Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2006-8-3
pubmed:abstractText
Infection and bacteremia are common in sickle cell disease. We hypothesized that, consistent with evidence for the genetic modulation of other disease complications, the risk of developing bacteremia might also be genetically modulated. Accordingly, we studied the association of single nucleotide polymorphisms (SNPs) in candidate genes with the risk of bacteremia in sickle cell anemia. We found significant associations with SNPs in IGF1R and genes of the TGF-beta /BMP pathway (BMP6, TGFBR3, BMPR1A, SMAD6 and SMAD3). We suggest that both IGF1R and the TGF-beta /BMP pathway could play important roles in immune function in sickle cell anemia and their polymorphisms may help identify a "bacteremia-prone" phenotype.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/BMP6 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/BMPR1A protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Bone Morphogenetic Protein 6, http://linkedlifedata.com/resource/pubmed/chemical/Bone Morphogenetic Protein..., http://linkedlifedata.com/resource/pubmed/chemical/Bone Morphogenetic Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Proteoglycans, http://linkedlifedata.com/resource/pubmed/chemical/Receptor, IGF Type 1, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Transforming Growth..., http://linkedlifedata.com/resource/pubmed/chemical/SMAD3 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/SMAD6 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Smad3 Protein, http://linkedlifedata.com/resource/pubmed/chemical/Smad6 Protein, http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta, http://linkedlifedata.com/resource/pubmed/chemical/betaglycan
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1537-6591
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
43
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
593-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:16886151-Adolescent, pubmed-meshheading:16886151-Adult, pubmed-meshheading:16886151-Anemia, Sickle Cell, pubmed-meshheading:16886151-Bacteremia, pubmed-meshheading:16886151-Bone Morphogenetic Protein 6, pubmed-meshheading:16886151-Bone Morphogenetic Protein Receptors, Type I, pubmed-meshheading:16886151-Bone Morphogenetic Proteins, pubmed-meshheading:16886151-Child, pubmed-meshheading:16886151-Child, Preschool, pubmed-meshheading:16886151-Female, pubmed-meshheading:16886151-Genetic Predisposition to Disease, pubmed-meshheading:16886151-Humans, pubmed-meshheading:16886151-Linkage Disequilibrium, pubmed-meshheading:16886151-Male, pubmed-meshheading:16886151-Polymorphism, Genetic, pubmed-meshheading:16886151-Proteoglycans, pubmed-meshheading:16886151-Receptor, IGF Type 1, pubmed-meshheading:16886151-Receptors, Transforming Growth Factor beta, pubmed-meshheading:16886151-Smad3 Protein, pubmed-meshheading:16886151-Smad6 Protein, pubmed-meshheading:16886151-Transforming Growth Factor beta
pubmed:year
2006
pubmed:articleTitle
Association of polymorphisms of IGF1R and genes in the transforming growth factor- beta /bone morphogenetic protein pathway with bacteremia in sickle cell anemia.
pubmed:affiliation
Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural