed |
| pubmed-article:16475990 | pubmed:author | pubmed-author:KirchnerHH | lld:pubmed |
| pubmed-article:16475990 | pubmed:author | pubmed-author:HennigHH | lld:pubmed |
| pubmed-article:16475990 | pubmed:author | pubmed-author:WarneckeJJ | lld:pubmed |
| pubmed-article:16475990 | pubmed:author | pubmed-author:HartwigDD | lld:pubmed |
| pubmed-article:16475990 | pubmed:author | pubmed-author:DoseSS | lld:pubmed |
| pubmed-article:16475990 | pubmed:author | pubmed-author:SchütteCC | lld:pubmed |
| pubmed-article:16475990 | pubmed:author | pubmed-author:SchlenkePP | lld:pubmed |
| pubmed-article:16475990 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16475990 | pubmed:volume | 13 | lld:pubmed |
| pubmed-article:16475990 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16475990 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16475990 | pubmed:pagination | 150-7 | lld:pubmed |
| pubmed-article:16475990 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:16475990 | pubmed:meshHeading | pubmed-meshheading:16475990... | lld:pubmed |
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| pubmed-article:16475990 | pubmed:meshHeading | pubmed-meshheading:16475990... | lld:pubmed |
| pubmed-article:16475990 | pubmed:meshHeading | pubmed-meshheading:16475990... | lld:pubmed |
| pubmed-article:16475990 | pubmed:meshHeading | pubmed-meshheading:16475990... | lld:pubmed |
| pubmed-article:16475990 | pubmed:meshHeading | pubmed-meshheading:16475990... | lld:pubmed |
| pubmed-article:16475990 | pubmed:meshHeading | pubmed-meshheading:16475990... | lld:pubmed |
| pubmed-article:16475990 | pubmed:meshHeading | pubmed-meshheading:16475990... | lld:pubmed |
| pubmed-article:16475990 | pubmed:meshHeading | pubmed-meshheading:16475990... | lld:pubmed |
| pubmed-article:16475990 | pubmed:meshHeading | pubmed-meshheading:16475990... | lld:pubmed |
| pubmed-article:16475990 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16475990 | pubmed:articleTitle | The large form of ADAR 1 is responsible for enhanced hepatitis delta virus RNA editing in interferon-alpha-stimulated host cells. | lld:pubmed |
| pubmed-article:16475990 | pubmed:affiliation | Institut für Immunologie und Transfusionsmedizin, Universität zu Lübeck, Germany. hartwig@klinchem.mu-luebeck.de | lld:pubmed |
| pubmed-article:16475990 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16475990 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:103 | entrezgene:pubmed | pubmed-article:16475990 | lld:entrezgene |
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