Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2005-9-27
pubmed:abstractText
Mutations of the NOD2 gene increase the susceptibility of humans to Crohn's disease. NOD2 is a cytoplasmic receptor for the bacterial product peptidoglycan. There is considerable controversy in the literature whether the most common mutation in Crohn's disease, the 3020insC NOD2, leads to a loss of function, i.e. decreased cytokine production, or to the reverse, i.e. a gain of function. In previous papers we proposed the former, since we could show decreased cytokine production with a net proinflammatory status after exposure to muramyl dipeptide (MDP).
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0300-2977
pubmed:author
pubmed:issnType
Print
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
305-8
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:16186640-Acetylmuramyl-Alanyl-Isoglutamine, pubmed-meshheading:16186640-Alleles, pubmed-meshheading:16186640-Case-Control Studies, pubmed-meshheading:16186640-Crohn Disease, pubmed-meshheading:16186640-Gene Expression Regulation, pubmed-meshheading:16186640-Genetic Predisposition to Disease, pubmed-meshheading:16186640-Homozygote, pubmed-meshheading:16186640-Humans, pubmed-meshheading:16186640-Interleukin-1, pubmed-meshheading:16186640-Intracellular Signaling Peptides and Proteins, pubmed-meshheading:16186640-Leukocytes, Mononuclear, pubmed-meshheading:16186640-Lipopeptides, pubmed-meshheading:16186640-Mutation, pubmed-meshheading:16186640-Nod2 Signaling Adaptor Protein, pubmed-meshheading:16186640-Oligopeptides, pubmed-meshheading:16186640-Peptidoglycan, pubmed-meshheading:16186640-Polymerase Chain Reaction, pubmed-meshheading:16186640-Signal Transduction, pubmed-meshheading:16186640-Toll-Like Receptor 2
pubmed:year
2005
pubmed:articleTitle
NOD2 3020insC mutation and the pathogenesis of Crohn's disease: impaired IL-1beta production points to a loss-of-function phenotype.
pubmed:affiliation
Departments of Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands. M.Netea@aig.umcn.nl
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't