Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-12-23
pubmed:abstractText
Evidence that a deficient innate immune response toward the bacterial flora of the gut plays a role in the pathogenesis of inflammatory bowel disease (IBD) is growing. This is underscored by the finding of the association between CARD15 variants and Crohn's disease (CD) and D299G in Toll-like receptor (TLR) 4 and IBD. Our aims were to study nonsynonymous polymorphisms in other TLR genes in IBD.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1078-0998
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-8
pubmed:dateRevised
2008-5-13
pubmed:meshHeading
pubmed-meshheading:16374251-Adult, pubmed-meshheading:16374251-Antibodies, Antineutrophil Cytoplasmic, pubmed-meshheading:16374251-Biological Markers, pubmed-meshheading:16374251-Colitis, Ulcerative, pubmed-meshheading:16374251-Crohn Disease, pubmed-meshheading:16374251-Female, pubmed-meshheading:16374251-Genetic Predisposition to Disease, pubmed-meshheading:16374251-Genotype, pubmed-meshheading:16374251-Humans, pubmed-meshheading:16374251-Intracellular Signaling Peptides and Proteins, pubmed-meshheading:16374251-Male, pubmed-meshheading:16374251-Multivariate Analysis, pubmed-meshheading:16374251-Nod2 Signaling Adaptor Protein, pubmed-meshheading:16374251-Phenotype, pubmed-meshheading:16374251-Polymorphism, Single Nucleotide, pubmed-meshheading:16374251-Saccharomyces cerevisiae, pubmed-meshheading:16374251-Toll-Like Receptors
pubmed:year
2006
pubmed:articleTitle
Toll-like receptor-1, -2, and -6 polymorphisms influence disease extension in inflammatory bowel diseases.
pubmed:affiliation
Department of Gastroenterology, University Hospital Gasthuisberg, Leuven, Belgium. Marieke.Pierik@uz.kuleuven.ac.be
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't