Source:http://linkedlifedata.com/resource/pubmed/id/21966559
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2011-10-3
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pubmed:abstractText |
Pattern recognition receptors (PRRs) constitute the first line of host defense against bacterial, fungal and viral pathogens. Upon sensing microbial infection, PRRs initiate a cascade of signal transduction and transcriptional events to induce the production of inflammatory cytokines. As a result, many pathogens have evolved to evade PRR detection and activation in order to establish a successful infection. In a recent report, we described how a viral protein named Orf63 encoded by Kaposi's sarcoma-associated herpesvirus (KSHV) inhibits activation of several members of a family of PRRs called NLRs (nucleotide-binding and oligomerization, leucine-rich repeat) by functionally inhibiting the NLR response. This resulted in reduced NLR-dependent pro-inflammatory cytokine secretion and cell death. Moreover, Orf63 was essential in the KSHV lifecycle. Thus, our work suggests KSHV has evolved to encode a functional homolog of NLR proteins in an effort to suppress the host inflammatory response.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:status |
PubMed-not-MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1942-0889
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
4
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
416-8
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pubmed:year |
2011
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pubmed:articleTitle |
Inhibition of the inflammasome response by a viral protein that interacts with NLRs.
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pubmed:affiliation |
Lineberger Comprehensive Cancer Center and Department of Microbiology & Immunology; University of North Carolina; Chapel Hill, NC USA.
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pubmed:publicationType |
Journal Article
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