Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-7-26
pubmed:abstractText
Recent studies have revealed that negative regulatory molecules, including interleukin-1 receptor-associated kinase-M (IRAK-M), control the overactivation of Toll-like receptor (TLR) signaling. The role of IRAK-M in human gingival epithelial cells (HGECs), which express TLRs, remains unclear. The present study examined the role of IRAK-M on interleukin-8 and macrophage chemoattractant protein-1 (MCP-1) expression in HGECs stimulated with Porphyromonas gingivalis and TLR ligands.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
D
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/CCL2 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL2, http://linkedlifedata.com/resource/pubmed/chemical/IRAK3 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1 Receptor-Associated..., http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-8, http://linkedlifedata.com/resource/pubmed/chemical/Ligands, http://linkedlifedata.com/resource/pubmed/chemical/Lipopeptides, http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides, http://linkedlifedata.com/resource/pubmed/chemical/Pam(3)CSK(4) peptide, http://linkedlifedata.com/resource/pubmed/chemical/Phosphoric Monoester Hydrolases, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering, http://linkedlifedata.com/resource/pubmed/chemical/SOCS1 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Suppressor of Cytokine Signaling..., http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors, http://linkedlifedata.com/resource/pubmed/chemical/inositol-1,4,5-trisphosphate...
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1600-0765
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
512-9
pubmed:meshHeading
pubmed-meshheading:20412419-Cell Line, pubmed-meshheading:20412419-Cells, Cultured, pubmed-meshheading:20412419-Chemokine CCL2, pubmed-meshheading:20412419-Down-Regulation, pubmed-meshheading:20412419-Epithelial Cells, pubmed-meshheading:20412419-Gene Silencing, pubmed-meshheading:20412419-Gingiva, pubmed-meshheading:20412419-Humans, pubmed-meshheading:20412419-Interleukin-1 Receptor-Associated Kinases, pubmed-meshheading:20412419-Interleukin-8, pubmed-meshheading:20412419-Ligands, pubmed-meshheading:20412419-Lipopeptides, pubmed-meshheading:20412419-Lipopolysaccharides, pubmed-meshheading:20412419-Phosphoric Monoester Hydrolases, pubmed-meshheading:20412419-Porphyromonas gingivalis, pubmed-meshheading:20412419-Protein Processing, Post-Translational, pubmed-meshheading:20412419-RNA, Small Interfering, pubmed-meshheading:20412419-RNA Interference, pubmed-meshheading:20412419-Signal Transduction, pubmed-meshheading:20412419-Suppressor of Cytokine Signaling Proteins, pubmed-meshheading:20412419-Toll-Like Receptors, pubmed-meshheading:20412419-Up-Regulation
pubmed:year
2010
pubmed:articleTitle
Interleukin-1 receptor-associated kinase-M in gingival epithelial cells attenuates the inflammatory response elicited by Porphyromonas gingivalis.
pubmed:affiliation
Center for Transdisciplinary Research, Niigata University, Niigata, Japan.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't