Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2010-2-24
pubmed:abstractText
The Receptor for Advanced Glycation End-products (RAGE) belongs to the family of pattern-recognition receptors and is significantly involved in the molecular mechanisms mediating pro-inflammatory action of hyperglycemia in diabetes. The aim of the current study was to elucidate the possible functional impact of the genetic variability in the AGER gene constituting previously identified risk haplotype for diabetic nephropathy (-429C/-374T/2184G) by testing the haplotype-specific effect on the AGER gene transcriptional activity IN VITRO. Promotor and intron 8 constructs carrying respective substitutions were amplified and cloned into pGL3-Basic reporter vector and subsequently used for transfection of HEK293 cells. Following 48hrs incubation in either normo- (5 mM/L) or hyperglycemic (25 mM/L) culture medium luciferase activity was measured to assess transcriptional efficiency. Risk haplotype was associated with the highest transcriptional activity in hyperglycemia and greatest relative increase of activity between normo- and hyperglycemia conditions (approx. 3-times). We conclude that ascertained functional differences in the regulatory regions of the AGER gene might have significant consequences for the development of hyperglycemia-related pathology in diabetics.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1439-3646
pubmed:author
pubmed:copyrightInfo
J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart. New York.
pubmed:issnType
Electronic
pubmed:volume
118
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
93-5
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Functional analysis of the common haplotype in the receptor for advanced glycation end-products gene previously identified as a susceptibility factor for diabetic nephropathy.
pubmed:affiliation
Masaryk University, Dept. of Pathophysiology, Faculty of Medicine, 625 00 Brno, Czech Republic. kankov@med.muni.cz
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't