Linked Life Data

17259397

Source:http://linkedlifedata.com/resource/pubmed/id/17259397

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-1-29
pubmed:abstractText
A20 or tumor necrosis factor (TNF)-induced protein 3 (TNFAIP3) is a negative regulator of nuclear factor-kappaB (NF-kappaB). We have investigated whether polymorphisms in this gene are associated with increased atherosclerosis in diabetic patients. Five tag single nucleotide polymorphisms (SNPs) were typed in 479 type 2 diabetic patients from Boston, including 239 coronary artery disease (CAD)-positive case subjects and 240 CAD-negative control subjects. Two tag SNPs (rs5029930 and rs610604) were independently associated with CAD; adjusted odds ratios (ORs) for minor allele carriers were 2.3 (95% CI 1.4-3.8, P = 0.001) and 2.0 (1.3-2.9, P = 0.0008), respectively. The association with rs610604 was dependent on glycemic control, with ORs of 3.9 among subjects with A1C < or =7.0% and 1.2 for those with A1C >7.0% (P for interaction = 0.015). A similar interaction pattern was found among 231 CAD-positive and 332 CAD-negative type 2 diabetic patients from Italy (OR 2.2, P = 0.05 vs. OR 0.9, P = 0.63 in the low vs. high A1C strata, P for interaction = 0.05). Quantitative RT-PCR in blood mononuclear cells from 83 nondiabetic subjects showed that rs610604 and rs5029930 minor allele homozygotes have 30-45% lower levels of A20 mRNA than major allele homozygotes, and heterozygotes have intermediate levels (P = 0.04 and 0.028, respectively). These findings point to variability in the A20/TNFAIP3 gene as a modulator of CAD risk in type 2 diabetes. This effect is mediated by allelic differences in A20 expression.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
56
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
499-505
pubmed:dateRevised
2011-2-3
pubmed:meshHeading
pubmed-meshheading:17259397-Aged, pubmed-meshheading:17259397-Alleles, pubmed-meshheading:17259397-Boston, pubmed-meshheading:17259397-Coronary Artery Disease, pubmed-meshheading:17259397-Diabetes Complications, pubmed-meshheading:17259397-Diabetes Mellitus, Type 2, pubmed-meshheading:17259397-Exons, pubmed-meshheading:17259397-Female, pubmed-meshheading:17259397-Gene Expression Regulation, pubmed-meshheading:17259397-Genotype, pubmed-meshheading:17259397-Homozygote, pubmed-meshheading:17259397-Humans, pubmed-meshheading:17259397-Intracellular Signaling Peptides and Proteins, pubmed-meshheading:17259397-Italy, pubmed-meshheading:17259397-Linkage Disequilibrium, pubmed-meshheading:17259397-Male, pubmed-meshheading:17259397-Middle Aged, pubmed-meshheading:17259397-Nuclear Proteins, pubmed-meshheading:17259397-Polymorphism, Single Nucleotide, pubmed-meshheading:17259397-Risk
pubmed:year
2007
pubmed:articleTitle
Tag polymorphisms at the A20 (TNFAIP3) locus are associated with lower gene expression and increased risk of coronary artery disease in type 2 diabetes.
pubmed:affiliation
Section on Genetics and Epidemiology, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural